---
_id: '6158'
abstract:
- lang: eng
text: Wild isolates of Caenorhabditis elegans can feed either alone or in groups1,2.
This natural variation in behaviour is associated with a single residue difference
in NPR-1, a predicted G-protein-coupled neuropeptide receptor related to Neuropeptide
Y receptors2. Here we show that the NPR-1 isoform associated with solitary feeding
acts in neurons exposed to the body fluid to inhibit social feeding. Furthermore,
suppressing the activity of these neurons, called AQR, PQR and URX, using an activated
K+ channel, inhibits social feeding. NPR-1 activity in AQR, PQR and URX neurons
seems to suppress social feeding by antagonizing signalling through a cyclic GMP-gated
ion channel encoded by tax-2 and tax-4. We show that mutations in tax-2 or tax-4
disrupt social feeding, and that tax-4 is required in several neurons for social
feeding, including one or more of AQR, PQR and URX. The AQR, PQR and URX neurons
are unusual in C. elegans because they are directly exposed to the pseudocoelomic
body fluid3. Our data suggest a model in which these neurons integrate antagonistic
signals to control the choice between social and solitary feeding behaviour.
author:
- first_name: Juliet C.
full_name: Coates, Juliet C.
last_name: Coates
- first_name: Mario
full_name: de Bono, Mario
id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
last_name: de Bono
orcid: 0000-0001-8347-0443
citation:
ama: Coates JC, de Bono M. Antagonistic pathways in neurons exposed to body fluid
regulate social feeding in Caenorhabditis elegans. Nature. 2002;419(6910):925-929.
doi:10.1038/nature01170
apa: Coates, J. C., & de Bono, M. (2002). Antagonistic pathways in neurons exposed
to body fluid regulate social feeding in Caenorhabditis elegans. Nature.
Springer Nature. https://doi.org/10.1038/nature01170
chicago: Coates, Juliet C., and Mario de Bono. “Antagonistic Pathways in Neurons
Exposed to Body Fluid Regulate Social Feeding in Caenorhabditis Elegans.” Nature.
Springer Nature, 2002. https://doi.org/10.1038/nature01170.
ieee: J. C. Coates and M. de Bono, “Antagonistic pathways in neurons exposed to
body fluid regulate social feeding in Caenorhabditis elegans,” Nature,
vol. 419, no. 6910. Springer Nature, pp. 925–929, 2002.
ista: Coates JC, de Bono M. 2002. Antagonistic pathways in neurons exposed to body
fluid regulate social feeding in Caenorhabditis elegans. Nature. 419(6910), 925–929.
mla: Coates, Juliet C., and Mario de Bono. “Antagonistic Pathways in Neurons Exposed
to Body Fluid Regulate Social Feeding in Caenorhabditis Elegans.” Nature,
vol. 419, no. 6910, Springer Nature, 2002, pp. 925–29, doi:10.1038/nature01170.
short: J.C. Coates, M. de Bono, Nature 419 (2002) 925–929.
date_created: 2019-03-21T10:09:20Z
date_published: 2002-10-31T00:00:00Z
date_updated: 2021-01-12T08:06:26Z
day: '31'
doi: 10.1038/nature01170
extern: '1'
external_id:
pmid:
- '12410311'
intvolume: ' 419'
issue: '6910'
language:
- iso: eng
month: '10'
oa_version: None
page: 925-929
pmid: 1
publication: Nature
publication_identifier:
issn:
- 0028-0836
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
status: public
title: Antagonistic pathways in neurons exposed to body fluid regulate social feeding
in Caenorhabditis elegans
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 419
year: '2002'
...
---
_id: '6159'
abstract:
- lang: eng
text: 'Natural Caenorhabditis elegans isolates exhibit either social or solitary
feeding on bacteria. We show here that social feeding is induced by nociceptive
neurons that detect adverse or stressful conditions. Ablation of the nociceptive
neurons ASH and ADL transforms social animals into solitary feeders. Social feeding
is probably due to the sensation of noxious chemicals by ASH and ADL neurons;
it requires the genes ocr-2 and osm-9, which encode TRP-related transduction channels,
and odr-4 and odr-8, which are required to localize sensory chemoreceptors to
cilia. Other sensory neurons may suppress social feeding, as social feeding in
ocr-2 and odr-4 mutants is restored by mutations in osm-3, a gene required for
the development of 26 ciliated sensory neurons. Our data suggest a model for regulation
of social feeding by opposing sensory inputs: aversive inputs to nociceptive neurons
promote social feeding, whereas antagonistic inputs from neurons that express
osm-3 inhibit aggregation.'
author:
- first_name: Mario
full_name: de Bono, Mario
id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
last_name: de Bono
orcid: 0000-0001-8347-0443
- first_name: David M.
full_name: Tobin, David M.
last_name: Tobin
- first_name: M. Wayne
full_name: Davis, M. Wayne
last_name: Davis
- first_name: Leon
full_name: Avery, Leon
last_name: Avery
- first_name: Cornelia I.
full_name: Bargmann, Cornelia I.
last_name: Bargmann
citation:
ama: de Bono M, Tobin DM, Davis MW, Avery L, Bargmann CI. Social feeding in Caenorhabditis
elegans is induced by neurons that detect aversive stimuli. Nature. 2002;419(6910):899-903.
doi:10.1038/nature01169
apa: de Bono, M., Tobin, D. M., Davis, M. W., Avery, L., & Bargmann, C. I. (2002).
Social feeding in Caenorhabditis elegans is induced by neurons that detect aversive
stimuli. Nature. Springer Nature. https://doi.org/10.1038/nature01169
chicago: Bono, Mario de, David M. Tobin, M. Wayne Davis, Leon Avery, and Cornelia
I. Bargmann. “Social Feeding in Caenorhabditis Elegans Is Induced by Neurons That
Detect Aversive Stimuli.” Nature. Springer Nature, 2002. https://doi.org/10.1038/nature01169.
ieee: M. de Bono, D. M. Tobin, M. W. Davis, L. Avery, and C. I. Bargmann, “Social
feeding in Caenorhabditis elegans is induced by neurons that detect aversive stimuli,”
Nature, vol. 419, no. 6910. Springer Nature, pp. 899–903, 2002.
ista: de Bono M, Tobin DM, Davis MW, Avery L, Bargmann CI. 2002. Social feeding
in Caenorhabditis elegans is induced by neurons that detect aversive stimuli.
Nature. 419(6910), 899–903.
mla: de Bono, Mario, et al. “Social Feeding in Caenorhabditis Elegans Is Induced
by Neurons That Detect Aversive Stimuli.” Nature, vol. 419, no. 6910, Springer
Nature, 2002, pp. 899–903, doi:10.1038/nature01169.
short: M. de Bono, D.M. Tobin, M.W. Davis, L. Avery, C.I. Bargmann, Nature 419 (2002)
899–903.
date_created: 2019-03-21T10:27:04Z
date_published: 2002-10-31T00:00:00Z
date_updated: 2021-01-12T08:06:27Z
day: '31'
doi: 10.1038/nature01169
extern: '1'
external_id:
pmid:
- '12410303'
intvolume: ' 419'
issue: '6910'
language:
- iso: eng
month: '10'
oa_version: None
page: 899-903
pmid: 1
publication: Nature
publication_identifier:
issn:
- 0028-0836
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
status: public
title: Social feeding in Caenorhabditis elegans is induced by neurons that detect
aversive stimuli
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 419
year: '2002'
...
---
_id: '204'
abstract:
- lang: eng
text: Let k⩾5 be an integer, and let x⩾1 be an arbitrary real number. We derive
a bound[Formula presented] for the number of positive integers less than or equal
to x which can be represented as a sum of two non-negative coprime kth powers,
in essentially more than one way.
article_processing_charge: No
article_type: original
author:
- first_name: Timothy D
full_name: Browning, Timothy D
id: 35827D50-F248-11E8-B48F-1D18A9856A87
last_name: Browning
orcid: 0000-0002-8314-0177
citation:
ama: Browning TD. Equal Sums of Two kth Powers. Journal of Number Theory.
2002;96(2):293-318. doi:10.1006/jnth.2002.2800
apa: Browning, T. D. (2002). Equal Sums of Two kth Powers. Journal of Number
Theory. Academic Press. https://doi.org/10.1006/jnth.2002.2800
chicago: Browning, Timothy D. “Equal Sums of Two Kth Powers.” Journal of Number
Theory. Academic Press, 2002. https://doi.org/10.1006/jnth.2002.2800.
ieee: T. D. Browning, “Equal Sums of Two kth Powers,” Journal of Number Theory,
vol. 96, no. 2. Academic Press, pp. 293–318, 2002.
ista: Browning TD. 2002. Equal Sums of Two kth Powers. Journal of Number Theory.
96(2), 293–318.
mla: Browning, Timothy D. “Equal Sums of Two Kth Powers.” Journal of Number Theory,
vol. 96, no. 2, Academic Press, 2002, pp. 293–318, doi:10.1006/jnth.2002.2800.
short: T.D. Browning, Journal of Number Theory 96 (2002) 293–318.
date_created: 2018-12-11T11:45:11Z
date_published: 2002-10-02T00:00:00Z
date_updated: 2023-07-26T12:15:14Z
day: '02'
doi: 10.1006/jnth.2002.2800
extern: '1'
intvolume: ' 96'
issue: '2'
language:
- iso: eng
license: https://creativecommons.org/licenses/by/4.0/
month: '10'
oa_version: Published Version
page: 293 - 318
publication: Journal of Number Theory
publication_identifier:
issn:
- 0022-314X
publication_status: published
publisher: Academic Press
publist_id: '7708'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Equal Sums of Two kth Powers
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 96
year: '2002'
...
