---
_id: '3541'
abstract:
- lang: eng
text: 'The contribution of the various hippocampal regions to the maintenance of
epileptic activity, induced by stimulation of the perforant path or commissural
system, was examined in the awake rat. Combination of multiple-site recordings
with silicon probes, current source density analysis and unit recordings allowed
for a high spatial resolution of the field events. Following perforant path stimulation,
seizures began in the dentate gyrus, followed by events in the CA3-CA1 regions.
After commissural stimulation, rhythmic bursts in the CA3-CA1 circuitry preceded
the activation of the dentate gyrus. Correlation of events in the different subregions
indicated that the sustained rhythmic afterdischarge (2-6 Hz) could not be explained
by a cycle-by-cycle excitation of principal cell populations in the hippocampal-entorhinal
loop. The primary afterdischarge always terminated in the CA1 region, followed
by the dentate gyrus, CA3 region and the entorhinal cortex. The duration and pattern
of the hippocampal afterdischarge was essentially unaffected by removal of the
entorhinal cortex. The emergence of large population spike bursts coincided with
a decreased discharge of interneurons in both CAI and hilar regions. The majority
of hilar interneurons displayed a strong amplitude decrement prior to the onset
of population spike phase of the afterdischarge. These findings suggest that (i)
afterdischarges can independently arise in the CA3-CA1 and entorhinal-dentate
gyrus circuitries, (ii) reverberation of excitation in the hippocampal-entorhinal
loop is not critical for the maintenance of afterdischarges and (iii) decreased
activity of the interneuronal network may release population bursting of principal
cells. '
acknowledgement: We thank K. Wise and J. Hetke for providing us the silicon probes,
J. J. Chrobak, S. L-W. Leung, G. G. Somjen and R. D. Traub for their comments on
the manuscript. This work was supported by NINDS (NS34994; 1P41RR09754; NS33310)
and the Whitehall Foundation. M. Penttonen was a visiting scholar at Rutgers University,
supported by the Finnish Academy of Sciences and the A. I. Virtanen Institute.
article_processing_charge: No
article_type: original
author:
- first_name: Anatol
full_name: Bragin, Anatol
last_name: Bragin
- first_name: Jozsef L
full_name: Csicsvari, Jozsef L
id: 3FA14672-F248-11E8-B48F-1D18A9856A87
last_name: Csicsvari
orcid: 0000-0002-5193-4036
- first_name: Markku
full_name: Penttonen, Markku
last_name: Penttonen
- first_name: György
full_name: Buzsáki, György
last_name: Buzsáki
citation:
ama: 'Bragin A, Csicsvari JL, Penttonen M, Buzsáki G. Epileptic afterdischarge in
the hippocampal-entorhinal system: Current source density and unit studies. Neuroscience.
1997;76(4):1187-1203. doi:10.1016/S0306-4522(96)00446-0'
apa: 'Bragin, A., Csicsvari, J. L., Penttonen, M., & Buzsáki, G. (1997). Epileptic
afterdischarge in the hippocampal-entorhinal system: Current source density and
unit studies. Neuroscience. Elsevier. https://doi.org/10.1016/S0306-4522(96)00446-0'
chicago: 'Bragin, Anatol, Jozsef L Csicsvari, Markku Penttonen, and György Buzsáki.
“Epileptic Afterdischarge in the Hippocampal-Entorhinal System: Current Source
Density and Unit Studies.” Neuroscience. Elsevier, 1997. https://doi.org/10.1016/S0306-4522(96)00446-0.'
ieee: 'A. Bragin, J. L. Csicsvari, M. Penttonen, and G. Buzsáki, “Epileptic afterdischarge
in the hippocampal-entorhinal system: Current source density and unit studies,”
Neuroscience, vol. 76, no. 4. Elsevier, pp. 1187–1203, 1997.'
ista: 'Bragin A, Csicsvari JL, Penttonen M, Buzsáki G. 1997. Epileptic afterdischarge
in the hippocampal-entorhinal system: Current source density and unit studies.
Neuroscience. 76(4), 1187–1203.'
mla: 'Bragin, Anatol, et al. “Epileptic Afterdischarge in the Hippocampal-Entorhinal
System: Current Source Density and Unit Studies.” Neuroscience, vol. 76,
no. 4, Elsevier, 1997, pp. 1187–203, doi:10.1016/S0306-4522(96)00446-0.'
short: A. Bragin, J.L. Csicsvari, M. Penttonen, G. Buzsáki, Neuroscience 76 (1997)
1187–1203.
date_created: 2018-12-11T12:03:52Z
date_published: 1997-01-15T00:00:00Z
date_updated: 2022-08-19T11:53:06Z
day: '15'
doi: 10.1016/S0306-4522(96)00446-0
extern: '1'
external_id:
pmid:
- '9027878'
fulldoi: https://doi.org/10.1016/S0306-4522(96)00446-0
intvolume: ' 76'
issue: '4'
language:
- iso: eng
month: '01'
oa_version: None
page: 1187 - 1203
pmid: 1
publication: Neuroscience
publication_identifier:
issn:
- 0306-4522
publication_status: published
publisher: Elsevier
publist_id: '2844'
quality_controlled: '1'
status: public
title: 'Epileptic afterdischarge in the hippocampal-entorhinal system: Current source
density and unit studies'
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 76
year: '1997'
...
---
_id: '4289'
abstract:
- lang: eng
text: A worldwide survey of polymorphic molecular markers shows that the human population
is genetically homogeneous, in close agreement with evidence from quite different
genes and traits.
article_processing_charge: No
article_type: letter_note
author:
- first_name: Nicholas H
full_name: Barton, Nicholas H
id: 4880FE40-F248-11E8-B48F-1D18A9856A87
last_name: Barton
orcid: 0000-0002-8548-5240
citation:
ama: 'Barton NH. Population genetics: A new apportionment of human diversity. Current
Biology. 1997;7(12):757-758. doi:10.1016/S0960-9822(06)00397-6'
apa: 'Barton, N. H. (1997). Population genetics: A new apportionment of human diversity.
Current Biology. Cell Press. https://doi.org/10.1016/S0960-9822(06)00397-6'
chicago: 'Barton, Nicholas H. “Population Genetics: A New Apportionment of Human
Diversity.” Current Biology. Cell Press, 1997. https://doi.org/10.1016/S0960-9822(06)00397-6.'
ieee: 'N. H. Barton, “Population genetics: A new apportionment of human diversity,”
Current Biology, vol. 7, no. 12. Cell Press, pp. 757–758, 1997.'
ista: 'Barton NH. 1997. Population genetics: A new apportionment of human diversity.
Current Biology. 7(12), 757–758.'
mla: 'Barton, Nicholas H. “Population Genetics: A New Apportionment of Human Diversity.”
Current Biology, vol. 7, no. 12, Cell Press, 1997, pp. 757–58, doi:10.1016/S0960-9822(06)00397-6.'
short: N.H. Barton, Current Biology 7 (1997) 757–758.
date_created: 2018-12-11T12:08:04Z
date_published: 1997-12-01T00:00:00Z
date_updated: 2022-08-17T13:07:08Z
day: '01'
doi: 10.1016/S0960-9822(06)00397-6
extern: '1'
fulldoi: https://doi.org/10.1016/S0960-9822(06)00397-6
intvolume: ' 7'
issue: '12'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.sciencedirect.com/science/article/pii/S0960982206003976?via%3Dihub
month: '12'
oa: 1
oa_version: Published Version
page: 757 - 758
publication: Current Biology
publication_identifier:
issn:
- 0960-9822
publication_status: published
publisher: Cell Press
publist_id: '1788'
quality_controlled: '1'
status: public
title: 'Population genetics: A new apportionment of human diversity'
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 7
year: '1997'
...
---
OA_place: repository
OA_type: green
_id: '17828'
abstract:
- lang: eng
text: We quantify the consequences of intergalactic dust produced by the first Type
II supernovae in the universe. The fraction of gas converted into stars is calibrated
based on the observed C/H ratio in the intergalactic medium at z = 3, assuming
a Scalo mass function for the stars. The associated dust absorbs starlight energy
and emits it at longer wavelengths. For a uniform mix of metals and dust with
the intergalactic gas, we find that the dust distorts the microwave background
spectrum by a y-parameter in the range (0.06-6) × 10-5 (MSN/0.3 M☉), where MSN
is the average mass of dust produced per supernova. The opacity of intergalactic
dust to infrared sources at redshifts of z ≳ 10 is significant, τdust = (0.1-1)
× (MSN/0.3 M☉), and could be detected with the Next Generation Space Telescope.
Although dust suppresses the Lyα emission from early sources, the redshifts of
star clusters at z = 10-35 can be easily inferred from the Lyman limit break in
their infrared spectrum between 1 and 3.5 μm.
article_processing_charge: No
article_type: original
arxiv: 1
author:
- first_name: Abraham
full_name: Loeb, Abraham
last_name: Loeb
- first_name: Zoltán
full_name: Haiman, Zoltán
id: 7c006e8c-cc0d-11ee-8322-cb904ef76f36
last_name: Haiman
orcid: 0000-0003-3633-5403
citation:
ama: Loeb A, Haiman Z. Signatures of intergalactic dust from the first supernovae.
The Astrophysical Journal. 1997;490(2):571-576. doi:10.1086/304919
apa: Loeb, A., & Haiman, Z. (1997). Signatures of intergalactic dust from the
first supernovae. The Astrophysical Journal. American Astronomical Society.
https://doi.org/10.1086/304919
chicago: Loeb, Abraham, and Zoltán Haiman. “Signatures of Intergalactic Dust from
the First Supernovae.” The Astrophysical Journal. American Astronomical
Society, 1997. https://doi.org/10.1086/304919.
ieee: A. Loeb and Z. Haiman, “Signatures of intergalactic dust from the first supernovae,”
The Astrophysical Journal, vol. 490, no. 2. American Astronomical Society,
pp. 571–576, 1997.
ista: Loeb A, Haiman Z. 1997. Signatures of intergalactic dust from the first supernovae.
The Astrophysical Journal. 490(2), 571–576.
mla: Loeb, Abraham, and Zoltán Haiman. “Signatures of Intergalactic Dust from the
First Supernovae.” The Astrophysical Journal, vol. 490, no. 2, American
Astronomical Society, 1997, pp. 571–76, doi:10.1086/304919.
short: A. Loeb, Z. Haiman, The Astrophysical Journal 490 (1997) 571–576.
date_created: 2024-09-06T12:08:42Z
date_published: 1997-12-01T00:00:00Z
date_updated: 2024-11-13T07:14:38Z
day: '01'
doi: 10.1086/304919
extern: '1'
external_id:
arxiv:
- astro-ph/9704133
fulldoi: https://doi.org/10.1086/304919
intvolume: ' 490'
issue: '2'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.48550/arXiv.astro-ph/9704133
month: '12'
oa: 1
oa_version: Preprint
page: 571-576
publication: The Astrophysical Journal
publication_identifier:
eissn:
- 1538-4357
issn:
- 0004-637X
publication_status: published
publisher: American Astronomical Society
quality_controlled: '1'
scopus_import: '1'
status: public
title: Signatures of intergalactic dust from the first supernovae
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 490
year: '1997'
...
---
_id: '2562'
abstract:
- lang: eng
text: A monoclonal antibody against a metabotropic glutamate receptor, mGluR2, was
produced by using a glutathione S-transferase (GST) fusion protein containing
an N-terminal sequence of rat mGluR2. Intense mGluR2-like immunoreactivity (mGluR2-LI)
was seen mainly in neuropil of the cerebral cortical regions, hippocampus, olfactory
bulb, some diencephalic nuclei, dorsal cochlear nucleus and cerebellar cortex.
In the cerebellar cortex, mGluR2-LI was seen only in Golgi cells. In Ammon's hem,
mGluR2-LI was marked in the stratum lucidum of CA3 and the stratum lacunosum-moleculare
of CA1-CA3, but not detected in the stratum pyramidale. The results indicate that
mGluR2 is located not only presynaptically but also postsynaptically.
acknowledgement: We are grateful to Mr. Akira Uesugi for photographic help.
article_processing_charge: No
article_type: original
author:
- first_name: Akio
full_name: Neki, Akio
last_name: Neki
- first_name: Hitoshi
full_name: Ohishi, Hitoshi
last_name: Ohishi
- first_name: Takeshi
full_name: Kaneko, Takeshi
last_name: Kaneko
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Shigetada
full_name: Nakanishi, Shigetada
last_name: Nakanishi
- first_name: Noboru
full_name: Mizuno, Noboru
last_name: Mizuno
citation:
ama: 'Neki A, Ohishi H, Kaneko T, Shigemoto R, Nakanishi S, Mizuno N. Pre- and postsynaptic
localization of a metabotropic glutamate receptor, mGluR2, in the rat brain: An
immunohistochemical study with a monoclonal antibody. Neuroscience Letters.
