---
OA_place: publisher
OA_type: hybrid
_id: '1546'
abstract:
- lang: eng
text: Synaptic efficacy and precision are influenced by the coupling of voltage-gated
Ca2+ channels (VGCCs) to vesicles. But because the topography of VGCCs and their
proximity to vesicles is unknown, a quantitative understanding of the determinants
of vesicular release at nanometer scale is lacking. To investigate this, we combined
freeze-fracture replica immunogold labeling of Cav2.1 channels, local [Ca2+] imaging,
and patch pipette perfusion of EGTA at the calyx of Held. Between postnatal day
7 and 21, VGCCs formed variable sized clusters and vesicular release became less
sensitive to EGTA, whereas fixed Ca2+ buffer properties remained constant. Experimentally
constrained reaction-diffusion simulations suggest that Ca2+ sensors for vesicular
release are located at the perimeter of VGCC clusters (<30nm) and predict that
VGCC number per cluster determines vesicular release probability without altering
release time course. This "perimeter release model" provides a unifying
framework accounting for developmental changes in both synaptic efficacy and time
course.
acknowledgement: This work was supported by the Core Research for Evolutional Science
and Technology (CREST) of Japan Science and Technology Agency to T.T. and R.S.;
by the funding provided by Okinawa Institute of Science and Technology (OIST) to
T.T. and Y.N.; by JSPS Core-to-Core Program, A. Advanced Networks to T.T.; by the
Grant-in-Aid for Young Scientists from the Japanese Ministry of Education, Culture,
Sports, Science and Technology (#23700474) to Y.N.; by the Centre National de la
Recherche Scientifique through the Actions Thematiques et Initatives sur Programme,
Fondation Fyssen, Fondation pour la Recherche Medicale, Federation pour la Recherche
sur le Cerveau, Agence Nationale de la Recherche (ANR-2007-Neuro-008-01 and ANR-2010-BLAN-1411-01)
to D.D. and Y.N.; and by the European Commission Coordination Action ENINET (LSHM-CT-2005-19063)
to D.D. and R.A.S. R.A.S. and J.S.R. were funded by Wellcome Trust Senior (064413)
and Principal (095667) Research Fellowship and an ERC advance grant (294667) to
RAS.
article_processing_charge: Yes (in subscription journal)
article_type: original
author:
- first_name: Yukihiro
full_name: Nakamura, Yukihiro
last_name: Nakamura
- first_name: Harumi
full_name: Harada, Harumi
id: 2E55CDF2-F248-11E8-B48F-1D18A9856A87
last_name: Harada
orcid: 0000-0001-7429-7896
- first_name: Naomi
full_name: Kamasawa, Naomi
last_name: Kamasawa
- first_name: Ko
full_name: Matsui, Ko
last_name: Matsui
- first_name: Jason
full_name: Rothman, Jason
last_name: Rothman
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: R Angus
full_name: Silver, R Angus
last_name: Silver
- first_name: David
full_name: Digregorio, David
last_name: Digregorio
- first_name: Tomoyuki
full_name: Takahashi, Tomoyuki
last_name: Takahashi
citation:
ama: Nakamura Y, Harada H, Kamasawa N, et al. Nanoscale distribution of presynaptic
Ca2+ channels and its impact on vesicular release during development. Neuron.
2015;85(1):145-158. doi:10.1016/j.neuron.2014.11.019
apa: Nakamura, Y., Harada, H., Kamasawa, N., Matsui, K., Rothman, J., Shigemoto,
R., … Takahashi, T. (2015). Nanoscale distribution of presynaptic Ca2+ channels
and its impact on vesicular release during development. Neuron. Elsevier.
https://doi.org/10.1016/j.neuron.2014.11.019
chicago: Nakamura, Yukihiro, Harumi Harada, Naomi Kamasawa, Ko Matsui, Jason Rothman,
Ryuichi Shigemoto, R Angus Silver, David Digregorio, and Tomoyuki Takahashi. “Nanoscale
Distribution of Presynaptic Ca2+ Channels and Its Impact on Vesicular Release
during Development.” Neuron. Elsevier, 2015. https://doi.org/10.1016/j.neuron.2014.11.019.
ieee: Y. Nakamura et al., “Nanoscale distribution of presynaptic Ca2+ channels
and its impact on vesicular release during development,” Neuron, vol. 85,
no. 1. Elsevier, pp. 145–158, 2015.
ista: Nakamura Y, Harada H, Kamasawa N, Matsui K, Rothman J, Shigemoto R, Silver
RA, Digregorio D, Takahashi T. 2015. Nanoscale distribution of presynaptic Ca2+
channels and its impact on vesicular release during development. Neuron. 85(1),
145–158.
mla: Nakamura, Yukihiro, et al. “Nanoscale Distribution of Presynaptic Ca2+ Channels
and Its Impact on Vesicular Release during Development.” Neuron, vol. 85,
no. 1, Elsevier, 2015, pp. 145–58, doi:10.1016/j.neuron.2014.11.019.