---
_id: '859'
abstract:
- lang: eng
text: The polymeric ubiquitin (poly-u) genes are composed of tandem 228-bp repeats
with no spacer sequences between individual monomer units. Ubiquitin is one of
the most conserved proteins known to date, and the individual units within a number
of poly-u genes are significantly more similar to each other than would be expected
if each unit evolved independently. It has been proposed that the rather striking
similarity among poly-u monomers in some lineages is caused by a series of homogenization
events. Here we report the sequences of the polyubiquitin-C (Ubc) genes in two
mouse strains. Analysis of these sequences, as well as those of the previously
reported Chinese hamster and rat poly-u genes, supports the assertion that the
homogenization of the ubiquitin-C gene in rodents is due to unequal crossing-over
events. The sequence divergence of noncoding DNA was used to estimate the frequency
of unequal crossing-over events (6.3 x 10-5 events per generation) in the Ubc
gene, as well as to provide evidence of apparent selection in the poly-u gene.
acknowledgement: We are thankful to J.A. Southerland and P.L. Jiang for technical
assistance in DNA sequencing, as well as to Y.I. Pavlov for helpful discussions.
This work was supported by public Health Service Research Grant AI45135 from the
Institute of Allergy and Infectious Diseases, National Institutes of Health.
article_processing_charge: No
article_type: original
author:
- first_name: Andrey
full_name: Perelygin, Andrey
last_name: Perelygin
- first_name: Fyodor
full_name: Kondrashov, Fyodor
id: 44FDEF62-F248-11E8-B48F-1D18A9856A87
last_name: Kondrashov
orcid: 0000-0001-8243-4694
- first_name: Igor
full_name: Rogozin, Igor
last_name: Rogozin
- first_name: Margo
full_name: Brinton, Margo
last_name: Brinton
citation:
ama: Perelygin A, Kondrashov F, Rogozin I, Brinton M. Evolution of the mouse polyubiquitin
C gene. Journal of Molecular Evolution. 2002;55(2):202-210. doi:10.1007/s00239-002-2318-0
apa: Perelygin, A., Kondrashov, F., Rogozin, I., & Brinton, M. (2002). Evolution
of the mouse polyubiquitin C gene. Journal of Molecular Evolution. Springer.
https://doi.org/10.1007/s00239-002-2318-0
chicago: Perelygin, Andrey, Fyodor Kondrashov, Igor Rogozin, and Margo Brinton.
“Evolution of the Mouse Polyubiquitin C Gene.” Journal of Molecular Evolution.
Springer, 2002. https://doi.org/10.1007/s00239-002-2318-0.
ieee: A. Perelygin, F. Kondrashov, I. Rogozin, and M. Brinton, “Evolution of the
mouse polyubiquitin C gene,” Journal of Molecular Evolution, vol. 55, no.
2. Springer, pp. 202–210, 2002.
ista: Perelygin A, Kondrashov F, Rogozin I, Brinton M. 2002. Evolution of the mouse
polyubiquitin C gene. Journal of Molecular Evolution. 55(2), 202–210.
mla: Perelygin, Andrey, et al. “Evolution of the Mouse Polyubiquitin C Gene.” Journal
of Molecular Evolution, vol. 55, no. 2, Springer, 2002, pp. 202–10, doi:10.1007/s00239-002-2318-0.
short: A. Perelygin, F. Kondrashov, I. Rogozin, M. Brinton, Journal of Molecular
Evolution 55 (2002) 202–210.
date_created: 2018-12-11T11:48:53Z
date_published: 2002-01-01T00:00:00Z
date_updated: 2023-07-26T12:01:34Z
day: '01'
doi: 10.1007/s00239-002-2318-0
extern: '1'
external_id:
pmid:
- '12107596'
intvolume: ' 55'
issue: '2'
language:
- iso: eng
month: '01'
oa_version: None
page: 202 - 210
pmid: 1
publication: Journal of Molecular Evolution
publication_identifier:
issn:
- 0022-2844
publication_status: published
publisher: Springer
publist_id: '6787'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Evolution of the mouse polyubiquitin C gene
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 55
year: '2002'
...
---
_id: '871'
abstract:
- lang: eng
text: 'BACKGROUND: Gene duplications have a major role in the evolution of new biological
functions. Theoretical studies often assume that a duplication per se is selectively
neutral and that, following a duplication, one of the gene copies is freed from
purifying (stabilizing) selection, which creates the potential for evolution of
a new function. RESULTS: In search of systematic evidence of accelerated evolution
after duplication, we used data from 26 bacterial, six archaeal, and seven eukaryotic
genomes to compare the mode and strength of selection acting on recently duplicated
genes (paralogs) and on similarly diverged, unduplicated orthologous genes in
different species. We find that the ratio of nonsynonymous to synonymous substitutions
(Kn/Ks) in most paralogous pairs is <<1 and that paralogs typically evolve
at similar rates, without significant asymmetry, indicating that both paralogs
produced by a duplication are subject to purifying selection. This selection is,
however, substantially weaker than the purifying selection affecting unduplicated
orthologs that have diverged to the same extent as the analyzed paralogs. Most
of the recently duplicated genes appear to be involved in various forms of environmental
response; in particular, many of them encode membrane and secreted proteins. CONCLUSIONS:
The results of this analysis indicate that recently duplicated paralogs evolve
faster than orthologs with the same level of divergence and similar functions,
but apparently do not experience a phase of neutral evolution. We hypothesize
that gene duplications that persist in an evolving lineage are beneficial from
the time of their origin, due primarily to a protein dosage effect in response
to variable environmental conditions; duplications are likely to give rise to
new functions at a later phase of their evolution once a higher level of divergence
is reached.'
acknowledgement: We are grateful to A.S. Kondrashov for numerous helpful suggestions,
to I. King Jordan, M.A. Roytberg, J.L. Spouge and D.A. Kondrashov for useful discussions
and to A.S. Kondrashov, I. King Jordan and D.J. Lipman for critical reading of the
manuscript.
article_processing_charge: No
article_type: original
author:
- first_name: Fyodor
full_name: Kondrashov, Fyodor
id: 44FDEF62-F248-11E8-B48F-1D18A9856A87
last_name: Kondrashov
orcid: 0000-0001-8243-4694
- first_name: Igor
full_name: Rogozin, Igor
last_name: Rogozin
- first_name: Yuri
full_name: Wolf, Yuri
last_name: Wolf
- first_name: Eugene
full_name: Koonin, Eugene
last_name: Koonin
citation:
ama: Kondrashov F, Rogozin I, Wolf Y, Koonin E. Selection in the evolution of gene
duplications . Genome Biology. 2002;3(2). doi:10.1186/gb-2002-3-2-research0008
apa: Kondrashov, F., Rogozin, I., Wolf, Y., & Koonin, E. (2002). Selection in
the evolution of gene duplications . Genome Biology. BioMed Central. https://doi.org/10.1186/gb-2002-3-2-research0008
chicago: Kondrashov, Fyodor, Igor Rogozin, Yuri Wolf, and Eugene Koonin. “Selection
in the Evolution of Gene Duplications .” Genome Biology. BioMed Central,
2002. https://doi.org/10.1186/gb-2002-3-2-research0008.
ieee: F. Kondrashov, I. Rogozin, Y. Wolf, and E. Koonin, “Selection in the evolution
of gene duplications ,” Genome Biology, vol. 3, no. 2. BioMed Central,
2002.
ista: Kondrashov F, Rogozin I, Wolf Y, Koonin E. 2002. Selection in the evolution
of gene duplications . Genome Biology. 3(2).
mla: Kondrashov, Fyodor, et al. “Selection in the Evolution of Gene Duplications
.” Genome Biology, vol. 3, no. 2, BioMed Central, 2002, doi:10.1186/gb-2002-3-2-research0008.
short: F. Kondrashov, I. Rogozin, Y. Wolf, E. Koonin, Genome Biology 3 (2002).
date_created: 2018-12-11T11:48:57Z
date_published: 2002-01-01T00:00:00Z
date_updated: 2023-07-26T11:48:27Z
day: '01'
doi: 10.1186/gb-2002-3-2-research0008
extern: '1'
external_id:
pmid:
- '11864370'
intvolume: ' 3'
issue: '2'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC65685/
month: '01'
oa: 1
oa_version: Published Version
pmid: 1
publication: Genome Biology
publication_identifier:
issn:
- 1465-6906
publication_status: published
publisher: BioMed Central
publist_id: '6781'
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Selection in the evolution of gene duplications '
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 3
year: '2002'
...