1996;202(3):197-200. doi:10.1016/0304-3940(95)12248-6'
apa: 'Neki, A., Ohishi, H., Kaneko, T., Shigemoto, R., Nakanishi, S., & Mizuno,
N. (1996). Pre- and postsynaptic localization of a metabotropic glutamate receptor,
mGluR2, in the rat brain: An immunohistochemical study with a monoclonal antibody.
Neuroscience Letters. Elsevier. https://doi.org/10.1016/0304-3940(95)12248-6'
chicago: 'Neki, Akio, Hitoshi Ohishi, Takeshi Kaneko, Ryuichi Shigemoto, Shigetada
Nakanishi, and Noboru Mizuno. “Pre- and Postsynaptic Localization of a Metabotropic
Glutamate Receptor, MGluR2, in the Rat Brain: An Immunohistochemical Study with
a Monoclonal Antibody.” Neuroscience Letters. Elsevier, 1996. https://doi.org/10.1016/0304-3940(95)12248-6.'
ieee: 'A. Neki, H. Ohishi, T. Kaneko, R. Shigemoto, S. Nakanishi, and N. Mizuno,
“Pre- and postsynaptic localization of a metabotropic glutamate receptor, mGluR2,
in the rat brain: An immunohistochemical study with a monoclonal antibody,” Neuroscience
Letters, vol. 202, no. 3. Elsevier, pp. 197–200, 1996.'
ista: 'Neki A, Ohishi H, Kaneko T, Shigemoto R, Nakanishi S, Mizuno N. 1996. Pre-
and postsynaptic localization of a metabotropic glutamate receptor, mGluR2, in
the rat brain: An immunohistochemical study with a monoclonal antibody. Neuroscience
Letters. 202(3), 197–200.'
mla: 'Neki, Akio, et al. “Pre- and Postsynaptic Localization of a Metabotropic Glutamate
Receptor, MGluR2, in the Rat Brain: An Immunohistochemical Study with a Monoclonal
Antibody.” Neuroscience Letters, vol. 202, no. 3, Elsevier, 1996, pp. 197–200,
doi:10.1016/0304-3940(95)12248-6.'
short: A. Neki, H. Ohishi, T. Kaneko, R. Shigemoto, S. Nakanishi, N. Mizuno, Neuroscience
Letters 202 (1996) 197–200.
date_created: 2018-12-11T11:58:24Z
date_published: 1996-01-05T00:00:00Z
date_updated: 2022-08-12T12:04:18Z
day: '05'
doi: 10.1016/0304-3940(95)12248-6
extern: '1'
external_id:
pmid:
- '8848265'
fulldoi: https://doi.org/10.1016/0304-3940(95)12248-6
intvolume: ' 202'
issue: '3'
language:
- iso: eng
month: '01'
oa_version: None
page: 197 - 200
pmid: 1
publication: Neuroscience Letters
publication_identifier:
issn:
- 0304-3940
publication_status: published
publisher: Elsevier
publist_id: '4335'
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Pre- and postsynaptic localization of a metabotropic glutamate receptor, mGluR2,
in the rat brain: An immunohistochemical study with a monoclonal antibody'
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 202
year: '1996'
...
---
_id: '2573'
abstract:
- lang: eng
text: Developmental changes of the distribution pattern of substance P receptor
(SPR) were investigated immunohistochemically in the rat striatum. The SPR immunoreactivity
in the striatum first emerged at postnatal day 1 and transiently showed a patchy
pattern of distribution until it displayed the adult pattern of homogeneous distribution
by the end of the third postnatal week. The SPR-immunoreactive patches were most
marked in the medial and dorsolateral parts of the striatum, as well as in the
subcallosal streak. They matched tyrosine hydroxylase-enriched areas and, conversely,
avoided calbindin-enriched zones. No neurons within the SPR-immunoreactive patches
contained either choline acetyltransferase or somatostatin, which is known to
be contained in intrinsic neurons in the striatum. The vast majority of SPR-immunoreactive
patch neurons also contained DARPP-32, a phosphoprotein that is expressed in striatal
projection neurons with D1 dopamine receptor. The results indicate that SPR-immunoreactive
patches which appear transiently in the developing striatum are in register with
the striatal patch compartment, and that SPR immunoreactivity within these patches
may be expressed on projection neurons rather than intrinsic neurons. Such SPR
immunoreactivity in projection neurons in striatal patches may fade out in adulthood.
acknowledgement: "We thank Mr. Akira Uesugi and Ms. Miao-Li Zhang for their photographic
help. We are also grateful for the support of Dr. Kajitaro Morita in the Morita
Clinic of Internal Medicine and Pediatrics at Kadoma, Osaka, Japan, and for the
support of Drs. Satoru Fukuchi, Ritsu Hayashi, Sozaburo Hayashi, Mizuho Katsurada,
Yutaka Kitani, Keiko Kumagai, Toshihiko Kuroda., Hiroshi Matsubara, Hiroshi Matsushita,
Chisato Minakuchi, Gonpei Niwa, Hajime Oda, Masahiko Ohbayashi, Sei-ichi Ohbayashi,
Hiroyasu Ohtsuka, Shigeo Tamaki, Eizo Watanabe, Kazuo Yoshino, and Toshiaki Yoshino.
This work was supported in part by Grants-in-Aid for Special Research on Priority
Areas 05267104, Scientific Research (B) \r\n5454658, and Scientific Research (C)
05680658 and 06680735 from the Ministry of Education, Science and Culture of Japan."
article_processing_charge: No
article_type: original
author:
- first_name: Hironobu
full_name: Tokuno, Hironobu
last_name: Tokuno
- first_name: Masahiko
full_name: Takada, Masahiko
last_name: Takada
- first_name: Takeshi
full_name: Kaneko, Takeshi
last_name: Kaneko
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Noboru
full_name: Mizuno, Noboru
last_name: Mizuno
citation:
ama: Tokuno H, Takada M, Kaneko T, Shigemoto R, Mizuno N. Patchy distribution of
substance P receptor immunoreactivity in the developing rat striatum. Developmental
Brain Research. 1996;95(1):107-117. doi:10.1016/0165-3806(96)00080-6
apa: Tokuno, H., Takada, M., Kaneko, T., Shigemoto, R., & Mizuno, N. (1996).
Patchy distribution of substance P receptor immunoreactivity in the developing
rat striatum. Developmental Brain Research. Elsevier. https://doi.org/10.1016/0165-3806(96)00080-6
chicago: Tokuno, Hironobu, Masahiko Takada, Takeshi Kaneko, Ryuichi Shigemoto, and
Noboru Mizuno. “Patchy Distribution of Substance P Receptor Immunoreactivity in
the Developing Rat Striatum.” Developmental Brain Research. Elsevier, 1996.
https://doi.org/10.1016/0165-3806(96)00080-6.
ieee: H. Tokuno, M. Takada, T. Kaneko, R. Shigemoto, and N. Mizuno, “Patchy distribution
of substance P receptor immunoreactivity in the developing rat striatum,” Developmental
Brain Research, vol. 95, no. 1. Elsevier, pp. 107–117, 1996.
ista: Tokuno H, Takada M, Kaneko T, Shigemoto R, Mizuno N. 1996. Patchy distribution
of substance P receptor immunoreactivity in the developing rat striatum. Developmental
Brain Research. 95(1), 107–117.
mla: Tokuno, Hironobu, et al. “Patchy Distribution of Substance P Receptor Immunoreactivity
in the Developing Rat Striatum.” Developmental Brain Research, vol. 95,
no. 1, Elsevier, 1996, pp. 107–17, doi:10.1016/0165-3806(96)00080-6.
short: H. Tokuno, M. Takada, T. Kaneko, R. Shigemoto, N. Mizuno, Developmental Brain
Research 95 (1996) 107–117.
date_created: 2018-12-11T11:58:28Z
date_published: 1996-08-20T00:00:00Z
date_updated: 2022-08-11T12:07:34Z
day: '20'
doi: 10.1016/0165-3806(96)00080-6
extern: '1'
external_id:
pmid:
- '8873981 '
fulldoi: https://doi.org/10.1016/0165-3806(96)00080-6
intvolume: ' 95'
issue: '1'
language:
- iso: eng
month: '08'
oa_version: None
page: 107 - 117
pmid: 1
publication: Developmental Brain Research
publication_identifier:
issn:
- 0165-3806
publication_status: published
publisher: Elsevier
publist_id: '4325'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Patchy distribution of substance P receptor immunoreactivity in the developing
rat striatum
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 95
year: '1996'
...
---
_id: '4025'
abstract:
- lang: eng
text: Questions of chemical reactivity can often be cast as questions of molecular
geometry. Common geometric models for proteins and other molecules are the space-filling
diagram, the solvent accessible surface and the molecular surface. In this paper
we present a new approach to triangulating the surface of a molecule under the
three models, which is fast, robust, and results in topologically correct triangulations.
Our computations are based on a simplicial complex dual to the molecule models.
All proposed algorithms are parallelizable.
acknowledgement: 'The research of both authors is partially supported by the Office
of Naval Research. Herbert Edelsbrunner is also supported through the Alan T. Waterman
award, grant CCR-9118874. '
article_processing_charge: No
article_type: original
author:
- first_name: Nataraj
full_name: Akkiraju, Nataraj
last_name: Akkiraju
- first_name: Herbert
full_name: Edelsbrunner, Herbert
id: 3FB178DA-F248-11E8-B48F-1D18A9856A87
last_name: Edelsbrunner
orcid: 0000-0002-9823-6833
citation:
ama: Akkiraju N, Edelsbrunner H. Triangulating the surface of a molecule. Discrete
Applied Mathematics. 1996;71(1-3):5-22. doi:10.1016/S0166-218X(96)00054-6
apa: Akkiraju, N., & Edelsbrunner, H. (1996). Triangulating the surface of a
molecule. Discrete Applied Mathematics. Elsevier. https://doi.org/10.1016/S0166-218X(96)00054-6
chicago: Akkiraju, Nataraj, and Herbert Edelsbrunner. “Triangulating the Surface
of a Molecule.” Discrete Applied Mathematics. Elsevier, 1996. https://doi.org/10.1016/S0166-218X(96)00054-6.
ieee: N. Akkiraju and H. Edelsbrunner, “Triangulating the surface of a molecule,”
Discrete Applied Mathematics, vol. 71, no. 1–3. Elsevier, pp. 5–22, 1996.
ista: Akkiraju N, Edelsbrunner H. 1996. Triangulating the surface of a molecule.
Discrete Applied Mathematics. 71(1–3), 5–22.
mla: Akkiraju, Nataraj, and Herbert Edelsbrunner. “Triangulating the Surface of
a Molecule.” Discrete Applied Mathematics, vol. 71, no. 1–3, Elsevier,
1996, pp. 5–22, doi:10.1016/S0166-218X(96)00054-6.
short: N. Akkiraju, H. Edelsbrunner, Discrete Applied Mathematics 71 (1996) 5–22.
date_created: 2018-12-11T12:06:30Z
date_published: 1996-12-05T00:00:00Z
date_updated: 2022-08-09T14:06:12Z
day: '05'
doi: 10.1016/S0166-218X(96)00054-6
extern: '1'
fulldoi: https://doi.org/10.1016/S0166-218X(96)00054-6
intvolume: ' 71'
issue: 1-3
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.sciencedirect.com/science/article/pii/S0166218X96000546?via%3Dihub
month: '12'
oa: 1
oa_version: Published Version
page: 5 - 22
publication: Discrete Applied Mathematics
publication_identifier:
issn:
- 0166-218X
publication_status: published
publisher: Elsevier
publist_id: '2102'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Triangulating the surface of a molecule
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 71
year: '1996'
...
---
_id: '4151'
abstract:
- lang: eng
text: 'Jaws and branchial arches together are a basic, segmented feature of the
vertebrate head, Seven arches develop in the zebrafish embryo (Danio rerio), derived
largely from neural crest cells that form the cartilaginous skeleton, In this
and the following paper we describe the phenotypes of 109 arch mutants, focusing
here on three classes that affect the posterior pharyngeal arches, including the
hyoid and five gill-bearing arches, In lockjaw, the hyoid arch is strongly reduced
and subsets of branchial arches do not develop, Mutants of a large second class,
designated the flathead group, lack several adjacent branchial arches and their
associated cartilages. Five alleles at the flathead locus all lead to larvae that
lack arches 4-6, Among 34 other flathead group members complementation tests are
incomplete, but at least six unique phenotypes can be distinguished, These all
delete continuous stretches of adjacent branchial arches and unpaired cartilages
in the ventral midline, Many show cell death in the midbrain, from which some
neural crest precursors of the arches originate, lockjaw and a few mutants in
the flathead group, including pistachio, affect both jaw cartilage and pigmentation,
reflecting essential functions of these genes in at least two neural crest lineages,
Mutants of a third class, including boxer, dackel and pincher, affect pectoral
fins and axonal trajectories in the brain, as well as the arches. Their skeletal
phenotypes suggest that they disrupt cartilage morphogenesis in all arches, Our
results suggest that there are sets of genes that: (1) specify neural crest cells
in groups of adjacent head segments, and (2) function in common genetic pathways
in a variety of tissues including the brain, pectoral fins and pigment cells as
well as pharyngeal arches.'
acknowledgement: We thank Drs Charles Kimmel, Philip Ingham, Paula Mabee and members
of the Ingham lab for critical comments on the manuscript.
article_processing_charge: No
article_type: original
author:
- first_name: Thomas
full_name: Schilling, Thomas
last_name: Schilling
- first_name: Tatjana
full_name: Piotrowski, Tatjana
last_name: Piotrowski
- first_name: Heiner
full_name: Grandel, Heiner
last_name: Grandel
- first_name: Michael
full_name: Brand, Michael
last_name: Brand
- first_name: Carl-Philipp J
full_name: Heisenberg, Carl-Philipp J
id: 39427864-F248-11E8-B48F-1D18A9856A87
last_name: Heisenberg
orcid: 0000-0002-0912-4566
- first_name: Yunjin
full_name: Jiang, Yunjin
last_name: Jiang
- first_name: Dirk
full_name: Beuchle, Dirk
last_name: Beuchle
- first_name: Matthias
full_name: Hammerschmidt, Matthias
last_name: Hammerschmidt
- first_name: Donald
full_name: Kane, Donald
last_name: Kane
- first_name: Mary
full_name: Mullins, Mary
last_name: Mullins
- first_name: Fredericus
full_name: Van Eeden, Fredericus
last_name: Van Eeden
- first_name: Robert
full_name: Kelsh, Robert
last_name: Kelsh
- first_name: Makoto
full_name: Furutani Seiki, Makoto
last_name: Furutani Seiki
- first_name: Michael
full_name: Granato, Michael
last_name: Granato
- first_name: Pascal
full_name: Haffter, Pascal
last_name: Haffter
- first_name: Jörg
full_name: Odenthal, Jörg
last_name: Odenthal
- first_name: Rachel
full_name: Warga, Rachel
last_name: Warga
- first_name: Torsten
full_name: Trowe, Torsten
last_name: Trowe
- first_name: Christiane
full_name: Nüsslein Volhard, Christiane
last_name: Nüsslein Volhard
citation:
ama: 'Schilling T, Piotrowski T, Grandel H, et al. Jaw and branchial arch mutants
in zebrafish I: Branchial arches. Development. 1996;123(1):329-344. doi:10.1242/dev.123.1.329'
apa: 'Schilling, T., Piotrowski, T., Grandel, H., Brand, M., Heisenberg, C.-P. J.,
Jiang, Y., … Nüsslein Volhard, C. (1996). Jaw and branchial arch mutants in zebrafish
I: Branchial arches. Development. Company of Biologists. https://doi.org/10.1242/dev.123.1.329'
chicago: 'Schilling, Thomas, Tatjana Piotrowski, Heiner Grandel, Michael Brand,
Carl-Philipp J Heisenberg, Yunjin Jiang, Dirk Beuchle, et al. “Jaw and Branchial
Arch Mutants in Zebrafish I: Branchial Arches.” Development. Company of
Biologists, 1996. https://doi.org/10.1242/dev.123.1.329.'
ieee: 'T. Schilling et al., “Jaw and branchial arch mutants in zebrafish
I: Branchial arches,” Development, vol. 123, no. 1. Company of Biologists,
pp. 329–344, 1996.'
ista: 'Schilling T, Piotrowski T, Grandel H, Brand M, Heisenberg C-PJ, Jiang Y,
Beuchle D, Hammerschmidt M, Kane D, Mullins M, Van Eeden F, Kelsh R, Furutani
Seiki M, Granato M, Haffter P, Odenthal J, Warga R, Trowe T, Nüsslein Volhard
C. 1996. Jaw and branchial arch mutants in zebrafish I: Branchial arches. Development.
123(1), 329–344.'
mla: 'Schilling, Thomas, et al. “Jaw and Branchial Arch Mutants in Zebrafish I:
Branchial Arches.” Development, vol. 123, no. 1, Company of Biologists,
1996, pp. 329–44, doi:10.1242/dev.123.1.329.'
short: T. Schilling, T. Piotrowski, H. Grandel, M. Brand, C.-P.J. Heisenberg, Y.
Jiang, D. Beuchle, M. Hammerschmidt, D. Kane, M. Mullins, F. Van Eeden, R. Kelsh,
M. Furutani Seiki, M. Granato, P. Haffter, J. Odenthal, R. Warga, T. Trowe, C.
Nüsslein Volhard, Development 123 (1996) 329–344.
date_created: 2018-12-11T12:07:15Z
date_published: 1996-12-01T00:00:00Z
date_updated: 2022-08-08T08:41:00Z
day: '01'
doi: 10.1242/dev.123.1.329
extern: '1'
external_id:
pmid:
- '9007253'
fulldoi: https://doi.org/10.1242/dev.123.1.329
intvolume: ' 123'
issue: '1'
language:
- iso: eng
month: '12'
oa_version: None
page: 329 - 344
pmid: 1
publication: Development
publication_identifier:
issn:
- 0950-1991
publication_status: published
publisher: Company of Biologists
publist_id: '1968'
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Jaw and branchial arch mutants in zebrafish I: Branchial arches'
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 123
year: '1996'
...
---
_id: '4170'
abstract:
- lang: eng
text: We identified 6 genes that are essential for specifying ventral regions of
the early zebrafish embryo, Mutations in these genes cause an expansion of structures
normally derived from dorsal-lateral regions of the blastula at the expense of
ventrally derived structures, A series of phenotypes of varied strengths is observed
with different alleles of these mutants, The weakest phenotype is a reduction
in the ventral tail fin, observed as a dominant phenotype of swirl, piggytail,
and somitabun and a recessive phenotype of min fin, lost-a-fin and some piggytail
alleles, With increasing phenotypic strength, the blood and pronephric anlagen
are also reduced or absent, while the paraxial mesoderm and anterior neuroectoderm
is progressively expanded, In the strong phenotypes, displayed by homozygous embryos
of snailhouse, swirl and somitabun, the somites circle around the embryo and the
midbrain region is expanded laterally, Several mutations in this group of genes
are semidominant as well as recessive indicating a strong dosage sensitivity of
the processes involved, Mutations in the piggytail gene display an unusual dominance
that depends on both a maternal and zygotic heterozygous genotype, while somitabun
is a fully penetrant dominant maternal-effect mutation, The similar and overlapping
phenotypes of mutants of the 6 genes identified suggest that they function in
a common pathway, which begins in oogenesis, but also depends on factors provided
after the onset of zygotic transcription, presumably during blastula stages, This
pathway provides ventral positional information, counteracting the dorsalizing
instructions of the organizer, which is localized in the dorsal shield.
acknowledgement: 'We would like to thank: Eric Weinberg, and David Ransom and Leonard
Zon for providing the myoD and gata1 cDNA clone, respectively, prior to publication;
David Ransom for pointing out the histological blood staining method; J. S. Joly
for the eve1 cDNA clone; Mary Ellen Lane, Siegfried Roth, Stefan Schulte-Merker,
Herbert Steinbeiser for helpful comments on the manuscript; and very special thanks
to Karin Finger-Miller for technical support, as well as to Hans-Martin Maischein,
Amanda Wilson, Jörg Zeller, and Cosima Fabian. This work was supported by an NIH
postdoctoral fellowship to M. C. M.'
article_processing_charge: No
article_type: original
author:
- first_name: Mary
full_name: Mullins, Mary
last_name: Mullins
- first_name: Matthias
full_name: Hammerschmidt, Matthias
last_name: Hammerschmidt
- first_name: Donald
full_name: Kane, Donald
last_name: Kane
- first_name: Jörg
full_name: Odenthal, Jörg
last_name: Odenthal
- first_name: Michael
full_name: Brand, Michael
last_name: Brand
- first_name: Fredericus
full_name: Van Eeden, Fredericus
last_name: Van Eeden
- first_name: Makoto
full_name: Furutani Seiki, Makoto
last_name: Furutani Seiki
- first_name: Michael
full_name: Granato, Michael
last_name: Granato
- first_name: Pascal
full_name: Haffter, Pascal
last_name: Haffter
- first_name: Carl-Philipp J
full_name: Heisenberg, Carl-Philipp J
id: 39427864-F248-11E8-B48F-1D18A9856A87
last_name: Heisenberg
orcid: 0000-0002-0912-4566
- first_name: Yunjin
full_name: Jiang, Yunjin
last_name: Jiang
- first_name: Robert
full_name: Kelsh, Robert
last_name: Kelsh
- first_name: Christiane
full_name: Nüsslein Volhard, Christiane
last_name: Nüsslein Volhard
citation:
ama: 'Mullins M, Hammerschmidt M, Kane D, et al. Genes establishing dorsoventral
pattern formation in the zebrafish embryo: The ventral specifying genes. Development.
1996;123(1):81-93. doi:10.1242/dev.123.1.81'
apa: 'Mullins, M., Hammerschmidt, M., Kane, D., Odenthal, J., Brand, M., Van Eeden,
F., … Nüsslein Volhard, C. (1996). Genes establishing dorsoventral pattern formation
in the zebrafish embryo: The ventral specifying genes. Development. Company
of Biologists. https://doi.org/10.1242/dev.123.1.81'
chicago: 'Mullins, Mary, Matthias Hammerschmidt, Donald Kane, Jörg Odenthal, Michael
Brand, Fredericus Van Eeden, Makoto Furutani Seiki, et al. “Genes Establishing
Dorsoventral Pattern Formation in the Zebrafish Embryo: The Ventral Specifying
Genes.” Development. Company of Biologists, 1996. https://doi.org/10.1242/dev.123.1.81.'
ieee: 'M. Mullins et al., “Genes establishing dorsoventral pattern formation
in the zebrafish embryo: The ventral specifying genes,” Development, vol.
123, no. 1. Company of Biologists, pp. 81–93, 1996.'
ista: 'Mullins M, Hammerschmidt M, Kane D, Odenthal J, Brand M, Van Eeden F, Furutani
Seiki M, Granato M, Haffter P, Heisenberg C-PJ, Jiang Y, Kelsh R, Nüsslein Volhard
C. 1996. Genes establishing dorsoventral pattern formation in the zebrafish embryo:
The ventral specifying genes. Development. 123(1), 81–93.'
mla: 'Mullins, Mary, et al. “Genes Establishing Dorsoventral Pattern Formation in
the Zebrafish Embryo: The Ventral Specifying Genes.” Development, vol.
123, no. 1, Company of Biologists, 1996, pp. 81–93, doi:10.1242/dev.123.1.81.'
short: M. Mullins, M. Hammerschmidt, D. Kane, J. Odenthal, M. Brand, F. Van Eeden,
M. Furutani Seiki, M. Granato, P. Haffter, C.-P.J. Heisenberg, Y. Jiang, R. Kelsh,
C. Nüsslein Volhard, Development 123 (1996) 81–93.
date_created: 2018-12-11T12:07:22Z
date_published: 1996-12-01T00:00:00Z
date_updated: 2022-08-05T12:01:06Z
day: '01'
doi: 10.1242/dev.123.1.81
extern: '1'
external_id:
pmid:
- '9007231'
fulldoi: https://doi.org/10.1242/dev.123.1.81
intvolume: ' 123'
issue: '1'
language:
- iso: eng
month: '12'
oa_version: None
page: 81 - 93
pmid: 1
publication: Development
publication_identifier:
issn:
- 0950-1991
publication_status: published
publisher: Company of Biologists
publist_id: '1951'
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Genes establishing dorsoventral pattern formation in the zebrafish embryo:
The ventral specifying genes'
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 123
year: '1996'
...