---
_id: '885'
abstract:
- lang: eng
text: We study fitness landscape in the space of protein sequences by relating sets
of human pathogenic missense mutations in 32 proteins to amino acid substitutions
that occurred in the course of evolution of these proteins. On average, ≈10% of
deviations of a nonhuman protein from its human ortholog are compensated pathogenic
deviations (CPDs), i.e., are caused by an amino acid substitution that, at this
site, would be pathogenic to humans. Normal functioning of a CPD-containing protein
must be caused by other, compensatory deviations of the nonhuman species from
humans. Together, a CPD and the corresponding compensatory deviation form a Dobzhansky-Muller
incompatibility that can be visualized as the corner on a fitness ridge. Thus,
proteins evolve along fitness ridges which contain only ≈10 steps between sucessive
corners. The fraction of CPDs among all deviations of a protein from its human
ortholog does not increase with the evolutionary distance between the proteins,
indicating that subtitutions that carry evolving proteins around these corners
occur in rapid succession, driven by positive selection. Data on fitness of interspecies
hybrids suggest that the compensatory change that makes a CPD fit usually occurs
within the same protein. Data on protein structures and on cooccurrence of amino
acids at different sites of multiple orthologous proteins often make it possible
to provisionally identify the substitution that compensates a partiCUlar CPD.
article_processing_charge: No
article_type: original
author:
- first_name: Alexey
full_name: Kondrashov, Alexey
last_name: Kondrashov
- first_name: Shamil
full_name: Sunyaev, Shamil
last_name: Sunyaev
- first_name: Fyodor
full_name: Kondrashov, Fyodor
id: 44FDEF62-F248-11E8-B48F-1D18A9856A87
last_name: Kondrashov
orcid: 0000-0001-8243-4694
citation:
ama: Kondrashov A, Sunyaev S, Kondrashov F. Dobzhansky-Muller incompatibilities
in protein evolution. PNAS. 2002;99(23):14878-14883. doi:10.1073/pnas.232565499
apa: Kondrashov, A., Sunyaev, S., & Kondrashov, F. (2002). Dobzhansky-Muller
incompatibilities in protein evolution. PNAS. National Academy of Sciences.
https://doi.org/10.1073/pnas.232565499
chicago: Kondrashov, Alexey, Shamil Sunyaev, and Fyodor Kondrashov. “Dobzhansky-Muller
Incompatibilities in Protein Evolution.” PNAS. National Academy of Sciences,
2002. https://doi.org/10.1073/pnas.232565499.
ieee: A. Kondrashov, S. Sunyaev, and F. Kondrashov, “Dobzhansky-Muller incompatibilities
in protein evolution,” PNAS, vol. 99, no. 23. National Academy of Sciences,
pp. 14878–14883, 2002.
ista: Kondrashov A, Sunyaev S, Kondrashov F. 2002. Dobzhansky-Muller incompatibilities
in protein evolution. PNAS. 99(23), 14878–14883.
mla: Kondrashov, Alexey, et al. “Dobzhansky-Muller Incompatibilities in Protein
Evolution.” PNAS, vol. 99, no. 23, National Academy of Sciences, 2002,
pp. 14878–83, doi:10.1073/pnas.232565499.
short: A. Kondrashov, S. Sunyaev, F. Kondrashov, PNAS 99 (2002) 14878–14883.
date_created: 2018-12-11T11:49:01Z
date_published: 2002-11-12T00:00:00Z
date_updated: 2023-07-26T09:48:37Z
day: '12'
doi: 10.1073/pnas.232565499
extern: '1'
external_id:
pmid:
- '12403824'
intvolume: ' 99'
issue: '23'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC137512/
month: '11'
oa: 1
oa_version: Published Version
page: 14878 - 14883
pmid: 1
publication: PNAS
publication_identifier:
issn:
- 0027-8424
publication_status: published
publisher: National Academy of Sciences
publist_id: '6763'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Dobzhansky-Muller incompatibilities in protein evolution
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 99
year: '2002'
...
---
_id: '897'
abstract:
- lang: eng
text: "Transcription is a slow and expensive process: in eukaryotes, approximately
20 nucleotides can be transcribed per second at the expense of at least two ATP
molecules per nucleotide. Thus, at least for highly expressed genes, transcription
of long introns, which are particularly common in mammals, is costly. Using data
on the expression of genes that encode proteins in Caenorhabditis elegans and
Homo sapiens, we show that introns in highly expressed genes are substantially
shorter than those in genes that are expressed at low levels. This difference
is greater in humans, such that introns are, on average, 14 times shorter in highly
expressed genes than in genes with low expression, whereas in C. Elegans the difference
in intron length is only twofold. In contrast, the density of introns in a gene
does not strongly depend on the level of gene expression. Thus, natural selection
appears to favor short introns in highly expressed genes to minimize the cost
of transcription and other molecular processes, such as splicing.\r\n"
acknowledgement: We are grateful to A. Kondrashov, I. Rogozin and A. Feldman for reading
the manuscript and P. Bouman, J. Cherry, J. Blumensteil and T. Kim for discussion.
article_processing_charge: No
article_type: original
author:
- first_name: Cristian
full_name: Castillo Davis, Cristian
last_name: Castillo Davis
- first_name: Sergei
full_name: Mekhedov, Sergei
last_name: Mekhedov
- first_name: Daniel
full_name: Hartl, Daniel
last_name: Hartl
- first_name: Eugene
full_name: Koonin, Eugene
last_name: Koonin
- first_name: Fyodor
full_name: Kondrashov, Fyodor
id: 44FDEF62-F248-11E8-B48F-1D18A9856A87
last_name: Kondrashov
orcid: 0000-0001-8243-4694
citation:
ama: Castillo Davis C, Mekhedov S, Hartl D, Koonin E, Kondrashov F. Selection for
short introns in highly expressed genes. Nature Genetics. 2002;31(4):415-418.
doi:10.1038/ng940
apa: Castillo Davis, C., Mekhedov, S., Hartl, D., Koonin, E., & Kondrashov,
F. (2002). Selection for short introns in highly expressed genes. Nature Genetics.
Nature Publishing Group. https://doi.org/10.1038/ng940
chicago: Castillo Davis, Cristian, Sergei Mekhedov, Daniel Hartl, Eugene Koonin,
and Fyodor Kondrashov. “Selection for Short Introns in Highly Expressed Genes.”
Nature Genetics. Nature Publishing Group, 2002. https://doi.org/10.1038/ng940.
ieee: C. Castillo Davis, S. Mekhedov, D. Hartl, E. Koonin, and F. Kondrashov, “Selection
for short introns in highly expressed genes,” Nature Genetics, vol. 31,
no. 4. Nature Publishing Group, pp. 415–418, 2002.
ista: Castillo Davis C, Mekhedov S, Hartl D, Koonin E, Kondrashov F. 2002. Selection
for short introns in highly expressed genes. Nature Genetics. 31(4), 415–418.
mla: Castillo Davis, Cristian, et al. “Selection for Short Introns in Highly Expressed
Genes.” Nature Genetics, vol. 31, no. 4, Nature Publishing Group, 2002,
pp. 415–18, doi:10.1038/ng940.
short: C. Castillo Davis, S. Mekhedov, D. Hartl, E. Koonin, F. Kondrashov, Nature
Genetics 31 (2002) 415–418.
date_created: 2018-12-11T11:49:05Z
date_published: 2002-08-01T00:00:00Z
date_updated: 2023-07-26T09:45:30Z
day: '01'
doi: 10.1038/ng940
extern: '1'
external_id:
pmid:
- '12134150'
intvolume: ' 31'
issue: '4'
language:
- iso: eng
month: '08'
oa_version: None
page: 415 - 418
pmid: 1
publication: Nature Genetics
publication_status: published
publisher: Nature Publishing Group
publist_id: '6751'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Selection for short introns in highly expressed genes
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 31
year: '2002'
...
---
_id: '3140'
abstract:
- lang: eng
text: The maturation of synaptic structures depends on inductive interactions between
axons and their prospective targets. One example of such an interaction is the
influence of proprioceptive sensory axons on the differentiation of muscle spindles.
We have monitored the expression of three transcription factors, Egr3, Pea3, and
Erm, that delineate early muscle spindle development in an assay of muscle spindle-inducing
signals. We provide genetic evidence that Neuregulin1 (Nrg1) is required for proprioceptive
afferent-evoked induction of muscle spindle differentiation in the mouse. Ig-Nrg1
isoforms are preferentially expressed by proprioceptive sensory neurons and are
sufficient to induce muscle spindle differentiation in vivo, whereas CRD-Nrg1
isoforms are broadly expressed in sensory and motor neurons but are not required
for muscle spindle induction.
acknowledgement: We thank L. Role for generously providing the CRD-Nrg1 mutant allele
for these studies, L. Parada and D. Anderson for sharing the TrkC and Ngn1 mouse
strains, W. Tourtellotte for providing Egr3 mutant mice, E. Avetisova for expert
technical assistance, X. Yang for experimental help in the initial phase of these
studies, A. Garratt for advice with ErbB antibodies, and L. Role and G. Fischbach
for helpful discussions. The CRD-Nrg1 mutant allele was generated in the lab of
Dr. Lorna Role, with the support of NIH grant NS29071. S.A. and S.H. were supported
by a grant from the Swiss National Science Foundation and the Kanton of Basel-Stadt.
S.J.B. was supported by grants from the NINDS. N.A.S. was supported by a Howard
Hughes Medical Institute Postdoctoral Fellowship for Physicians and a Career Development
Award from the NINDS. T.M.J. was supported by grants from NINDS and is an Investigator
of the Howard Hughes Medical Institute.
article_processing_charge: No
article_type: original
author:
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Neil
full_name: Shneider, Neil
last_name: Shneider
- first_name: Carmen
full_name: Birchmeier, Carmen
last_name: Birchmeier
- first_name: Steven
full_name: Burden, Steven
last_name: Burden
- first_name: Thomas
full_name: Jessell, Thomas
last_name: Jessell
- first_name: Silvia
full_name: Arber, Silvia
last_name: Arber
citation:
ama: Hippenmeyer S, Shneider N, Birchmeier C, Burden S, Jessell T, Arber S. A role
for Neuregulin1 signaling in muscle spindle differentiation. Neuron. 2002;36(6):1035-1049.
doi:10.1016/S0896-6273(02)01101-7
apa: Hippenmeyer, S., Shneider, N., Birchmeier, C., Burden, S., Jessell, T., &
Arber, S. (2002). A role for Neuregulin1 signaling in muscle spindle differentiation.