---
_id: '4189'
abstract:
- lang: eng
text: 'This report describes mutants of the zebrafish having phenotypes causing
a general arrest in early morphogenesis. These mutants identify a group of loci
making up about 20% of the loci identified by mutants with visible morphological
phenotypes within the first day of development. There are 12 Class I mutants,
which fall into 5 complementation groups and have cells that lyse before morphological
defects are observed. Mutants at three loci, speed bump, ogre and zombie, display
abnormal nuclei. The 8 Class II mutants, which fall into 6 complementation groups,
arrest development before cell lysis is observed. These mutants seemingly stop
development in the late segmentation stages, and maintain a body shape similar
to a 20 hour embryo. Mutations in speed bump, ogre, zombie, specter, poltergeist
and troll were tested for cell lethality by transplanting mutant cells into wild-type
hosts. With poltergeist, transplanted mutant cells all survive. The remainder
of the mutants tested were autonomously but conditionally lethal: mutant cells,
most of which lyse, sometimes survive to become notochord, muscles, or, in rare
cases, large neurons, all cell types which become postmitotic in the gastrula.
Some of the genes of the early arrest group may be necessary for progression though
the cell cycle; if so, the survival of early differentiating cells may be based
on having their terminal mitosis before the zygotic requirement for these genes.'
acknowledgement: We thank Dr Adam Felsenfeld for his careful comments on earlier drafts
of this manuscript, D. A. K. also thanks the two anonymous referees who patiently
pointed out a number of ‘speed bumps’ in the first submitted draft of this manuscript.
This work was supported in part by a grant from the National Institutes of Health
to D. A. K.
article_processing_charge: No
article_type: original
author:
- first_name: Donald
full_name: Kane, Donald
last_name: Kane
- first_name: Hans
full_name: Maischein, Hans
last_name: Maischein
- first_name: Michael
full_name: Brand, Michael
last_name: Brand
- first_name: Fredericus
full_name: Van Eeden, Fredericus
last_name: Van Eeden
- first_name: Makoto
full_name: Furutani Seiki, Makoto
last_name: Furutani Seiki
- first_name: Michael
full_name: Granato, Michael
last_name: Granato
- first_name: Pascal
full_name: Haffter, Pascal
last_name: Haffter
- first_name: Matthias
full_name: Hammerschmidt, Matthias
last_name: Hammerschmidt
- first_name: Carl-Philipp J
full_name: Heisenberg, Carl-Philipp J
id: 39427864-F248-11E8-B48F-1D18A9856A87
last_name: Heisenberg
orcid: 0000-0002-0912-4566
- first_name: Yunjin
full_name: Jiang, Yunjin
last_name: Jiang
- first_name: Robert
full_name: Kelsh, Robert
last_name: Kelsh
- first_name: Mary
full_name: Mullins, Mary
last_name: Mullins
- first_name: Jörg
full_name: Odenthal, Jörg
last_name: Odenthal
- first_name: Rachel
full_name: Warga, Rachel
last_name: Warga
- first_name: Christiane
full_name: Nüsslein Volhard, Christiane
last_name: Nüsslein Volhard
citation:
ama: Kane D, Maischein H, Brand M, et al. The zebrafish early arrest mutants. Development.
1996;123(1):57-66. doi:10.1242/dev.123.1.57
apa: Kane, D., Maischein, H., Brand, M., Van Eeden, F., Furutani Seiki, M., Granato,
M., … Nüsslein Volhard, C. (1996). The zebrafish early arrest mutants. Development.
Company of Biologists. https://doi.org/10.1242/dev.123.1.57
chicago: Kane, Donald, Hans Maischein, Michael Brand, Fredericus Van Eeden, Makoto
Furutani Seiki, Michael Granato, Pascal Haffter, et al. “The Zebrafish Early Arrest
Mutants.” Development. Company of Biologists, 1996. https://doi.org/10.1242/dev.123.1.57 .
ieee: D. Kane et al., “The zebrafish early arrest mutants,” Development,
vol. 123, no. 1. Company of Biologists, pp. 57–66, 1996.
ista: Kane D, Maischein H, Brand M, Van Eeden F, Furutani Seiki M, Granato M, Haffter
P, Hammerschmidt M, Heisenberg C-PJ, Jiang Y, Kelsh R, Mullins M, Odenthal J,
Warga R, Nüsslein Volhard C. 1996. The zebrafish early arrest mutants. Development.
123(1), 57–66.
mla: Kane, Donald, et al. “The Zebrafish Early Arrest Mutants.” Development,
vol. 123, no. 1, Company of Biologists, 1996, pp. 57–66, doi:10.1242/dev.123.1.57 .
short: D. Kane, H. Maischein, M. Brand, F. Van Eeden, M. Furutani Seiki, M. Granato,
P. Haffter, M. Hammerschmidt, C.-P.J. Heisenberg, Y. Jiang, R. Kelsh, M. Mullins,
J. Odenthal, R. Warga, C. Nüsslein Volhard, Development 123 (1996) 57–66.
date_created: 2018-12-11T12:07:29Z
date_published: 1996-12-01T00:00:00Z
date_updated: 2022-08-05T09:43:44Z
day: '01'
doi: '10.1242/dev.123.1.57 '
extern: '1'
external_id:
pmid:
- '9007229 '
fulldoi: 'https://doi.org/10.1242/dev.123.1.57 '
intvolume: ' 123'
issue: '1'
language:
- iso: eng
month: '12'
oa_version: None
page: 57 - 66
pmid: 1
publication: Development
publication_identifier:
issn:
- 0950-1991
publication_status: published
publisher: Company of Biologists
publist_id: '1931'
quality_controlled: '1'
scopus_import: '1'
status: public
title: The zebrafish early arrest mutants
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 123
year: '1996'
...
---
_id: '4191'
abstract:
- lang: eng
text: In a screen for embryonic mutants in the zebrafish a large number of mutants
were isolated with abnormal brain morphology, We describe here 26 mutants in 13
complementation groups that show abnormal development of large regions of the
brain, Early neurogenesis is affected in white tail (wit), During segmentation
stages, homozygous wit embryos display an irregularly formed neural keel, particularly
in the hindbrain, Using a variety of molecular markers, a severe increase in the
number of various early differentiating neurons can be demonstrated, In contrast,
late differentiating neurons, radial glial cells and some nonneural cell types,
such as the neural crest-derived melanoblasts, are much reduced, Somitogenesis
appears delayed, In addition, very reduced numbers of melanophores are present
posterior to the mid-trunk, The wit phenotype is reminiscent of neurogenic mutants
in Drosophila, such as Notch or Delta, In mutant parachute (pac) embryos the general
organization of the hindbrain is disturbed and many rounded cells accumulate loosely
in the hindbrain and midbrain ventricles, Mutants in a group of 6 genes, snakehead(snk),
natter (nat), otter (ott) fullbrain (ful) viper (vip) and white snake (wis) develop
collapsed brain ventricles, before showing signs of general degeneration, atlantis
(atl), big head (bid), wicked brain (win), scabland (sbd) and eisspalte (ele)
mutants have different malformation of the brain folds, Some of them have transient
phenotypes, and mutant individuals may grow up to adults.
acknowledgement: We would like to thank Vladimir Korzh, Stefan Krauss, Monte Westerfield,
Tom Jessell, Mark Fishman, Eric Weinberg, Andreas Püschel, Trevor Jowett and Jóse
Campos-Ortega for providing antibodies and cDNA clones. We thank Suresh Jesuthasan
and Tanya Whitfield for many helpful suggestions on the manuscript. Y.-J. J. wants
to thank Christian Müller and Ralf Rupp for their instructive discussion. Y.-J.
J. is a predoctoral fellow supported by Deutscher Akademischer Austauschdienst (DAAD).
article_processing_charge: No
article_type: original
author:
- first_name: Yunjin
full_name: Jiang, Yunjin
last_name: Jiang
- first_name: Michael
full_name: Brand, Michael
last_name: Brand
- first_name: Carl-Philipp J
full_name: Heisenberg, Carl-Philipp J
id: 39427864-F248-11E8-B48F-1D18A9856A87
last_name: Heisenberg
orcid: 0000-0002-0912-4566
- first_name: Dirk
full_name: Beuchle, Dirk
last_name: Beuchle
- first_name: Makoto
full_name: Furutani Seiki, Makoto
last_name: Furutani Seiki
- first_name: Robert
full_name: Kelsh, Robert
last_name: Kelsh
- first_name: Rachel
full_name: Warga, Rachel
last_name: Warga
- first_name: Michael
full_name: Granato, Michael
last_name: Granato
- first_name: Pascal
full_name: Haffter, Pascal
last_name: Haffter
- first_name: Matthias
full_name: Hammerschmidt, Matthias
last_name: Hammerschmidt
- first_name: Donald
full_name: Kane, Donald
last_name: Kane
- first_name: Mary
full_name: Mullins, Mary
last_name: Mullins
- first_name: Jörg
full_name: Odenthal, Jörg
last_name: Odenthal
- first_name: Fredericus
full_name: Van Eeden, Fredericus
last_name: Van Eeden
- first_name: Christiane
full_name: Nüsslein Volhard, Christiane
last_name: Nüsslein Volhard
citation:
ama: Jiang Y, Brand M, Heisenberg C-PJ, et al. Mutations affecting neurogenesis
and brain morphology in the zebrafish, Danio rerio. Development. 1996;123(1):205-216.
doi:10.1242/dev.123.1.205
apa: Jiang, Y., Brand, M., Heisenberg, C.-P. J., Beuchle, D., Furutani Seiki, M.,
Kelsh, R., … Nüsslein Volhard, C. (1996). Mutations affecting neurogenesis and
brain morphology in the zebrafish, Danio rerio. Development. Company of
Biologists. https://doi.org/10.1242/dev.123.1.205
chicago: Jiang, Yunjin, Michael Brand, Carl-Philipp J Heisenberg, Dirk Beuchle,
Makoto Furutani Seiki, Robert Kelsh, Rachel Warga, et al. “Mutations Affecting
Neurogenesis and Brain Morphology in the Zebrafish, Danio Rerio.” Development.
Company of Biologists, 1996. https://doi.org/10.1242/dev.123.1.205.
ieee: Y. Jiang et al., “Mutations affecting neurogenesis and brain morphology
in the zebrafish, Danio rerio,” Development, vol. 123, no. 1. Company of
Biologists, pp. 205–216, 1996.
ista: Jiang Y, Brand M, Heisenberg C-PJ, Beuchle D, Furutani Seiki M, Kelsh R, Warga
R, Granato M, Haffter P, Hammerschmidt M, Kane D, Mullins M, Odenthal J, Van Eeden
F, Nüsslein Volhard C. 1996. Mutations affecting neurogenesis and brain morphology
in the zebrafish, Danio rerio. Development. 123(1), 205–216.
mla: Jiang, Yunjin, et al. “Mutations Affecting Neurogenesis and Brain Morphology
in the Zebrafish, Danio Rerio.” Development, vol. 123, no. 1, Company of
Biologists, 1996, pp. 205–16, doi:10.1242/dev.123.1.205.
short: Y. Jiang, M. Brand, C.-P.J. Heisenberg, D. Beuchle, M. Furutani Seiki, R.
Kelsh, R. Warga, M. Granato, P. Haffter, M. Hammerschmidt, D. Kane, M. Mullins,
J. Odenthal, F. Van Eeden, C. Nüsslein Volhard, Development 123 (1996) 205–216.
date_created: 2018-12-11T12:07:30Z
date_published: 1996-12-01T00:00:00Z
date_updated: 2022-08-05T09:13:51Z
day: '01'
doi: 10.1242/dev.123.1.205
extern: '1'
external_id:
pmid:
- '9007241'
fulldoi: https://doi.org/10.1242/dev.123.1.205
intvolume: ' 123'
issue: '1'
language:
- iso: eng
month: '12'
oa_version: None
page: 205 - 216
pmid: 1
publication: Development
publication_identifier:
issn:
- 0950-1991
publication_status: published
publisher: Company of Biologists
publist_id: '1926'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Mutations affecting neurogenesis and brain morphology in the zebrafish, Danio
rerio
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 123
year: '1996'
...
---
_id: '4215'
abstract:
- lang: eng
text: In a screen for early developmental mutants of the zebrafish, we have identified
mutations specifically affecting the internal organs, We identified 53 mutations
affecting the cardiovascular system, Nine of them affect specific landmarks of
heart morphogenesis. Mutations in four genes cause a failure in the fusion of
the bilateral heart primordia, resulting in cardia bifida. In lonely atrium, no
heart venticle is visible and the atrium is directly fused to the outflow tract.
In the overlooped mutant, the relative position of the two heart chambers is distorted,
The heart is enormously enlarged in the santa mutant, In two mutants, scotch tape
and superglue, the cardiac jelly between the two layers of the heart is significantly
reduced, We also identified a number of mutations affecting the function of the
heart, The mutations affecting heart function can be subdivided into two groups,
one affecting heart contraction and another affecting the rhythm of the heart
beat. Among the contractility group of mutants are 5 with no heart beat at all
and 15 with a reduced heart beat of one or both chambers, 6 mutations are in the
rhythmicity group and specifically affect the beating pattern of the heart, Mutations
in two genes, bypass and kurzschluss, cause specific defects in the circulatory
system, In addition to the heart mutants, we identified 23 mutations affecting
the integrity of the liver, the intestine or the kidney, In this report, we demonstrate
that it is feasible to screen for genes specific for the patterning or function
of certain internal organs in the zebrafish, The mutations presented here could
serve as an entrypoint to the establishment of a genetic hierarchy underlying
organogenesis.
acknowledgement: We thank Chris Simpson and Colleen Boggs for excellent technical
help. We thank Mark C. Fishman for the advice and providing fish for complementation;
Bernadette Fouquet, Kerri S. Warren and Brant M. Weinstein for critically reading
the manuscript. JNC is supported in part by NIH grant RO1-HL49579 to Mark C. Fishman.
article_processing_charge: No
article_type: original
author:
- first_name: Jaunian
full_name: Chen, Jaunian
last_name: Chen
- first_name: Pascal
full_name: Haffter, Pascal
last_name: Haffter
- first_name: Jörg
full_name: Odenthal, Jörg
last_name: Odenthal
- first_name: Elisabeth
full_name: Vogelsang, Elisabeth
last_name: Vogelsang
- first_name: Michael
full_name: Brand, Michael
last_name: Brand
- first_name: Fredericus
full_name: Van Eeden, Fredericus
last_name: Van Eeden
- first_name: Makoto
full_name: Furutani Seiki, Makoto
last_name: Furutani Seiki
- first_name: Michael
full_name: Granato, Michael
last_name: Granato
- first_name: Matthias
full_name: Hammerschmidt, Matthias
last_name: Hammerschmidt
- first_name: Carl-Philipp J
full_name: Heisenberg, Carl-Philipp J
id: 39427864-F248-11E8-B48F-1D18A9856A87
last_name: Heisenberg
orcid: 0000-0002-0912-4566
- first_name: Yunjin
full_name: Jiang, Yunjin
last_name: Jiang
- first_name: Donald
full_name: Kane, Donald
last_name: Kane
- first_name: Robert
full_name: Kelsh, Robert
last_name: Kelsh
- first_name: Mary
full_name: Mullins, Mary
last_name: Mullins
- first_name: Christiane
full_name: Nüsslein Volhard, Christiane
last_name: Nüsslein Volhard
citation:
ama: Chen J, Haffter P, Odenthal J, et al. Mutations affecting the cardiovascular
system and other internal organs in zebrafish. Development. 1996;123:293-302.
doi:10.1242/dev.123.1.293
apa: Chen, J., Haffter, P., Odenthal, J., Vogelsang, E., Brand, M., Van Eeden, F.,
… Nüsslein Volhard, C. (1996). Mutations affecting the cardiovascular system and
other internal organs in zebrafish. Development. Company of Biologists.
https://doi.org/10.1242/dev.123.1.293
chicago: Chen, Jaunian, Pascal Haffter, Jörg Odenthal, Elisabeth Vogelsang, Michael
Brand, Fredericus Van Eeden, Makoto Furutani Seiki, et al. “Mutations Affecting
the Cardiovascular System and Other Internal Organs in Zebrafish.” Development.
Company of Biologists, 1996. https://doi.org/10.1242/dev.123.1.293.
ieee: J. Chen et al., “Mutations affecting the cardiovascular system and
other internal organs in zebrafish,” Development, vol. 123. Company of
Biologists, pp. 293–302, 1996.
ista: Chen J, Haffter P, Odenthal J, Vogelsang E, Brand M, Van Eeden F, Furutani
Seiki M, Granato M, Hammerschmidt M, Heisenberg C-PJ, Jiang Y, Kane D, Kelsh R,
Mullins M, Nüsslein Volhard C. 1996. Mutations affecting the cardiovascular system
and other internal organs in zebrafish. Development. 123, 293–302.
mla: Chen, Jaunian, et al. “Mutations Affecting the Cardiovascular System and Other
Internal Organs in Zebrafish.” Development, vol. 123, Company of Biologists,
1996, pp. 293–302, doi:10.1242/dev.123.1.293.
short: J. Chen, P. Haffter, J. Odenthal, E. Vogelsang, M. Brand, F. Van Eeden, M.
Furutani Seiki, M. Granato, M. Hammerschmidt, C.-P.J. Heisenberg, Y. Jiang, D.
Kane, R. Kelsh, M. Mullins, C. Nüsslein Volhard, Development 123 (1996) 293–302.
date_created: 2018-12-11T12:07:38Z
date_published: 1996-12-01T00:00:00Z
date_updated: 2022-08-04T13:11:56Z
day: '01'
doi: 10.1242/dev.123.1.293
extern: '1'
external_id:
pmid:
- '9007249'
fulldoi: https://doi.org/10.1242/dev.123.1.293
intvolume: ' 123'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://journals.biologists.com/dev/article/123/1/293/39344/Mutations-affecting-the-cardiovascular-system-and
month: '12'
oa: 1
oa_version: Published Version
page: 293 - 302
pmid: 1
publication: Development
publication_identifier:
issn:
- 0950-1991
publication_status: published
publisher: Company of Biologists
publist_id: '1902'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Mutations affecting the cardiovascular system and other internal organs in
zebrafish
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 123
year: '1996'
...
---
_id: '2559'
abstract:
- lang: eng
text: Taking advantage of the restricted expression of metabotropic glutamate receptor
subtype 6 (mGIuR6) in retinal ON bipolar cells, we generated knockout mice lacking
mGIuR6 expression. The homozygous mutant mice showed a loss of ON responses but
unchanged OFF responses to light. The mutant mice displayed no obvious changes
in retinal cell organization nor in the projection of optic fibers to the brain.
Furthermore, the mGIuR6-deficient mice showed visual behavioral responses to light
stimulation as examined by shuttle box avoidance behavior experiments using light
exposure as a conditioned stimulus. The results demonstrate that mGIuR6 is essential
in synaptic transmission to the ON bipolar cell and that the OFF response provides
an important means for transmitting visual information.
acknowledgement: We thank Drs. N. Mizuno, M. Iso, M. Tachibana, A. Kaneko, M. Tessier-Lavigne,
and T. Hensch for useful advice and A. Uesugi for photographic assistance. This
work is supported by grants in aid for specially promoted research, for scientific
research on priority areas, and for scientific research (A) from the Ministry of
Education, Science, and Culture in Japan and by grants from the Ministry of Health
and Welfare of Japan, the Sankyo Foundation, and the Senri Life Science Foundation.
article_processing_charge: No
article_type: original
author:
- first_name: Masayuki
full_name: Masu, Masayuki
last_name: Masu
- first_name: Hideki
full_name: Iwakabe, Hideki
last_name: Iwakabe
- first_name: Yoshiaki
full_name: Tagawa, Yoshiaki
last_name: Tagawa
- first_name: Tomomitsu
full_name: Miyoshi, Tomomitsu
last_name: Miyoshi
- first_name: Masayuki
full_name: Yamashita, Masayuki
last_name: Yamashita
- first_name: Yutaka
full_name: Fukuda, Yutaka
last_name: Fukuda
- first_name: Hitoshi
full_name: Sasaki, Hitoshi
last_name: Sasaki
- first_name: Kano
full_name: Hiroi, Kano
last_name: Hiroi
- first_name: Yasuhisa
full_name: Nakamura, Yasuhisa
last_name: Nakamura
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Masahiko
full_name: Takada, Masahiko
last_name: Takada
- first_name: Kenji
full_name: Nakamura, Kenji
last_name: Nakamura
- first_name: Kazuki
full_name: Nakao, Kazuki
last_name: Nakao
- first_name: Motoya
full_name: Katsuki, Motoya
last_name: Katsuki
- first_name: Shigetada
full_name: Nakanishi, Shigetada
last_name: Nakanishi
citation:
ama: Masu M, Iwakabe H, Tagawa Y, et al. Specific deficit of the ON response in
visual transmission by targeted disruption of the mGIuR6 gene. Cell. 1995;80(5):757-765.
doi:10.1016/0092-8674(95)90354-2
apa: Masu, M., Iwakabe, H., Tagawa, Y., Miyoshi, T., Yamashita, M., Fukuda, Y.,
… Nakanishi, S. (1995). Specific deficit of the ON response in visual transmission
by targeted disruption of the mGIuR6 gene. Cell. Cell Press. https://doi.org/10.1016/0092-8674(95)90354-2
chicago: Masu, Masayuki, Hideki Iwakabe, Yoshiaki Tagawa, Tomomitsu Miyoshi, Masayuki
Yamashita, Yutaka Fukuda, Hitoshi Sasaki, et al. “Specific Deficit of the ON Response
in Visual Transmission by Targeted Disruption of the MGIuR6 Gene.” Cell.
Cell Press, 1995. https://doi.org/10.1016/0092-8674(95)90354-2.
ieee: M. Masu et al., “Specific deficit of the ON response in visual transmission
by targeted disruption of the mGIuR6 gene,” Cell, vol. 80, no. 5. Cell
Press, pp. 757–765, 1995.
ista: Masu M, Iwakabe H, Tagawa Y, Miyoshi T, Yamashita M, Fukuda Y, Sasaki H, Hiroi
K, Nakamura Y, Shigemoto R, Takada M, Nakamura K, Nakao K, Katsuki M, Nakanishi
S. 1995. Specific deficit of the ON response in visual transmission by targeted
disruption of the mGIuR6 gene. Cell. 80(5), 757–765.
mla: Masu, Masayuki, et al. “Specific Deficit of the ON Response in Visual Transmission
by Targeted Disruption of the MGIuR6 Gene.” Cell, vol. 80, no. 5, Cell
Press, 1995, pp. 757–65, doi:10.1016/0092-8674(95)90354-2.
short: M. Masu, H. Iwakabe, Y. Tagawa, T. Miyoshi, M. Yamashita, Y. Fukuda, H. Sasaki,
K. Hiroi, Y. Nakamura, R. Shigemoto, M. Takada, K. Nakamura, K. Nakao, M. Katsuki,
S. Nakanishi, Cell 80 (1995) 757–765.
date_created: 2018-12-11T11:58:23Z
date_published: 1995-02-10T00:00:00Z
date_updated: 2022-06-28T13:27:50Z
day: '10'
doi: 10.1016/0092-8674(95)90354-2
extern: '1'
external_id:
pmid:
- '7889569'
fulldoi: https://doi.org/10.1016/0092-8674(95)90354-2
intvolume: ' 80'
issue: '5'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.sciencedirect.com/science/article/pii/0092867495903542
month: '02'
oa: 1
oa_version: Published Version
page: 757 - 765
pmid: 1
publication: Cell
publication_identifier:
issn:
- 0092-8674
publication_status: published
publisher: Cell Press
publist_id: '4339'
quality_controlled: '1'
status: public
title: Specific deficit of the ON response in visual transmission by targeted disruption
of the mGIuR6 gene
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 80
year: '1995'
...