Neuron. Elsevier. https://doi.org/10.1016/S0896-6273(02)01101-7
chicago: Hippenmeyer, Simon, Neil Shneider, Carmen Birchmeier, Steven Burden, Thomas
Jessell, and Silvia Arber. “A Role for Neuregulin1 Signaling in Muscle Spindle
Differentiation.” Neuron. Elsevier, 2002. https://doi.org/10.1016/S0896-6273(02)01101-7.
ieee: S. Hippenmeyer, N. Shneider, C. Birchmeier, S. Burden, T. Jessell, and S.
Arber, “A role for Neuregulin1 signaling in muscle spindle differentiation,” Neuron,
vol. 36, no. 6. Elsevier, pp. 1035–1049, 2002.
ista: Hippenmeyer S, Shneider N, Birchmeier C, Burden S, Jessell T, Arber S. 2002.
A role for Neuregulin1 signaling in muscle spindle differentiation. Neuron. 36(6),
1035–1049.
mla: Hippenmeyer, Simon, et al. “A Role for Neuregulin1 Signaling in Muscle Spindle
Differentiation.” Neuron, vol. 36, no. 6, Elsevier, 2002, pp. 1035–49,
doi:10.1016/S0896-6273(02)01101-7.
short: S. Hippenmeyer, N. Shneider, C. Birchmeier, S. Burden, T. Jessell, S. Arber,
Neuron 36 (2002) 1035–1049.
date_created: 2018-12-11T12:01:37Z
date_published: 2002-12-19T00:00:00Z
date_updated: 2023-07-17T11:46:43Z
day: '19'
doi: 10.1016/S0896-6273(02)01101-7
extern: '1'
external_id:
pmid:
- '12495620'
intvolume: ' 36'
issue: '6'
language:
- iso: eng
month: '12'
oa_version: None
page: 1035 - 1049
pmid: 1
publication: Neuron
publication_identifier:
issn:
- 0896-6273
publication_status: published
publisher: Elsevier
publist_id: '3558'
quality_controlled: '1'
scopus_import: '1'
status: public
title: A role for Neuregulin1 signaling in muscle spindle differentiation
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 36
year: '2002'
...
---
_id: '3421'
abstract:
- lang: eng
text: Single molecule experiments provide insight into the individuality of biological
macromolecules, their unique function, reaction pathways, trajectories and molecular
interactions. The exceptional signal-to-noise ratio of the atomic force microscope
allows individual proteins to be imaged under physiologically relevant conditions
at a lateral resolution of 0.5–1 nm and a vertical resolution of 0.1–0.2 nm. Recently,
it has become possible to observe single molecule events using this technique.
This capability is reviewed on various water-soluble and membrane proteins. Examples
of the observation of function, variability, and assembly of single proteins are
discussed. Statistical analysis is important to extend conclusions derived from
single molecule experiments to protein species. Such approaches allow the classification
of protein conformations and movements. Recent developments of probe microscopy
techniques allow simultaneous measurement of multiple signals on individual macromolecules,
and greatly extend the range of experiments possible for probing biological systems
at the molecular level. Biologists exploring molecular mechanisms will benefit
from a burgeoning of scanning probe microscopes and of their future combination
with molecular biological experiments.
article_processing_charge: No
article_type: review
author:
- first_name: Daniel
full_name: Mueller, Daniel
last_name: Mueller
- first_name: Harald L
full_name: Janovjak, Harald L
id: 33BA6C30-F248-11E8-B48F-1D18A9856A87
last_name: Janovjak
orcid: 0000-0002-8023-9315
- first_name: Tiina
full_name: Lehto, Tiina
last_name: Lehto
- first_name: Lars
full_name: Kuerschner, Lars
last_name: Kuerschner
- first_name: Kurt
full_name: Anderson, Kurt
last_name: Anderson
citation:
ama: Mueller D, Janovjak HL, Lehto T, Kuerschner L, Anderson K. Observing structure,
function and assembly of single proteins by AFM. Progress in Biophysics and
Molecular Biology. 2002;79(1-3):1-43. doi:10.1016/S0079-6107(02)00009-3
apa: Mueller, D., Janovjak, H. L., Lehto, T., Kuerschner, L., & Anderson, K.
(2002). Observing structure, function and assembly of single proteins by AFM.
Progress in Biophysics and Molecular Biology. Elsevier. https://doi.org/10.1016/S0079-6107(02)00009-3
chicago: Mueller, Daniel, Harald L Janovjak, Tiina Lehto, Lars Kuerschner, and Kurt
Anderson. “Observing Structure, Function and Assembly of Single Proteins by AFM.”
Progress in Biophysics and Molecular Biology. Elsevier, 2002. https://doi.org/10.1016/S0079-6107(02)00009-3.
ieee: D. Mueller, H. L. Janovjak, T. Lehto, L. Kuerschner, and K. Anderson, “Observing
structure, function and assembly of single proteins by AFM,” Progress in Biophysics
and Molecular Biology, vol. 79, no. 1–3. Elsevier, pp. 1–43, 2002.
ista: Mueller D, Janovjak HL, Lehto T, Kuerschner L, Anderson K. 2002. Observing
structure, function and assembly of single proteins by AFM. Progress in Biophysics
and Molecular Biology. 79(1–3), 1–43.
mla: Mueller, Daniel, et al. “Observing Structure, Function and Assembly of Single
Proteins by AFM.” Progress in Biophysics and Molecular Biology, vol. 79,
no. 1–3, Elsevier, 2002, pp. 1–43, doi:10.1016/S0079-6107(02)00009-3.
short: D. Mueller, H.L. Janovjak, T. Lehto, L. Kuerschner, K. Anderson, Progress
in Biophysics and Molecular Biology 79 (2002) 1–43.
date_created: 2018-12-11T12:03:14Z
date_published: 2002-05-01T00:00:00Z
date_updated: 2023-07-17T11:36:32Z
day: '01'
doi: 10.1016/S0079-6107(02)00009-3
extern: '1'
external_id:
pmid:
- '12225775'
intvolume: ' 79'
issue: 1-3
language:
- iso: eng
month: '05'
oa_version: None
page: 1 - 43
pmid: 1
publication: Progress in Biophysics and Molecular Biology
publication_identifier:
issn:
- 0079-6107
publication_status: published
publisher: Elsevier
publist_id: '2980'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Observing structure, function and assembly of single proteins by AFM
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 79
year: '2002'
...
---
_id: '3422'
abstract:
- lang: eng
text: Quantitative real-time PCR represents a highly sensitive and powerful technique
for the quantitation of nucleic acids. It has a tremendous potential for the high-throughput
analysis of gene expression in research and routine diagnostics. However, the
major hurdle is not the practical performance of the experiments themselves but
rather the efficient evaluation and the mathematical and statistical analysis
of the enormous amount of data gained by this technology, as these functions are
not included in the software provided by the manufacturers of the detection systems.
In this work, we focus on the mathematical evaluation and analysis of the data
generated by quantitative real-time PCR, the calculation of the final results,
the propagation of experimental variation of the measured values to the final
results, and the statistical analysis. We developed a Microsoft Excel-based software
application coded in Visual Basic for Applications, called Q-Gene, which addresses
these points. Q-Gene manages and expedites the planning, performance, and evaluation
of quantitative real-time PCR experiments, as well as the mathematical and statistical
analysis, storage, and graphical presentation of the data. The Q-Gene software
application is a tool to cope with complex quantitative real-time PCR experiments
at a high-throughput scale and considerably expedites and rationalizes the experimental
setup, data analysis, and data management while ensuring highest reproducibility.
article_processing_charge: No
article_type: original
author:
- first_name: Patrick
full_name: Müller, Patrick
last_name: Müller
- first_name: Harald L
full_name: Janovjak, Harald L
id: 33BA6C30-F248-11E8-B48F-1D18A9856A87
last_name: Janovjak
orcid: 0000-0002-8023-9315
- first_name: Andre
full_name: Miserez, Andre
last_name: Miserez
- first_name: Zuzana
full_name: Dobbie, Zuzana
last_name: Dobbie
citation:
ama: Müller P, Janovjak HL, Miserez A, Dobbie Z. Processing of gene expression data
generated by quantitative real-time RT-PCR. Biotechniques. 2002;32(6):1372-1379.
apa: Müller, P., Janovjak, H. L., Miserez, A., & Dobbie, Z. (2002). Processing
of gene expression data generated by quantitative real-time RT-PCR. Biotechniques.
Informa Healthcare.
chicago: Müller, Patrick, Harald L Janovjak, Andre Miserez, and Zuzana Dobbie. “Processing
of Gene Expression Data Generated by Quantitative Real-Time RT-PCR.” Biotechniques.
Informa Healthcare, 2002.
ieee: P. Müller, H. L. Janovjak, A. Miserez, and Z. Dobbie, “Processing of gene
expression data generated by quantitative real-time RT-PCR,” Biotechniques,
vol. 32, no. 6. Informa Healthcare, pp. 1372–1379, 2002.
ista: Müller P, Janovjak HL, Miserez A, Dobbie Z. 2002. Processing of gene expression
data generated by quantitative real-time RT-PCR. Biotechniques. 32(6), 1372–1379.
mla: Müller, Patrick, et al. “Processing of Gene Expression Data Generated by Quantitative
Real-Time RT-PCR.” Biotechniques, vol. 32, no. 6, Informa Healthcare, 2002,
pp. 1372–79.
short: P. Müller, H.L. Janovjak, A. Miserez, Z. Dobbie, Biotechniques 32 (2002)
1372–1379.
date_created: 2018-12-11T12:03:15Z
date_published: 2002-06-01T00:00:00Z
date_updated: 2023-07-17T11:29:06Z
day: '01'
extern: '1'
external_id:
pmid:
- '12074169'
intvolume: ' 32'
issue: '6'
language:
- iso: eng
month: '06'
oa_version: None
page: 1372 - 1379
pmid: 1
publication: Biotechniques
publication_identifier:
issn:
- 0736-6205
publication_status: published
publisher: Informa Healthcare
publist_id: '2979'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Processing of gene expression data generated by quantitative real-time RT-PCR
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 32
year: '2002'
...
---
_id: '3423'
article_processing_charge: No
author:
- first_name: Wolfgang
full_name: Bauer, Wolfgang
last_name: Bauer
- first_name: Mark Tobias
full_name: Bollenbach, Mark Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
- first_name: Marko
full_name: Kleine Berkenbusch, Marko
last_name: Kleine Berkenbusch
- first_name: Holger
full_name: Harreis, Holger
last_name: Harreis
citation:
ama: 'Bauer W, Bollenbach MT, Kleine Berkenbusch M, Harreis H. The percolation interpretation
of the nuclear fragmentation phase transition. In: Proceedings of the 18th
Winter Workshop on Nuclear Dynamics. EP Systema; 2002:111-118.'
apa: 'Bauer, W., Bollenbach, M. T., Kleine Berkenbusch, M., & Harreis, H. (2002).
The percolation interpretation of the nuclear fragmentation phase transition.
In Proceedings of the 18th Winter Workshop on Nuclear Dynamics (pp. 111–118).
Nassau, Bahamas: EP Systema.'
chicago: Bauer, Wolfgang, Mark Tobias Bollenbach, Marko Kleine Berkenbusch, and
Holger Harreis. “The Percolation Interpretation of the Nuclear Fragmentation Phase
Transition.” In Proceedings of the 18th Winter Workshop on Nuclear Dynamics,
111–18. EP Systema, 2002.
ieee: W. Bauer, M. T. Bollenbach, M. Kleine Berkenbusch, and H. Harreis, “The percolation
interpretation of the nuclear fragmentation phase transition,” in Proceedings
of the 18th Winter Workshop on Nuclear Dynamics, Nassau, Bahamas, 2002, pp.
111–118.
ista: Bauer W, Bollenbach MT, Kleine Berkenbusch M, Harreis H. 2002. The percolation
interpretation of the nuclear fragmentation phase transition. Proceedings of the
18th Winter Workshop on Nuclear Dynamics. Winter Workshop on Nuclear Dynamics,
111–118.
mla: Bauer, Wolfgang, et al. “The Percolation Interpretation of the Nuclear Fragmentation
Phase Transition.” Proceedings of the 18th Winter Workshop on Nuclear Dynamics,
EP Systema, 2002, pp. 111–18.
short: W. Bauer, M.T. Bollenbach, M. Kleine Berkenbusch, H. Harreis, in:, Proceedings
of the 18th Winter Workshop on Nuclear Dynamics, EP Systema, 2002, pp. 111–118.
conference:
end_date: 2002-01-22
location: Nassau, Bahamas
name: Winter Workshop on Nuclear Dynamics
start_date: 2002-01-20
date_created: 2018-12-11T12:03:15Z
date_published: 2002-01-01T00:00:00Z
date_updated: 2023-07-17T11:15:14Z
day: '01'
extern: '1'
language:
- iso: eng
month: '01'
oa_version: None
page: 111 - 118
publication: Proceedings of the 18th Winter Workshop on Nuclear Dynamics
publication_status: published
publisher: EP Systema
publist_id: '2978'
status: public
title: The percolation interpretation of the nuclear fragmentation phase transition
type: conference
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
year: '2002'
...
---
_id: '3424'
abstract:
- lang: eng
text: "We give a brief overview of the current understanding of the explosion mechanism
of core collapse supernovae. Our main focus is the impact of rotation on the explosion.
Recent observations of the polarization of the light emitted by supernova explosions
indicate that there are large deviations from spherical symmetry in the very heart
of the explosion the origin of which is unknown. We use the new approach of a
three dimensional test particle based simulation to simulate the infall phase
of a supernova event. The underlying microphysics is simplified to make this computationally
possible. A systematic study of the influence of rotation mainly during the infall
phase of the collapse of a typical iron core is performed. Indications for significant
deviations from spherical symmetry are found in our very rapidly rotating models.
© 2002 American Institute of Physics\r\n"
alternative_title:
- Exotic Clustering, American Institute of Physics Conference Proceedings
article_processing_charge: No
author:
- first_name: Mark Tobias
full_name: Bollenbach, Mark Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
- first_name: Wolfgang
full_name: Bauer, Wolfgang
last_name: Bauer
citation:
ama: 'Bollenbach MT, Bauer W. 3d supernovae collapse calculations. In: Vol 644.
American Institute of Physics; 2002:219-232. doi:10.1063/1.1523196 '
apa: 'Bollenbach, M. T., & Bauer, W. (2002). 3d supernovae collapse calculations
(Vol. 644, pp. 219–232). Presented at the CRIS: Catania Relativistic Ion Studies
, Catania, Italy: American Institute of Physics. https://doi.org/10.1063/1.1523196 '
chicago: Bollenbach, Mark Tobias, and Wolfgang Bauer. “3d Supernovae Collapse Calculations,”
644:219–32. American Institute of Physics, 2002. https://doi.org/10.1063/1.1523196 .
ieee: 'M. T. Bollenbach and W. Bauer, “3d supernovae collapse calculations,” presented
at the CRIS: Catania Relativistic Ion Studies , Catania, Italy, 2002, vol. 644,
pp. 219–232.'
ista: 'Bollenbach MT, Bauer W. 2002. 3d supernovae collapse calculations. CRIS:
Catania Relativistic Ion Studies , Exotic Clustering, American Institute of Physics
Conference Proceedings, vol. 644, 219–232.'
mla: Bollenbach, Mark Tobias, and Wolfgang Bauer. 3d Supernovae Collapse Calculations.
Vol. 644, American Institute of Physics, 2002, pp. 219–32, doi:10.1063/1.1523196 .
short: M.T. Bollenbach, W. Bauer, in:, American Institute of Physics, 2002, pp.
219–232.
conference:
end_date: 2002-06-14
location: Catania, Italy
name: 'CRIS: Catania Relativistic Ion Studies '
start_date: 2002-06-10
date_created: 2018-12-11T12:03:15Z
date_published: 2002-11-26T00:00:00Z
date_updated: 2023-07-17T11:05:27Z
day: '26'
doi: '10.1063/1.1523196 '
extern: '1'
intvolume: ' 644'
language:
- iso: eng
month: '11'
oa_version: None
page: 219 - 232
publication_identifier:
isbn:
- '9781510832008'
publication_status: published
publisher: American Institute of Physics
publist_id: '2977'
quality_controlled: '1'
status: public
title: 3d supernovae collapse calculations
type: conference
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 644
year: '2002'
...
---
_id: '3448'
author:
- first_name: Sanhita
full_name: Mallick, Sanhita
last_name: Mallick
- first_name: Krishnendu
full_name: Krishnendu Chatterjee
id: 2E5DCA20-F248-11E8-B48F-1D18A9856A87
last_name: Chatterjee
orcid: 0000-0002-4561-241X
- first_name: Arif
full_name: Merchant, Arif N
last_name: Merchant
- first_name: Pallab
full_name: Dasgupta, Pallab
last_name: Dasgupta
citation:
ama: 'Mallick S, Chatterjee K, Merchant A, Dasgupta P. Implementation of shape grammar
for plan analysis. In: Elsevier; 2002.'
apa: 'Mallick, S., Chatterjee, K., Merchant, A., & Dasgupta, P. (2002). Implementation
of shape grammar for plan analysis. Presented at the IT-Built: Information Technology
For Built Environment, Elsevier.'
chicago: Mallick, Sanhita, Krishnendu Chatterjee, Arif Merchant, and Pallab Dasgupta.
“Implementation of Shape Grammar for Plan Analysis.” Elsevier, 2002.
ieee: 'S. Mallick, K. Chatterjee, A. Merchant, and P. Dasgupta, “Implementation
of shape grammar for plan analysis,” presented at the IT-Built: Information Technology
For Built Environment, 2002.'
ista: 'Mallick S, Chatterjee K, Merchant A, Dasgupta P. 2002. Implementation of
shape grammar for plan analysis. IT-Built: Information Technology For Built Environment.'
mla: Mallick, Sanhita, et al. Implementation of Shape Grammar for Plan Analysis.
Elsevier, 2002.
short: S. Mallick, K. Chatterjee, A. Merchant, P. Dasgupta, in:, Elsevier, 2002.
conference:
name: 'IT-Built: Information Technology For Built Environment'
date_created: 2018-12-11T12:03:23Z
date_published: 2002-01-15T00:00:00Z
date_updated: 2021-01-12T07:43:31Z
day: '15'
extern: 1
month: '01'
publication_status: published
publisher: Elsevier
publist_id: '2939'
quality_controlled: 0
status: public
title: Implementation of shape grammar for plan analysis
type: conference
year: '2002'
...