---
_id: '3454'
abstract:
- lang: eng
text: The study of gene expression and regulation in the central nervous system
(CNS) is a daunting task because of the diversity of neuronal phenotypes and the
complexity of many protein classes. Molecular cloning revealed the presence of
a large number of different protein families in the CNS, each comprising several
members. Ligand-gated ion channels may serve as an example to illustrate this
point (for review, see Unwin, 1993). Heterologous expression combined with electrophysiological
analysis suggests that ligand-gated channels are multimeric proteins with functional
properties depending on the subunit composition. Very little is known, however,
about how the functional properties of the recombinant and native receptors relate
to each other. Thus, it is of eminent importance to elucidate the subunit expression
profile in different types of neurons in the CNS and to correlate this with the
functional properties of the native receptors.
article_processing_charge: No
author:
- first_name: Hannah
full_name: Monyer, Hannah
last_name: Monyer
- first_name: Peter M
full_name: Jonas, Peter M
id: 353C1B58-F248-11E8-B48F-1D18A9856A87
last_name: Jonas
orcid: 0000-0001-5001-4804
citation:
ama: 'Monyer H, Jonas PM. Polymerase chain reaction analysis of ion channel expression
in single neurons of brain slices. In: Sakmann B, Neher E, eds. Single-Channel
Recording. Plenum; 1995:357-373. doi:10.1007/978-1-4419-1229-9_16'
apa: Monyer, H., & Jonas, P. M. (1995). Polymerase chain reaction analysis of
ion channel expression in single neurons of brain slices. In B. Sakmann &
E. Neher (Eds.), Single-channel recording (pp. 357–373). Plenum. https://doi.org/10.1007/978-1-4419-1229-9_16
chicago: Monyer, Hannah, and Peter M Jonas. “Polymerase Chain Reaction Analysis
of Ion Channel Expression in Single Neurons of Brain Slices.” In Single-Channel
Recording, edited by Bert Sakmann and Erwin Neher, 357–73. Plenum, 1995. https://doi.org/10.1007/978-1-4419-1229-9_16.
ieee: H. Monyer and P. M. Jonas, “Polymerase chain reaction analysis of ion channel
expression in single neurons of brain slices,” in Single-channel recording,
B. Sakmann and E. Neher, Eds. Plenum, 1995, pp. 357–373.
ista: 'Monyer H, Jonas PM. 1995.Polymerase chain reaction analysis of ion channel
expression in single neurons of brain slices. In: Single-channel recording. ,
357–373.'
mla: Monyer, Hannah, and Peter M. Jonas. “Polymerase Chain Reaction Analysis of
Ion Channel Expression in Single Neurons of Brain Slices.” Single-Channel Recording,
edited by Bert Sakmann and Erwin Neher, Plenum, 1995, pp. 357–73, doi:10.1007/978-1-4419-1229-9_16.
short: H. Monyer, P.M. Jonas, in:, B. Sakmann, E. Neher (Eds.), Single-Channel Recording,
Plenum, 1995, pp. 357–373.
date_created: 2018-12-11T12:03:25Z
date_published: 1995-01-01T00:00:00Z
date_updated: 2022-06-28T09:13:01Z
day: '01'
doi: 10.1007/978-1-4419-1229-9_16
editor:
- first_name: Bert
full_name: Sakmann, Bert
last_name: Sakmann
- first_name: Erwin
full_name: Neher, Erwin
last_name: Neher
extern: '1'
fulldoi: https://doi.org/10.1007/978-1-4419-1229-9_16
language:
- iso: eng
main_file_link:
- url: https://link.springer.com/chapter/10.1007/978-1-4419-1229-9_16
month: '01'
oa_version: None
page: 357 - 373
publication: Single-channel recording
publication_identifier:
isbn:
- 978-0-306-44870-6
publication_status: published
publisher: Plenum
publist_id: '2933'
quality_controlled: '1'
status: public
title: Polymerase chain reaction analysis of ion channel expression in single neurons
of brain slices
type: book_chapter
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
year: '1995'
...
---
_id: '3455'
abstract:
- lang: eng
text: At a synapse, the transmitter is stored in synaptic vesicles and is released
into the synaptic cleft almost instantaneously upon fusion of these vesicles with
the presynaptic membrane. Subsequently, the transmitter diffuses to ligand-gated
ion channels in the postsynaptic density, binds to them, and thereby causes channel
activation. Unfortunately, we have estimates neither of the exact amount of transmitter
in the synaptic vesicle nor of the concentration in the synaptic cleft reaching
the postsynaptic receptors, and in some cases even the identity of the transmitter
is unknown. These questions may be addressed by modeling of release and diffusion.
Such a theoretical approach, however, is based on several assumptions, some of
which lack experimental evidence.
article_processing_charge: No
author:
- first_name: Peter M
full_name: Jonas, Peter M
id: 353C1B58-F248-11E8-B48F-1D18A9856A87
last_name: Jonas
orcid: 0000-0001-5001-4804
citation:
ama: 'Jonas PM. Fast application of agonists to isolated membrane patches. In: Sakmann
B, Neher E, eds. Single-Channel Recording. Plenum; 1995:231-243. doi:10.1007/978-1-4419-1229-9_10'
apa: Jonas, P. M. (1995). Fast application of agonists to isolated membrane patches.
In B. Sakmann & E. Neher (Eds.), Single-channel recording (pp. 231–243).
Plenum. https://doi.org/10.1007/978-1-4419-1229-9_10
chicago: Jonas, Peter M. “Fast Application of Agonists to Isolated Membrane Patches.”
In Single-Channel Recording, edited by Bert Sakmann and Erwin Neher, 231–43.
Plenum, 1995. https://doi.org/10.1007/978-1-4419-1229-9_10.
ieee: P. M. Jonas, “Fast application of agonists to isolated membrane patches,”
in Single-channel recording, B. Sakmann and E. Neher, Eds. Plenum, 1995,
pp. 231–243.
ista: 'Jonas PM. 1995.Fast application of agonists to isolated membrane patches.
In: Single-channel recording. , 231–243.'
mla: Jonas, Peter M. “Fast Application of Agonists to Isolated Membrane Patches.”
Single-Channel Recording, edited by Bert Sakmann and Erwin Neher, Plenum,
1995, pp. 231–43, doi:10.1007/978-1-4419-1229-9_10.
short: P.M. Jonas, in:, B. Sakmann, E. Neher (Eds.), Single-Channel Recording, Plenum,
1995, pp. 231–243.
date_created: 2018-12-11T12:03:25Z
date_published: 1995-01-01T00:00:00Z
date_updated: 2022-06-28T08:51:40Z
day: '01'
doi: 10.1007/978-1-4419-1229-9_10
editor:
- first_name: Bert
full_name: Sakmann, Bert
last_name: Sakmann
- first_name: Erwin
full_name: Neher, Erwin
last_name: Neher
extern: '1'
fulldoi: https://doi.org/10.1007/978-1-4419-1229-9_10
language:
- iso: eng
main_file_link:
- url: https://link.springer.com/chapter/10.1007/978-1-4419-1229-9_10
month: '01'
oa_version: None
page: 231 - 243
publication: Single-channel recording
publication_identifier:
isbn:
- 978-0-306-44870-6
publication_status: published
publisher: Plenum
publist_id: '2932'
quality_controlled: '1'
status: public
title: Fast application of agonists to isolated membrane patches
type: book_chapter
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
year: '1995'
...
---
_id: '3478'
abstract:
- lang: eng
text: 1. Properties of dendritic glutamate receptor (GluR) channels were investigated
using fast application of glutamate to outside-out membrane patches isolated from
the apical dendrites of CA3 and CA1 pyramidal neurons in rat hippocampal slices.
CA3 patches were formed (15-76 μm from the soma) in the region of messy fibre
(MF) synapses, and CA1 patches (25-174 μm from the soma) in the region of Schaffer
collateral (SC) innervation. 2. Dual-component responses consisting of a rapidly
rising and decaying component followed by a second, substantially slower, component
were elicited by 1 ms pulses of 1 mM glutamate in the presence of 10 μM glycine
and absence of external Mg2+. The fast component was selectively blocked by 2-5
μM 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and the slow component by 30 μM
D-2-amino-5-phosphonopentanoic acid (D-AP5), suggesting that the fast and slow
components were mediated by the GluR channels of the L-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate
(AMPA) and NMDA type, respectively. The peak amplitude ratio of the NMDA to AMPA
receptor-mediated components varied between 0.03 and 0.62 in patches from both
CA3 and CA1 dendrites. Patches lacking either component were rarely observed.
3. The peak current-voltage (I-V) relationship of the fast component was almost
linear, whereas the I-V relationship of the slow component showed a region of
negative slope in the presence of 1 mM external Mg2+. The reversal potential for
both components was close to 0 mV. 4. Kainate-preferring GluR channels did not
contribute appreciably to the response to glutamate. The responses to 100 ms pulses
of 1 mM glutamate were mimicked by application of 1 mM AMPA, whereas 1 mM kainate
produced much smaller, weakly desensitizing currents. This suggests that the fast
component is primarily mediated by the action of glutamate on AMPA-preferring
receptors. 5. The mean elementary conductance of AMPA receptor channels was about
10 pS, as estimated by non-stationary fluctuation analysis. The permeability of
these channels to Ca2+ was low (~5% of the permeability to Cs+). 6. The elementary
conductance of NMDA receptor channels was larger, with a main conductance state
of about 45 pS. These channels were 3.6 times more permeable to Ca2+ than to Cs+.
7. AMPA receptor-mediated currents activated rapidly in response to 1 ms pulses
of 1 mM glutamate and deactivated with a predominant, fast time constant and a
smaller, slower component (τ1≃2 ms, τ2≃8 ms, contributing ~80 and ~20% to the
total decay amplitude, respectively). Desensitization of the current during a
100 ms pulse was best fitted by two time constants (τ1≃10 ms, ~60%; τ2≃34 ms,
~40%). 8. NMDA receptor-mediated currents in response to 1 ms pulses of 1 mM glutamate
activated and deactivated much more slowly than AMPA receptor-mediated currents.
The time course could be described by a single exponential rising phase (τ≃7 ms)
followed by a double exponential decay (τ1≃200 ms, ~80%; τ2≃1-3 s, ~20%). 9. Mg2+
blocked the NMDA component in a voltage-dependent manner, with a half-maximal
inhibitory concentration (IC50) of 21 μM at -80 mV. At physiological Mg2+ concentrations,
block of the NMDA component could be rapidly relieved with voltage jumps from
negative to positive potentials. Block of the current upon return to negative
potentials occurred almost instantaneously. 10. Zn2+ also selectively-blocked
the NMDA receptor-mediated current with an IC50 of 22 μM, but this block differed
from that of Mg2+ in that it showed little voltage dependence. Rapid application
of Zn2+ together with glutamate produced partial block of the current. More block
was observed if Zn2+ and glutamate were co-applied when NMDA receptor channels
were already open. 11. The functional properties of dendritic GluRs were similar
to those found at the soma. Knowledge of these properties facilitated simulations
investigating the contribution of coactivated AMPA and NMDA receptors to synaptic
depolarization and Ca2+ entry into dendritic spines. Because of its slow deactivation,
the NMDA receptor-mediated current contributes substantially to depolarization
and Ca2+ entry and is susceptible to modulation over a period of seconds, either
by backpropagating action potentials or by the release of Zn2+ from presynaptic
boutons.
acknowledgement: We thank M.Hausser, A.Roth, P.Ruppersberg, and G.Stuart for helpful
discussions and M.H. and G.S. for critically reading the manuscript. We also thank
M.Kaiser for expert technical assistance and F.Helmchen, M.Huke and A.Roth for computer
programming. Financial support from the Alexander von Humboldt Foundation and the
Deutsche Forschungsgemeinschaft (SFB317) is gratefully acknowledged.
article_processing_charge: No
article_type: original
author:
- first_name: Nelson
full_name: Spruston, Nelson
last_name: Spruston
- first_name: Peter M
full_name: Jonas, Peter M
id: 353C1B58-F248-11E8-B48F-1D18A9856A87
last_name: Jonas
orcid: 0000-0001-5001-4804
- first_name: Bert
full_name: Sakmann, Bert
last_name: Sakmann
citation:
ama: Spruston N, Jonas PM, Sakmann B. Dendritic glutamate receptor channels in rat
hippocampal CA3 and CA1 pyramidal neurons. Journal of Physiology. 1995;482(Pt
2):325-352. doi:10.1113/jphysiol.1995.sp020521
apa: Spruston, N., Jonas, P. M., & Sakmann, B. (1995). Dendritic glutamate receptor
channels in rat hippocampal CA3 and CA1 pyramidal neurons. Journal of Physiology.