---
_id: '3497'
abstract:
- lang: eng
text: The use of advanced patch-clamp recording techniques in brain slices, such
as simultaneous recording from multiple neurons and recording from dendrites or
presynaptic terminals, demands slices of the highest quality. In this context
the mechanics of the tissue slicer are an important factor. Ideally, a tissue
slicer should generate large-amplitude and high-frequency movements of the cutting
blade in a horizontal axis, with minimal vibrations in the vertical axis. We developed
a vibroslicer that fulfils these in part conflicting requirements. The oscillator
is a permanent-magnet-coil-leaf-spring system. Using an auto-resonant mechano-electrical
feedback circuit, large horizontal oscillations (up to 3 mm peak-to-peak) with
high frequency (,90 Hz) are generated. To minimize vertical vibrations, an adjustment
mechanism was employed that allowed alignment of the cutting edge of the blade
with the major axis of the oscillation. A vibroprobe device was used to monitor
vertical vibrations during adjustment. The system is based on the shading of the
light path between a light-emitting diode (LED) and a photodiode. Vibroprobe monitoring
revealed that the vibroslicer, after appropriate adjustment, generated vertical
vibrations of <1 µm, significantly less than many commercial tissue slicers.
Light- and electron-microscopic analysis of surface layers of slices cut with
the vibroslicer showed that cellular elements, dendritic processes and presynaptic
terminals are well preserved under these conditions, as required for patch-clamp
recording from these structures.
acknowledgement: "We thank Dr. M. Frotscher for reading the manuscript, and H. Kressner,
R. Laufersweiler, and A. Bühler for help with the construction of several prototypes
of vibroslicer and vibroprobe. We also thank A. Blomenkamp, K. Winterhalter, B.
Joch, and A. Schneider for technical assistance. This work was supported by grants
of the Deutsche Forschungsgemeinschaft\r\n(SFB 505/C5, C6) and the Human Frontiers
Science Program Organization (RG0017/1998-B)."
article_processing_charge: No
article_type: original
author:
- first_name: Jörg
full_name: Geiger, Jörg
last_name: Geiger
- first_name: Joseph
full_name: Bischofberger, Joseph
last_name: Bischofberger
- first_name: Imre
full_name: Vida, Imre
last_name: Vida
- first_name: Ulrich
full_name: Fröbe, Ulrich
last_name: Fröbe
- first_name: S
full_name: Pfitzinger, S
last_name: Pfitzinger
- first_name: H.
full_name: Weber, H.
last_name: Weber
- first_name: Klaus
full_name: Haverkampf, Klaus
last_name: Haverkampf
- 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: 'Geiger J, Bischofberger J, Vida I, et al. Patch-clamp recording in brain slices
with improved slicer technology. Pflugers Archiv : European Journal of Physiology.
2002;443(3):491-501. doi:10.1007/s00424-001-0735-3'
apa: 'Geiger, J., Bischofberger, J., Vida, I., Fröbe, U., Pfitzinger, S., Weber,
H., … Jonas, P. M. (2002). Patch-clamp recording in brain slices with improved
slicer technology. Pflugers Archiv : European Journal of Physiology. Springer.
https://doi.org/10.1007/s00424-001-0735-3'
chicago: 'Geiger, Jörg, Joseph Bischofberger, Imre Vida, Ulrich Fröbe, S Pfitzinger,
H. Weber, Klaus Haverkampf, and Peter M Jonas. “Patch-Clamp Recording in Brain
Slices with Improved Slicer Technology.” Pflugers Archiv : European Journal
of Physiology. Springer, 2002. https://doi.org/10.1007/s00424-001-0735-3.'
ieee: 'J. Geiger et al., “Patch-clamp recording in brain slices with improved
slicer technology,” Pflugers Archiv : European Journal of Physiology, vol.
443, no. 3. Springer, pp. 491–501, 2002.'
ista: 'Geiger J, Bischofberger J, Vida I, Fröbe U, Pfitzinger S, Weber H, Haverkampf
K, Jonas PM. 2002. Patch-clamp recording in brain slices with improved slicer
technology. Pflugers Archiv : European Journal of Physiology. 443(3), 491–501.'
mla: 'Geiger, Jörg, et al. “Patch-Clamp Recording in Brain Slices with Improved
Slicer Technology.” Pflugers Archiv : European Journal of Physiology, vol.
443, no. 3, Springer, 2002, pp. 491–501, doi:10.1007/s00424-001-0735-3.'
short: 'J. Geiger, J. Bischofberger, I. Vida, U. Fröbe, S. Pfitzinger, H. Weber,
K. Haverkampf, P.M. Jonas, Pflugers Archiv : European Journal of Physiology 443
(2002) 491–501.'
date_created: 2018-12-11T12:03:38Z
date_published: 2002-01-01T00:00:00Z
date_updated: 2023-07-17T07:36:37Z
day: '01'
doi: 10.1007/s00424-001-0735-3
extern: '1'
external_id:
pmid:
- '11810221'
intvolume: ' 443'
issue: '3'
language:
- iso: eng
month: '01'
oa_version: None
page: 491 - 501
pmid: 1
publication: 'Pflugers Archiv : European Journal of Physiology'
publication_identifier:
issn:
- 0031-6768
publication_status: published
publisher: Springer
publist_id: '2890'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Patch-clamp recording in brain slices with improved slicer technology
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 443
year: '2002'
...
---
_id: '3508'
abstract:
- lang: eng
text: A method of automatic conversion of a physical object into a three-dimensional
digital model. The method acquires a set of measured data points on the surface
of a physical model. From the measured data points, the method reconstructs a
digital model of the physical object using a Delaunay complex of the points, a
flow strcuture of the simplicies in the Delaunay complex and retracting the Delaunay
complex into a digital model of the physical object using the flow structure.
The method then outputs the digital model of the physical object.
applicant:
- Raindrop Geomagic, Inc.
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: Ping
full_name: Fu, Ping
last_name: Fu
citation:
ama: Edelsbrunner H, Fu P. Methods of generating three-dimensional digital models
of objects by wrapping point cloud data points. 2002.
apa: Edelsbrunner, H., & Fu, P. (2002). Methods of generating three-dimensional
digital models of objects by wrapping point cloud data points.
chicago: Edelsbrunner, Herbert, and Ping Fu. “Methods of Generating Three-Dimensional
Digital Models of Objects by Wrapping Point Cloud Data Points,” 2002.
ieee: H. Edelsbrunner and P. Fu, “Methods of generating three-dimensional digital
models of objects by wrapping point cloud data points.” 2002.
ista: Edelsbrunner H, Fu P. 2002. Methods of generating three-dimensional digital
models of objects by wrapping point cloud data points.
mla: Edelsbrunner, Herbert, and Ping Fu. Methods of Generating Three-Dimensional
Digital Models of Objects by Wrapping Point Cloud Data Points. 2002.
short: H. Edelsbrunner, P. Fu, (2002).
date_created: 2018-12-11T12:03:42Z
date_published: 2002-04-23T00:00:00Z
date_updated: 2022-01-05T14:09:36Z
day: '23'
extern: '1'
ipc: G16Z99/00 ; G06K9/28 ; G06T17/10 ; G06T17/20
ipn: US6377865B1
main_file_link:
- open_access: '1'
url: https://patents.google.com/patent/US6377865B1
month: '04'
oa: 1
oa_version: Published Version
publication_date: 2002-04-23
publist_id: '2879'
status: public
title: Methods of generating three-dimensional digital models of objects by wrapping
point cloud data points
type: patent
user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9
year: '2002'
...
---
_id: '3533'
abstract:
- lang: eng
text: 'Information in neuronal networks is thought to be represented by the rate
of discharge and the temporal relationship between the discharging neurons. The
discharge frequency of neurons is affected by their afferents and intrinsic properties,
and shows great individual variability. The temporal coordination of neurons is
greatly facilitated by network oscillations. In the hippocampus, population synchrony
fluctuates during theta and gamma oscillations (10-100 ms scale) and can increase
almost 10-fold during sharp wave bursts. Despite these large changes in excitability
in the sub-second scale, longer-term (minute-scale) firing rates of individual
neurons are relatively constant in an unchanging environment. As a result, mean
hippocampal output remains stable over time. To understand the mechanisms responsible
for this homeostasis, we address the following issues: (i) Can firing rates of
single cells be modified? (ii) Once modified, what mechanism(s) can maintain the
changes? We show that firing rates of hippocampal pyramidal cells can be altered
in a novel environment and by Hebbian pairing of physiological input patterns
with postsynaptic burst discharge. We also illustrate a competition between single
spikes and the occurrence of spike bursts. Since spike-inducing (suprathreshold)
inputs decrease the ability of strong (''teaching'') inputs to induce a burst
discharge, we propose that the single spike versus burst competition presents
a homeostatic regulatory mechanism to maintain synaptic strength and, consequently,
firing rate in pyramidal cells.'
article_processing_charge: No
article_type: original
author:
- first_name: György
full_name: Buzsáki, György
last_name: Buzsáki
- 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: George
full_name: Dragoi, George
last_name: Dragoi
- first_name: Kenneth
full_name: Harris, Kenneth
last_name: Harris
- first_name: D.
full_name: Henze, D.
last_name: Henze
- first_name: Hajima
full_name: Hirase, Hajima
last_name: Hirase
citation:
ama: Buzsáki G, Csicsvari JL, Dragoi G, Harris K, Henze D, Hirase H. Homeostatic
maintenance of neuronal excitability by burst discharges in vivo. Cerebral
Cortex. 2002;12(9):893-899. doi:10.1093/cercor/12.9.893
apa: Buzsáki, G., Csicsvari, J. L., Dragoi, G., Harris, K., Henze, D., & Hirase,
H. (2002). Homeostatic maintenance of neuronal excitability by burst discharges
in vivo. Cerebral Cortex. Oxford University Press. https://doi.org/10.1093/cercor/12.9.893
chicago: Buzsáki, György, Jozsef L Csicsvari, George Dragoi, Kenneth Harris, D.
Henze, and Hajima Hirase. “Homeostatic Maintenance of Neuronal Excitability by
Burst Discharges in Vivo.” Cerebral Cortex. Oxford University Press, 2002.
https://doi.org/10.1093/cercor/12.9.893.
ieee: G. Buzsáki, J. L. Csicsvari, G. Dragoi, K. Harris, D. Henze, and H. Hirase,
“Homeostatic maintenance of neuronal excitability by burst discharges in vivo,”
Cerebral Cortex, vol. 12, no. 9. Oxford University Press, pp. 893–899,
2002.
ista: Buzsáki G, Csicsvari JL, Dragoi G, Harris K, Henze D, Hirase H. 2002. Homeostatic
maintenance of neuronal excitability by burst discharges in vivo. Cerebral Cortex.
12(9), 893–899.
mla: Buzsáki, György, et al. “Homeostatic Maintenance of Neuronal Excitability by
Burst Discharges in Vivo.” Cerebral Cortex, vol. 12, no. 9, Oxford University
Press, 2002, pp. 893–99, doi:10.1093/cercor/12.9.893.
short: G. Buzsáki, J.L. Csicsvari, G. Dragoi, K. Harris, D. Henze, H. Hirase, Cerebral
Cortex 12 (2002) 893–899.
date_created: 2018-12-11T12:03:50Z
date_published: 2002-09-01T00:00:00Z
date_updated: 2023-07-17T07:27:12Z
day: '01'
doi: 10.1093/cercor/12.9.893
extern: '1'
external_id:
pmid:
- '12183388'
intvolume: ' 12'
issue: '9'
language:
- iso: eng
month: '09'
oa_version: None
page: 893 - 899
pmid: 1
publication: Cerebral Cortex
publication_identifier:
issn:
- 1047-3211
publication_status: published
publisher: Oxford University Press
publist_id: '2851'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Homeostatic maintenance of neuronal excitability by burst discharges in vivo
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 12
year: '2002'
...
---
_id: '3621'
abstract:
- lang: eng
text: In 1991, Barton and Turelli developed recursions to describe the evolution
of multilocus systems under arbitrary forms of selection. This article generalizes
their approach to allow for arbitrary modes of inheritance, including diploidy,
polyploidy, sex linkage, cytoplasmic inheritance, and genomic imprinting. The
framework is also extended to allow for other deterministic evolutionary forces,
including migration and mutation. Exact recursions that fully describe the state
of the population are presented; these are implemented in a computer algebra package
(available on the Web at http://helios.bto.ed.ac.uk/evolgen). Despite the generality
of our framework, it can describe evolutionary dynamics exactly by just two equations.
These recursions can be further simplified using a "quasi-linkage equilibrium"
(QLE) approximation. We illustrate the methods by finding the effect of natural
selection, sexual selection, mutation, and migration on the genetic composition
of a population.
article_processing_charge: No
article_type: original
author:
- first_name: Mark
full_name: Kirkpatrick, Mark
last_name: Kirkpatrick
- first_name: Toby
full_name: Johnson, Toby
last_name: Johnson
- 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: Kirkpatrick M, Johnson T, Barton NH. General models of multilocus evolution.
Genetics. 2002;161(4):1727-1750. doi:10.1093/genetics/161.4.1727
apa: Kirkpatrick, M., Johnson, T., & Barton, N. H. (2002). General models of
multilocus evolution. Genetics. Genetics Society of America. https://doi.org/10.1093/genetics/161.4.1727
chicago: Kirkpatrick, Mark, Toby Johnson, and Nicholas H Barton. “General Models
of Multilocus Evolution.” Genetics. Genetics Society of America, 2002.
https://doi.org/10.1093/genetics/161.4.1727.
ieee: M. Kirkpatrick, T. Johnson, and N. H. Barton, “General models of multilocus
evolution,” Genetics, vol. 161, no. 4. Genetics Society of America, pp.
1727–1750, 2002.
ista: Kirkpatrick M, Johnson T, Barton NH. 2002. General models of multilocus evolution.
Genetics. 161(4), 1727–1750.
mla: Kirkpatrick, Mark, et al. “General Models of Multilocus Evolution.” Genetics,
vol. 161, no. 4, Genetics Society of America, 2002, pp. 1727–50, doi:10.1093/genetics/161.4.1727.
short: M. Kirkpatrick, T. Johnson, N.H. Barton, Genetics 161 (2002) 1727–1750.
date_created: 2018-12-11T12:04:17Z
date_published: 2002-08-01T00:00:00Z
date_updated: 2023-07-11T13:20:26Z
day: '01'
doi: 10.1093/genetics/161.4.1727
extern: '1'
external_id:
pmid:
- '12196414'
intvolume: ' 161'
issue: '4'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1462196/
month: '08'
oa: 1
oa_version: Published Version
page: 1727 - 1750
pmid: 1
publication: Genetics
publication_identifier:
issn:
- 0016-6731
publication_status: published
publisher: Genetics Society of America
publist_id: '2762'
quality_controlled: '1'
scopus_import: '1'
status: public
title: General models of multilocus evolution
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 161
year: '2002'
...
---
_id: '3757'
abstract:
- lang: eng
text: A central problem in biology is determining how genes interact as parts of
functional networks. Creation and analysis of synthetic networks, composed of
well-characterized genetic elements, provide a framework for theoretical modeling.
Here, with the use of a combinatorial method, a library of networks with varying
connectivity was generated in Escherichia coli. These networks were composed of
genes encoding the transcriptional regulators Lacl, TetR, and lambda Cl, as well
as the corresponding promoters. They displayed phenotypic behaviors resembling
binary logical circuits, with two chemical “inputs” and a fluorescent protein
“output.” Within this simple system, diverse computational functions arose through
changes in network connectivity. Combinatorial synthesis provides an alternative
approach for studying biological networks, as well as an efficient method for
producing diverse phenotypes in vivo.
article_processing_charge: No
article_type: original
author:
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
- first_name: Michael
full_name: Elowitz, Michael
last_name: Elowitz
- first_name: Weihong
full_name: Hsing, Weihong
last_name: Hsing
- first_name: Stanislas
full_name: Leibler, Stanislas
last_name: Leibler
citation:
ama: Guet CC, Elowitz M, Hsing W, Leibler S. Combinatorial synthesis of genetic
networks. Science. 2002;296(5572):1466-1470. doi:10.1126/science.1067407
apa: Guet, C. C., Elowitz, M., Hsing, W., & Leibler, S. (2002). Combinatorial
synthesis of genetic networks. Science. American Association for the Advancement
of Science. https://doi.org/10.1126/science.1067407
chicago: Guet, Calin C, Michael Elowitz, Weihong Hsing, and Stanislas Leibler. “Combinatorial
Synthesis of Genetic Networks.” Science. American Association for the Advancement
of Science, 2002. https://doi.org/10.1126/science.1067407.
ieee: C. C. Guet, M. Elowitz, W. Hsing, and S. Leibler, “Combinatorial synthesis
of genetic networks,” Science, vol. 296, no. 5572. American Association
for the Advancement of Science, pp. 1466–1470, 2002.
ista: Guet CC, Elowitz M, Hsing W, Leibler S. 2002. Combinatorial synthesis of genetic
networks. Science. 296(5572), 1466–1470.
mla: Guet, Calin C., et al. “Combinatorial Synthesis of Genetic Networks.” Science,
vol. 296, no. 5572, American Association for the Advancement of Science, 2002,
pp. 1466–70, doi:10.1126/science.1067407.
short: C.C. Guet, M. Elowitz, W. Hsing, S. Leibler, Science 296 (2002) 1466–1470.
date_created: 2018-12-11T12:05:00Z
date_published: 2002-05-24T00:00:00Z
date_updated: 2023-07-11T12:48:53Z
day: '24'
doi: 10.1126/science.1067407
extern: '1'
external_id:
pmid:
- '12029133'
intvolume: ' 296'
issue: '5572'
language:
- iso: eng
month: '05'
oa_version: None
page: 1466 - 1470
pmid: 1
publication: Science
publication_identifier:
issn:
- 0036-8075
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '2471'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Combinatorial synthesis of genetic networks
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 296
year: '2002'
...
---
_id: '3799'
abstract:
- lang: eng
text: 'GABAergic interneurones are diverse in their morphological and functional
properties. Perisomatic inhibitory cells show fast spiking during sustained current
injection, whereas dendritic inhibitory cells fire action potentials with lower
frequency. We examined functional and molecular properties of K(+) channels in
interneurones with horizontal dendrites in stratum oriens-alveus (OA) of the hippocampal
CA1 region, which mainly comprise somatostatin-positive dendritic inhibitory cells.
Voltage-gated K(+) currents in nucleated patches isolated from OA interneurones
consisted of three major components: a fast delayed rectifier K(+) current component
that was highly sensitive to external 4-aminopyridine (4-AP) and tetraethylammonium
(TEA) (half-maximal inhibitory concentrations < 0.1 mM for both blockers),
a slow delayed rectifier K(+) current component that was sensitive to high concentrations
of TEA, but insensitive to 4-AP, and a rapidly inactivating A-type K(+) current
component that was blocked by high concentrations of 4-AP, but resistant to TEA.
The relative contributions of these components to the macroscopic K(+) current
were estimated as 57 +/- 5, 25 +/- 6, and 19 +/- 2 %, respectively. Dendrotoxin,
a selective blocker of Kv1 channels had only minimal effects on K(+) currents
in nucleated patches. Coapplication of the membrane-permeant cAMP analogue 8-(4-chlorophenylthio)-adenosine
3'':5''-cyclic monophosphate (cpt-cAMP) and the phosphodiesterase blocker isobutyl-methylxanthine
(IBMX) resulted in a selective inhibition of the fast delayed rectifier K(+) current
component. This inhibition was absent in the presence of the protein kinase A
(PKA) inhibitor H-89, implying the involvement of PKA-mediated phosphorylation.