Wiley-Blackwell. https://doi.org/10.1113/jphysiol.1995.sp020521
chicago: Spruston, Nelson, Peter M Jonas, and Bert Sakmann. “Dendritic Glutamate
Receptor Channels in Rat Hippocampal CA3 and CA1 Pyramidal Neurons.” Journal
of Physiology. Wiley-Blackwell, 1995. https://doi.org/10.1113/jphysiol.1995.sp020521.
ieee: N. Spruston, P. M. Jonas, and B. Sakmann, “Dendritic glutamate receptor channels
in rat hippocampal CA3 and CA1 pyramidal neurons,” Journal of Physiology,
vol. 482, no. Pt 2. Wiley-Blackwell, pp. 325–352, 1995.
ista: Spruston N, Jonas PM, Sakmann B. 1995. Dendritic glutamate receptor channels
in rat hippocampal CA3 and CA1 pyramidal neurons. Journal of Physiology. 482(Pt
2), 325–352.
mla: Spruston, Nelson, et al. “Dendritic Glutamate Receptor Channels in Rat Hippocampal
CA3 and CA1 Pyramidal Neurons.” Journal of Physiology, vol. 482, no. Pt
2, Wiley-Blackwell, 1995, pp. 325–52, doi:10.1113/jphysiol.1995.sp020521.
short: N. Spruston, P.M. Jonas, B. Sakmann, Journal of Physiology 482 (1995) 325–352.
date_created: 2018-12-11T12:03:32Z
date_published: 1995-01-15T00:00:00Z
date_updated: 2022-06-28T08:08:40Z
day: '15'
doi: 10.1113/jphysiol.1995.sp020521
extern: '1'
external_id:
pmid:
- '7536248'
fulldoi: https://doi.org/10.1113/jphysiol.1995.sp020521
intvolume: ' 482'
issue: Pt 2
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://physoc.onlinelibrary.wiley.com/doi/abs/10.1113/jphysiol.1995.sp020521
month: '01'
oa: 1
oa_version: Published Version
page: 325 - 352
pmid: 1
publication: Journal of Physiology
publication_identifier:
issn:
- 0022-3751
publication_status: published
publisher: Wiley-Blackwell
publist_id: '2909'
quality_controlled: '1'
status: public
title: Dendritic glutamate receptor channels in rat hippocampal CA3 and CA1 pyramidal
neurons
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 482
year: '1995'
...
---
_id: '3479'
abstract:
- lang: eng
text: 1. Glutamate receptor (GluR) channels were studied in basket cells in the
dentate gyrus of rat hippocampal slices. Basket cells were identified by their
location, dendritic morphology and high frequency of action potentials generated
during sustained current injection. 2. Dual-component currents were activated
by fast application of glutamate to outside-out membrane patches isolated from
basket cell somata (10 μM glycine, no external Mg2+). The fast component was selectively
blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), the slow component by
D-2-amino-5-phosphonopentanoic acid (D-AP5). This suggests that the two components
were mediated by α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptor (AMPAR)/kainate
receptor and N-methyl-D-aspartate receptor (NMDAR) channels, respectively. The
mean ratio of the peak current of the NMDAR component to that of the AMPAR/kainate
receptor component was 0.22 (1 ms pulses of 10 mM glutamate). 3. The AMPAR/kainate
receptor component, which was studied in isolation in the presence of D-AP5, was
identified as AMPAR mediated on the basis of the preferential activation by AMPA
as compared with kainate, the weak desensitization of kainate-activated currents,
the cross-desensitization between AMPA and kainate, and the reduction of desensitization
by cyclothiazide. 4. Deactivation of basket cell AMPARs following 1 ms pulses
of glutamate occurred with a time constant (τ) of 1.2 ± 0.1 ms (mean ± S.E.M.).
During 100 ms glutamate pulses, AMPARs desensitized with a τ of 3.7 ± 0.2 ms.
5. The peak current-voltage (I-V) relation of AMPAR-mediated currents in Na+-rich
extracellular solution showed a reversal potential of -4.0 ± 2.6 mV and was characterized
by a doubly rectifying shape. The conductance of single AMPAR channels was estimated
as 22.6 ± 1.6 pS using non-stationary fluctuation analysis. AMPARs expressed in
hippocampal basket cells mere highly Ca2+ permeable (P(Ca)/P(K) = 1.79). 6. NMDARs
in hippocampal basket cells were studied in isolation in the presence of CNQX.
Deactivation of NMDARs activated by glutamate pulses occurred bi-exponentially
with mean τ values of 266 ± 23 ms (76%) and 2620 ± 383 ms (24%). 7. The peak I-V
relation of the NMDAR-mediated component in Na+-rich extracellular solution showed
a reversal potential of 1.5 ± 0.6 mV and a region of negative slope at negative
membrane potentials in the presence of external Mg2+, due to voltage-dependent
block by these ions. The conductance of single NMDAR channels in the main open
state was 50.2 ± 1.8 pS. NMDARs in hippocampal basket cells were highly permeable
to Ca2+ (P(Ca)/P(K) = 6.68). 8. AMPARs in hippocampal basket cells are characterized
by about threefold faster kinetics and twentyfold higher Ca2+ permeability than
AMPARs in hippocampal granule or pyramidal cells. Simulations show that the Ca2+
influx through basket cell AMPARs is comparable to that through NMDARs at negative
membrane potentials with physiological concentrations of Ca2+ and Mg2+. This suggests
a dual pathway of synaptically mediated Ca2+ entry into interneurones.
acknowledgement: We thank Drs M.Häusser and H.Markram for critically reading the manuscript
and M.Kaiser for technical assistance. Supported by the Deutsche Forschungsgemeinschaft
(SFB-317/B14 grant to P.J. and a Graduiertenkollegstipendium to J.R.P.G.)
article_processing_charge: No
article_type: original
author:
- first_name: Duk
full_name: Koh, Duk
last_name: Koh
- first_name: Jörg
full_name: Geiger, Jörg
last_name: Geiger
- first_name: Peter M
full_name: Jonas, Peter M
id: 353C1B58-F248-11E8-B48F-1D18A9856A87
last_name: Jonas
orcid: 0000-0001-5001-4804
- first_name: Bert
full_name: Sakmann, Bert
last_name: Sakmann
citation:
ama: Koh D, Geiger J, Jonas PM, Sakmann B. Ca(2+)-permeable AMPA and NMDA receptor
channels in basket cells of rat hippocampal dentate gyrus. Journal of Physiology.
1995;485(Pt 2):383-402. doi:10.1113/jphysiol.1995.sp020737
apa: Koh, D., Geiger, J., Jonas, P. M., & Sakmann, B. (1995). Ca(2+)-permeable
AMPA and NMDA receptor channels in basket cells of rat hippocampal dentate gyrus.
Journal of Physiology. Wiley-Blackwell. https://doi.org/10.1113/jphysiol.1995.sp020737
chicago: Koh, Duk, Jörg Geiger, Peter M Jonas, and Bert Sakmann. “Ca(2+)-Permeable
AMPA and NMDA Receptor Channels in Basket Cells of Rat Hippocampal Dentate Gyrus.”
Journal of Physiology. Wiley-Blackwell, 1995. https://doi.org/10.1113/jphysiol.1995.sp020737.
ieee: D. Koh, J. Geiger, P. M. Jonas, and B. Sakmann, “Ca(2+)-permeable AMPA and
NMDA receptor channels in basket cells of rat hippocampal dentate gyrus,” Journal
of Physiology, vol. 485, no. Pt 2. Wiley-Blackwell, pp. 383–402, 1995.
ista: Koh D, Geiger J, Jonas PM, Sakmann B. 1995. Ca(2+)-permeable AMPA and NMDA
receptor channels in basket cells of rat hippocampal dentate gyrus. Journal of
Physiology. 485(Pt 2), 383–402.
mla: Koh, Duk, et al. “Ca(2+)-Permeable AMPA and NMDA Receptor Channels in Basket
Cells of Rat Hippocampal Dentate Gyrus.” Journal of Physiology, vol. 485,
no. Pt 2, Wiley-Blackwell, 1995, pp. 383–402, doi:10.1113/jphysiol.1995.sp020737.
short: D. Koh, J. Geiger, P.M. Jonas, B. Sakmann, Journal of Physiology 485 (1995)
383–402.
date_created: 2018-12-11T12:03:33Z
date_published: 1995-06-01T00:00:00Z
date_updated: 2022-06-28T07:54:44Z
day: '01'
doi: 10.1113/jphysiol.1995.sp020737
extern: '1'
external_id:
pmid:
- '7545230'
fulldoi: https://doi.org/10.1113/jphysiol.1995.sp020737
intvolume: ' 485'
issue: Pt 2
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1158000/pdf/jphysiol00319-0104.pdf
month: '06'
oa: 1
oa_version: Published Version
page: 383 - 402
pmid: 1
publication: Journal of Physiology
publication_identifier:
issn:
- 0022-3751
publication_status: published
publisher: Wiley-Blackwell
publist_id: '2908'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Ca(2+)-permeable AMPA and NMDA receptor channels in basket cells of rat hippocampal
dentate gyrus
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 485
year: '1995'
...
---
_id: '3551'
abstract:
- lang: eng
text: Common geometric models for proteins and other molecules are the space filling
diagram, the solvent accessible surface, and the molecular surface. We describe
software that computes metric properties of these models, including volume and
surface area. It also measures voids or empty space enclosed by the protein, and
it keeps track of surface area contributions of individual atoms. The software
is based on 3-dimensional alpha complexes and on inclusion-exclusion formulas
with terms derived from the simplices in this complex.
article_processing_charge: No
author:
- first_name: Herbert
full_name: Edelsbrunner, Herbert
id: 3FB178DA-F248-11E8-B48F-1D18A9856A87
last_name: Edelsbrunner
orcid: 0000-0002-9823-6833
- first_name: Michael
full_name: Facello, Michael
last_name: Facello
- first_name: Ping
full_name: Fu, Ping
last_name: Fu
- first_name: Jie
full_name: Liang, Jie
last_name: Liang
citation:
ama: 'Edelsbrunner H, Facello M, Fu P, Liang J. Measuring proteins and voids in
proteins. In: Proceedings of the 28th Annual Hawaii International Conference
on System Sciences. IEEE; 1995:256-264. doi:10.1109/HICSS.1995.375331'
apa: 'Edelsbrunner, H., Facello, M., Fu, P., & Liang, J. (1995). Measuring proteins
and voids in proteins. In Proceedings of the 28th Annual Hawaii International
Conference on System Sciences (pp. 256–264). Wailea, HI, United States of
America: IEEE. https://doi.org/10.1109/HICSS.1995.375331'
chicago: Edelsbrunner, Herbert, Michael Facello, Ping Fu, and Jie Liang. “Measuring
Proteins and Voids in Proteins.” In Proceedings of the 28th Annual Hawaii International
Conference on System Sciences, 256–64. IEEE, 1995. https://doi.org/10.1109/HICSS.1995.375331.
ieee: H. Edelsbrunner, M. Facello, P. Fu, and J. Liang, “Measuring proteins and
voids in proteins,” in Proceedings of the 28th Annual Hawaii International
Conference on System Sciences, Wailea, HI, United States of America, 1995,
pp. 256–264.
ista: 'Edelsbrunner H, Facello M, Fu P, Liang J. 1995. Measuring proteins and voids
in proteins. Proceedings of the 28th Annual Hawaii International Conference on
System Sciences. HICSS: Hawaii International Conference on System Sciences, 256–264.'
mla: Edelsbrunner, Herbert, et al. “Measuring Proteins and Voids in Proteins.” Proceedings
of the 28th Annual Hawaii International Conference on System Sciences, IEEE,
1995, pp. 256–64, doi:10.1109/HICSS.1995.375331.
short: H. Edelsbrunner, M. Facello, P. Fu, J. Liang, in:, Proceedings of the 28th
Annual Hawaii International Conference on System Sciences, IEEE, 1995, pp. 256–264.
conference:
end_date: 1995-01-06
location: Wailea, HI, United States of America
name: 'HICSS: Hawaii International Conference on System Sciences'
start_date: 1995-01-03
date_created: 2018-12-11T12:03:55Z
date_published: 1995-01-04T00:00:00Z
date_updated: 2022-06-27T13:54:41Z
day: '04'
doi: 10.1109/HICSS.1995.375331
extern: '1'
fulldoi: https://doi.org/10.1109/HICSS.1995.375331
language:
- iso: eng
main_file_link:
- url: https://ieeexplore.ieee.org/document/375331
month: '01'
oa_version: None
page: 256 - 264
publication: Proceedings of the 28th Annual Hawaii International Conference on System
Sciences
publication_identifier:
isbn:
- 0-8186-6930-6
publication_status: published
publisher: IEEE
publist_id: '2834'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Measuring proteins and voids in proteins
type: conference
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
year: '1995'
...
---
_id: '3640'
abstract:
- lang: eng
text: 'The probability of fixation of a favorable mutation is reduced if selection
at other loci causes inherited variation in fitness. A general method for calculating
the fixation probability of an allele that can find itself in a variety of genetic
backgrounds is applied to find the effect of substitutions, fluctuating polymorphisms,
and deleterious mutations in a large population. With loose linkage, r, the effects
depend on the additive genetic variance in relative fitness, var(W), and act by
reducing effective population size by (N/Ne) = 1 + var(W)/2r2. However, tightly
linked loci can have a substantial effect not predictable from Ne. Linked deleterious
mutations reduce the fixation probability of weakly favored alleles by exp (-2U/R),
where U is the total mutation rate and R is the map length in Morgans. Substitutions
can cause a greater reduction: an allele with advantage s < scrit = (pi 2/6)
loge (S/s) [var(W)/R] is very unlikely to be fixed. (S is the advantage of the
substitution impeding fixation.) Fluctuating polymorphisms at many (n) linked
loci can also have a substantial effect, reducing fixation probability by exp
[square root of 2Kn var(W)/R] [K = -1/E((u-u)2/uv) depending on the frequencies
(u,v) at the selected polymorphisms]. Hitchhiking due to all three kinds of selection
may substantially impede adaptation that depends on weakly favored alleles.'
article_processing_charge: No
article_type: original
author:
- first_name: Nicholas H
full_name: Barton, Nicholas H
id: 4880FE40-F248-11E8-B48F-1D18A9856A87
last_name: Barton
orcid: 0000-0002-8548-5240
citation:
ama: Barton NH. Linkage and the limits to natural selection. Genetics. 1995;140(2):821-841.
doi: 10.1093/genetics/140.2.821
apa: Barton, N. H. (1995). Linkage and the limits to natural selection. Genetics.
Genetics Society of America. https://doi.org/
10.1093/genetics/140.2.821
chicago: Barton, Nicholas H. “Linkage and the Limits to Natural Selection.” Genetics.
Genetics Society of America, 1995. https://doi.org/
10.1093/genetics/140.2.821.
ieee: N. H. Barton, “Linkage and the limits to natural selection,” Genetics,
vol. 140, no. 2. Genetics Society of America, pp. 821–841, 1995.
ista: Barton NH. 1995. Linkage and the limits to natural selection. Genetics. 140(2),
821–841.
mla: Barton, Nicholas H. “Linkage and the Limits to Natural Selection.” Genetics,
vol. 140, no. 2, Genetics Society of America, 1995, pp. 821–41, doi: 10.1093/genetics/140.2.821.
short: N.H. Barton, Genetics 140 (1995) 821–841.
date_created: 2018-12-11T12:04:23Z
date_published: 1995-06-01T00:00:00Z
date_updated: 2025-06-30T10:18:45Z
day: '01'
doi: ' 10.1093/genetics/140.2.821'
extern: '1'
external_id:
pmid:
- '7498757'
fulldoi: https://doi.org/ 10.1093/genetics/140.2.821
intvolume: ' 140'
issue: '2'
language:
- iso: eng
month: '06'
oa_version: Published Version
page: 821 - 841
pmid: 1
publication: Genetics
publication_identifier:
issn:
- 0016-6731
publication_status: published
publisher: Genetics Society of America
publist_id: '2743'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Linkage and the limits to natural selection
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 140
year: '1995'
...
---
_id: '2557'
abstract:
- lang: eng
text: The distribution of the metabotropic glutamate receptors mGluR2 and mGluR3
was immunohistochemically examined in the rat cerebellar cortex at both light
and electron microscope levels. An antibody was raised against a fusion protein
containing a C-terminal portion of mGluR2. On immunoblot, the antibody reacted
with both mGluR2 and mGluR3 in rat brain. mGluR2/3 immunoreactivity was expressed
in cell bodies, dendrites, and axon terminals of Golgi cells, as well as in presumed
glial processes. Golgi axon terminals with mGluR2/3 immunoreactivity were often
encountered in the vicinity of glutamatergic mossy fiber terminals. The results
suggest that transmitter glutamate may exert control influences upon Golgi cells
not only through dendritic mGluR2/3, but also through axonal mGluR2/3.
acknowledgement: "We are grateful to Mr. Akira Uesugi for photographic help. This
work has been supported in part by research grants from the Ministry of Education,
Science and Culture of Japan. The costs of publication of this article were defrayed
in part\r\nby the payment of page charges. This article must therefore be hereby
marked “advertisement” in accordance with 18 USC Section 1734 solely to indicate
this fact. "
article_processing_charge: No
article_type: original
author:
- first_name: Hitoshi
full_name: Ohishi, Hitoshi
last_name: Ohishi
- first_name: Reiko
full_name: Ogawa Meguro, Reiko
last_name: Ogawa Meguro
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Takeshi
full_name: Kaneko, Takeshi
last_name: Kaneko
- first_name: Shigetada
full_name: Nakanishi, Shigetada
last_name: Nakanishi
- first_name: Noboru
full_name: Mizuno, Noboru
last_name: Mizuno
citation:
ama: Ohishi H, Ogawa Meguro R, Shigemoto R, Kaneko T, Nakanishi S, Mizuno N. Immunohistochemical
localization of metabotropic glutamate receptors, mGluR2 and mGluR3, in rat cerebellar
cortex. Neuron. 1994;13(1):55-66. doi:10.1016/0896-6273(94)90459-6
apa: Ohishi, H., Ogawa Meguro, R., Shigemoto, R., Kaneko, T., Nakanishi, S., &
Mizuno, N. (1994). Immunohistochemical localization of metabotropic glutamate
receptors, mGluR2 and mGluR3, in rat cerebellar cortex. Neuron. Elsevier.
https://doi.org/10.1016/0896-6273(94)90459-6
chicago: Ohishi, Hitoshi, Reiko Ogawa Meguro, Ryuichi Shigemoto, Takeshi Kaneko,
Shigetada Nakanishi, and Noboru Mizuno. “Immunohistochemical Localization of Metabotropic
Glutamate Receptors, MGluR2 and MGluR3, in Rat Cerebellar Cortex.” Neuron.
Elsevier, 1994. https://doi.org/10.1016/0896-6273(94)90459-6.
ieee: H. Ohishi, R. Ogawa Meguro, R. Shigemoto, T. Kaneko, S. Nakanishi, and N.
Mizuno, “Immunohistochemical localization of metabotropic glutamate receptors,
mGluR2 and mGluR3, in rat cerebellar cortex,” Neuron, vol. 13, no. 1. Elsevier,
pp. 55–66, 1994.
ista: Ohishi H, Ogawa Meguro R, Shigemoto R, Kaneko T, Nakanishi S, Mizuno N. 1994.
Immunohistochemical localization of metabotropic glutamate receptors, mGluR2 and
mGluR3, in rat cerebellar cortex. Neuron. 13(1), 55–66.
mla: Ohishi, Hitoshi, et al. “Immunohistochemical Localization of Metabotropic Glutamate
Receptors, MGluR2 and MGluR3, in Rat Cerebellar Cortex.” Neuron, vol. 13,
no. 1, Elsevier, 1994, pp. 55–66, doi:10.1016/0896-6273(94)90459-6.
short: H. Ohishi, R. Ogawa Meguro, R. Shigemoto, T. Kaneko, S. Nakanishi, N. Mizuno,
Neuron 13 (1994) 55–66.
date_created: 2018-12-11T11:58:22Z
date_published: 1994-07-01T00:00:00Z
date_updated: 2022-06-07T13:21:58Z
day: '01'
doi: 10.1016/0896-6273(94)90459-6
extern: '1'
external_id:
pmid:
- '8043281'
fulldoi: https://doi.org/10.1016/0896-6273(94)90459-6
intvolume: ' 13'
issue: '1'
language:
- iso: eng
main_file_link:
- url: https://www.sciencedirect.com/science/article/pii/0896627394904596?via%3Dihub
month: '07'
oa_version: None
page: 55 - 66
pmid: 1
publication: Neuron
publication_identifier:
issn:
- 0896-6273
publication_status: published
publisher: Elsevier
publist_id: '4342'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Immunohistochemical localization of metabotropic glutamate receptors, mGluR2
and mGluR3, in rat cerebellar cortex
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 13
year: '1994'
...
---
_id: '3475'
abstract:
- lang: eng
text: '1. A potassium channel activated by internal Na+ ions (K+Na channel) was
identified in peripheral myelinated axons of Xenopus laevis using the cell-attached
and excised configurations of the patch clamp technique. 2. The single-channel
conductance for the main open state was 88 pS with [K+]o = 105 mM and pS with
[K+]o = 2.5 mM ([K+]i = 105 mM). The channel was selectively permeable to K+ over
Na+ ions. A characteristic feature of the K+Na channel was the frequent occurrence
of subconductance states. 3. The open probability of the channel was strongly
dependent on the concentration of Na+ ions at the inner side of the membrane.
The half-maximal activating Na+ concentration and the Hill coefficient were 33
mM and 2.9, respectively. The open probability of the channel showed only weak
potential dependence. 4. The K+Na channel was relatively insensitive to external
tetraethylammonium (TEA+) in comparison with voltage-dependent axonal K+ channels;
the half-maximal inhibitory concentration (IC50) was 21.3 mM (at -90 mV). In contrast,
the channel was blocked by low concentrations of external Ba2+ and Cs+ ions, with
IC50 values of 0.7 and 1.1 mM, respectively (at -90 mV). The block by Ba2+ and
Cs+ was more pronounced at negative than at positive membrane potentials. 5. A
comparison of the number of K+Na channels in nodal and paranodal patches from
the same axon revealed that the channel density was about 10-fold higher at the
node of Ranvier than at the paranode. Moreover, a correlation between the number
of K+Na channels and voltage-dependent Na+ channels in the same patches was found,
suggesting co-localization of both channel types. 6. As weakly potential-dependent
(''leakage'') channels, axonal K+Na channels may be involved in setting the resting
potential of vertebrate axons. Simulations of Na+ ion diffusion suggest two possible
mechanisms of activation of K+Na channels: the local increase of Na+ concentration
in a cluster of Na+ channels during a single action potential or the accumulation
in the intracellular axonal compartment during a train of action potentials.'
acknowledgement: 'We thank Drs M.Häusser and A. Villarroel for critically reading
the manuscript, Dr E. v. Kitzing and A. Roth for many helpful discussions. This
work was supported by the Deutsche Forschungsgemeinschaft (Vo188/13-2). '
article_processing_charge: No
article_type: original
author:
- first_name: Duk
full_name: Koh, Duk
last_name: Koh
- first_name: Peter M
full_name: Jonas, Peter M
id: 353C1B58-F248-11E8-B48F-1D18A9856A87
last_name: Jonas
orcid: 0000-0001-5001-4804
- first_name: Werner
full_name: Vogel, Werner
last_name: Vogel
citation:
ama: Koh D, Jonas PM, Vogel W. Na+-activated K+ channels localized in the nodal
region of myelinated axons of Xenopus. Journal of Physiology. 1994;479:183-197.
doi:10.1113/jphysiol.1994.sp020287
apa: Koh, D., Jonas, P. M., & Vogel, W. (1994). Na+-activated K+ channels localized
in the nodal region of myelinated axons of Xenopus. Journal of Physiology.
Wiley-Blackwell. https://doi.org/10.1113/jphysiol.1994.sp020287
chicago: Koh, Duk, Peter M Jonas, and Werner Vogel. “Na+-Activated K+ Channels Localized
in the Nodal Region of Myelinated Axons of Xenopus.” Journal of Physiology.
Wiley-Blackwell, 1994. https://doi.org/10.1113/jphysiol.1994.sp020287.
ieee: D. Koh, P. M. Jonas, and W. Vogel, “Na+-activated K+ channels localized in
the nodal region of myelinated axons of Xenopus,” Journal of Physiology,
vol. 479. Wiley-Blackwell, pp. 183–197, 1994.
ista: Koh D, Jonas PM, Vogel W. 1994. Na+-activated K+ channels localized in the
nodal region of myelinated axons of Xenopus. Journal of Physiology. 479, 183–197.
mla: Koh, Duk, et al. “Na+-Activated K+ Channels Localized in the Nodal Region of
Myelinated Axons of Xenopus.” Journal of Physiology, vol. 479, Wiley-Blackwell,
1994, pp. 183–97, doi:10.1113/jphysiol.1994.sp020287.
short: D. Koh, P.M. Jonas, W. Vogel, Journal of Physiology 479 (1994) 183–197.
date_created: 2018-12-11T12:03:31Z
date_published: 1994-01-01T00:00:00Z
date_updated: 2022-06-03T11:09:21Z
day: '01'
doi: 10.1113/jphysiol.1994.sp020287
extern: '1'
external_id:
pmid:
- '7799220 '
fulldoi: https://doi.org/10.1113/jphysiol.1994.sp020287
intvolume: ' 479'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1155738/
month: '01'
oa: 1
oa_version: Published Version
page: 183 - 197
pmid: 1
publication: Journal of Physiology
publication_identifier:
issn:
- 0022-3751
publication_status: published
publisher: Wiley-Blackwell
publist_id: '2912'
quality_controlled: '1'
status: public
title: Na+-activated K+ channels localized in the nodal region of myelinated axons
of Xenopus
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 479
year: '1994'
...