Single-cell reverse transcription-polymerase chain reaction (RT-PCR) analysis
revealed a high abundance of Kv3.2 mRNA in OA interneurones, whereas the expression
level of Kv3.1 mRNA was markedly lower. Similarly, RT-PCR analysis showed a high
abundance of Kv4.3 mRNA, whereas Kv4.2 mRNA was undetectable. This suggests that
the fast delayed rectifier K(+) current and the A-type K(+) current component
are mediated predominantly by homomeric Kv3.2 and Kv4.3 channels. Selective modulation
of Kv3.2 channels in OA interneurones by cAMP is likely to be an important factor
regulating the activity of dendritic inhibitory cells in principal neurone-interneurone
microcircuits.'
acknowledgement: We thank Drs J. Bischofberger, M. Heckmann, and I. Vida for critically
reading the manuscript, and A. Blomenkamp and K. Winterhalter for technical assistance.
This work was supported by a scholarship from the Deutscher Akademischer Austansch
dienst to C.-C. L., a Deutsche Forschungsgemeinschaft grant to P. J. (SFB 505/C5),
and the Alexander-von-Humboldt foundation.
article_processing_charge: No
article_type: original
author:
- first_name: Cheng
full_name: Lien, Cheng
last_name: Lien
- first_name: Marco
full_name: Martina, Marco
last_name: Martina
- first_name: Jobst
full_name: Schultz, Jobst
last_name: Schultz
- first_name: Heimo
full_name: Ehmke, Heimo
last_name: Ehmke
- 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: Lien C, Martina M, Schultz J, Ehmke H, Jonas PM. Gating, modulation and subunit
composition of voltage-gated K(+) channels in dendritic inhibitory interneurones
of rat hippocampus. Journal of Physiology. 2002;538(Pt 2):405-419. doi:10.1113/jphysiol.2001.013066
apa: Lien, C., Martina, M., Schultz, J., Ehmke, H., & Jonas, P. M. (2002). Gating,
modulation and subunit composition of voltage-gated K(+) channels in dendritic
inhibitory interneurones of rat hippocampus. Journal of Physiology. Wiley-Blackwell.
https://doi.org/10.1113/jphysiol.2001.013066
chicago: Lien, Cheng, Marco Martina, Jobst Schultz, Heimo Ehmke, and Peter M Jonas.
“Gating, Modulation and Subunit Composition of Voltage-Gated K(+) Channels in
Dendritic Inhibitory Interneurones of Rat Hippocampus.” Journal of Physiology.
Wiley-Blackwell, 2002. https://doi.org/10.1113/jphysiol.2001.013066.
ieee: C. Lien, M. Martina, J. Schultz, H. Ehmke, and P. M. Jonas, “Gating, modulation
and subunit composition of voltage-gated K(+) channels in dendritic inhibitory
interneurones of rat hippocampus,” Journal of Physiology, vol. 538, no.
Pt 2. Wiley-Blackwell, pp. 405–419, 2002.
ista: Lien C, Martina M, Schultz J, Ehmke H, Jonas PM. 2002. Gating, modulation
and subunit composition of voltage-gated K(+) channels in dendritic inhibitory
interneurones of rat hippocampus. Journal of Physiology. 538(Pt 2), 405–419.
mla: Lien, Cheng, et al. “Gating, Modulation and Subunit Composition of Voltage-Gated
K(+) Channels in Dendritic Inhibitory Interneurones of Rat Hippocampus.” Journal
of Physiology, vol. 538, no. Pt 2, Wiley-Blackwell, 2002, pp. 405–19, doi:10.1113/jphysiol.2001.013066.
short: C. Lien, M. Martina, J. Schultz, H. Ehmke, P.M. Jonas, Journal of Physiology
538 (2002) 405–419.
date_created: 2018-12-11T12:05:14Z
date_published: 2002-01-01T00:00:00Z
date_updated: 2023-07-11T12:32:26Z
day: '01'
doi: 10.1113/jphysiol.2001.013066
extern: '1'
external_id:
pmid:
- '11790809'
intvolume: ' 538'
issue: Pt 2
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2290075/
month: '01'
oa: 1
oa_version: Published Version
page: 405 - 419
pmid: 1
publication: Journal of Physiology
publication_identifier:
issn:
- 0022-3751
publication_status: published
publisher: Wiley-Blackwell
publist_id: '2411'
quality_controlled: '1'
status: public
title: Gating, modulation and subunit composition of voltage-gated K(+) channels in
dendritic inhibitory interneurones of rat hippocampus
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 538
year: '2002'
...
---
_id: '3800'
abstract:
- lang: eng
text: Networks of GABAergic interneurons are of critical importance for the generation
of gamma frequency oscillations in the brain. To examine the underlying synaptic
mechanisms, we made paired recordings from "basket cells" (BCs) in different
subfields of hippocampal slices, using transgenic mice that express enhanced green
fluorescent protein (EGFP) under the control of the parvalbumin promoter. Unitary
inhibitory postsynaptic currents (IPSCs) showed large amplitude and fast time
course with mean amplitude-weighted decay time constants of 2.5, 1.2, and 1.8
ms in the dentate gyrus, and the cornu ammonis area 3 (CA3) and 1 (CA1), respectively
(33-34 degrees C). The decay of unitary IPSCs at BC-BC synapses was significantly
faster than that at BC-principal cell synapses, indicating target cell-specific
differences in IPSC kinetics. In addition, electrical coupling was found in a
subset of BC-BC pairs. To examine whether an interneuron network with fast inhibitory
synapses can act as a gamma frequency oscillator, we developed an interneuron
network model based on experimentally determined properties. In comparison to
previous interneuron network models, our model was able to generate oscillatory
activity with higher coherence over a broad range of frequencies (20-110 Hz).
In this model, high coherence and flexibility in frequency control emerge from
the combination of synaptic properties, network structure, and electrical coupling.
acknowledgement: We thank Drs. J. Bischofberger, M. Heckmann, and R. Traub for critically
reading the manuscript. This work was supported by Deutsche Forschungsgemeinschaft
Grants SFB 505/C5 (to P.J.) and SFB 505/C6 (to M.F. and P.J.), Human Frontiers Science
Program Organization Grant RG0017/1998-B (to P.J.), and grants from the Alexander-von-Humboldt
Foundation (to P.J. and M.F.), the Schilling Foundation (to H.M.), and Novartis
(to H.M.).
article_processing_charge: No
article_type: original
author:
- first_name: Marlene
full_name: Bartos, Marlene
last_name: Bartos
- first_name: Imre
full_name: Vida, Imre
last_name: Vida
- first_name: Michael
full_name: Frotscher, Michael
last_name: Frotscher
- first_name: Axel
full_name: Meyer, Axel
last_name: Meyer
- first_name: Hannah
full_name: Monyer, Hannah
last_name: Monyer
- 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
citation:
ama: Bartos M, Vida I, Frotscher M, et al. Fast synaptic inhibition promotes synchronized
gamma oscillations in hippocampal interneuron networks. PNAS. 2002;99(20):13222-13227.
doi:10.1073/pnas.192233099
apa: Bartos, M., Vida, I., Frotscher, M., Meyer, A., Monyer, H., Geiger, J., &
Jonas, P. M. (2002). Fast synaptic inhibition promotes synchronized gamma oscillations
in hippocampal interneuron networks. PNAS. National Academy of Sciences.
https://doi.org/10.1073/pnas.192233099
chicago: Bartos, Marlene, Imre Vida, Michael Frotscher, Axel Meyer, Hannah Monyer,
Jörg Geiger, and Peter M Jonas. “Fast Synaptic Inhibition Promotes Synchronized
Gamma Oscillations in Hippocampal Interneuron Networks.” PNAS. National
Academy of Sciences, 2002. https://doi.org/10.1073/pnas.192233099.
ieee: M. Bartos et al., “Fast synaptic inhibition promotes synchronized gamma
oscillations in hippocampal interneuron networks,” PNAS, vol. 99, no. 20.
National Academy of Sciences, pp. 13222–13227, 2002.
ista: Bartos M, Vida I, Frotscher M, Meyer A, Monyer H, Geiger J, Jonas PM. 2002.
Fast synaptic inhibition promotes synchronized gamma oscillations in hippocampal
interneuron networks. PNAS. 99(20), 13222–13227.
mla: Bartos, Marlene, et al. “Fast Synaptic Inhibition Promotes Synchronized Gamma
Oscillations in Hippocampal Interneuron Networks.” PNAS, vol. 99, no. 20,
National Academy of Sciences, 2002, pp. 13222–27, doi:10.1073/pnas.192233099.
short: M. Bartos, I. Vida, M. Frotscher, A. Meyer, H. Monyer, J. Geiger, P.M. Jonas,
PNAS 99 (2002) 13222–13227.
date_created: 2018-12-11T12:05:14Z
date_published: 2002-09-16T00:00:00Z
date_updated: 2023-07-10T13:35:18Z
day: '16'
doi: 10.1073/pnas.192233099
extern: '1'
external_id:
pmid:
- '12235359'
intvolume: ' 99'
issue: '20'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC130614/
month: '09'
oa: 1
oa_version: Published Version
page: 13222 - 13227
pmid: 1
publication: PNAS
publication_identifier:
issn:
- 0027-8424
publication_status: published
publisher: National Academy of Sciences
publist_id: '2409'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Fast synaptic inhibition promotes synchronized gamma oscillations in hippocampal
interneuron networks
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 99
year: '2002'
...