short: Y. Nakamura, H. Harada, N. Kamasawa, K. Matsui, J. Rothman, R. Shigemoto,
R.A. Silver, D. Digregorio, T. Takahashi, Neuron 85 (2015) 145–158.
date_created: 2018-12-11T11:52:39Z
date_published: 2015-01-07T00:00:00Z
date_updated: 2025-09-23T09:38:39Z
day: '07'
ddc:
- '570'
department:
- _id: RySh
doi: 10.1016/j.neuron.2014.11.019
external_id:
isi:
- '000348295100015'
pmid:
- '25533484'
file:
- access_level: open_access
checksum: 725f4d5be2dbb44b283ce722645ef37d
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:15:47Z
date_updated: 2020-07-14T12:45:01Z
file_id: '5170'
file_name: IST-2016-482-v1+1_1-s2.0-S0896627314010472-main.pdf
file_size: 3080111
relation: main_file
file_date_updated: 2020-07-14T12:45:01Z
has_accepted_license: '1'
intvolume: ' 85'
isi: 1
issue: '1'
language:
- iso: eng
license: https://creativecommons.org/licenses/by/3.0/
month: '01'
oa: 1
oa_version: Published Version
page: 145 - 158
pmid: 1
publication: Neuron
publication_identifier:
eissn:
- 1097-4199
issn:
- 0896-6273
publication_status: published
publisher: Elsevier
publist_id: '5625'
pubrep_id: '482'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Nanoscale distribution of presynaptic Ca2+ channels and its impact on vesicular
release during development
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/3.0/legalcode
name: Creative Commons Attribution 3.0 Unported (CC BY 3.0)
short: CC BY (3.0)
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 85
year: '2015'
...
---
_id: '1557'
abstract:
- lang: eng
text: γ-Aminobutyric acid (GABA)- and glycine-mediated hyperpolarizing inhibition
is associated with a chloride influx that depends on the inwardly directed chloride
electrochemical gradient. In neurons, the extrusion of chloride from the cytosol
primarily depends on the expression of an isoform of potassium-chloride cotransporters
(KCC2s). KCC2 is crucial in the regulation of the inhibitory tone of neural circuits,
including pain processing neural assemblies. Thus we investigated the cellular
distribution of KCC2 in neurons underlying pain processing in the superficial
spinal dorsal horn of rats by using high-resolution immunocytochemical methods.
We demonstrated that perikarya and dendrites widely expressed KCC2, but axon terminals
proved to be negative for KCC2. In single ultrathin sections, silver deposits
labeling KCC2 molecules showed different densities on the surface of dendritic
profiles, some of which were negative for KCC2. In freeze fracture replicas and
tissue sections double stained for the β3-subunit of GABAA receptors and KCC2,
GABAA receptors were revealed on dendritic segments with high and also with low
KCC2 densities. By measuring the distances between spots immunoreactive for gephyrin
(a scaffolding protein of GABAA and glycine receptors) and KCC2 on the surface
of neurokinin 1 (NK1) receptor-immunoreactive dendrites, we found that gephyrin-immunoreactive
spots were located at various distances from KCC2 cotransporters; 5.7 % of them
were recovered in the middle of 4-10-μm-long dendritic segments that were free
of KCC2 immunostaining. The variable local densities of KCC2 may result in variable
postsynaptic potentials evoked by the activation of GABAA and glycine receptors
along the dendrites of spinal neurons.
acknowledgement: "Funded by:\r\nHungarian Academy of Sciences. Grant Number: MTA-TKI
242\r\nHungarian Brain Research Program. Grant Number: KTIA_NAP_13-1-2013-0001\r\nSolution
Oriented Research for Science and Technology from the Japan Science and Technology
Agency Japanese Ministry of Education, Culture, Sports, Science and Technology"
article_processing_charge: No
author:
- first_name: Fariba
full_name: Javdani, Fariba
last_name: Javdani
- first_name: Krisztina
full_name: Holló, Krisztina
last_name: Holló
- first_name: Krisztina
full_name: Hegedűs, Krisztina
last_name: Hegedűs
- first_name: Gréta
full_name: Kis, Gréta
last_name: Kis
- first_name: Zoltán
full_name: Hegyi, Zoltán
last_name: Hegyi
- first_name: Klaudia
full_name: Dócs, Klaudia
last_name: Dócs
- first_name: Yu
full_name: Kasugai, Yu
last_name: Kasugai
- first_name: Yugo
full_name: Fukazawa, Yugo
last_name: Fukazawa
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Miklós
full_name: Antal, Miklós
last_name: Antal
citation:
ama: Javdani F, Holló K, Hegedűs K, et al. Differential expression patterns of K+Cl-
cotransporter 2 in neurons within the superficial spinal dorsal horn of rats.
Journal of Comparative Neurology. 2015;523(13):1967-1983. doi:10.1002/cne.23774
apa: Javdani, F., Holló, K., Hegedűs, K., Kis, G., Hegyi, Z., Dócs, K., … Antal,
M. (2015). Differential expression patterns of K+Cl- cotransporter 2 in neurons
within the superficial spinal dorsal horn of rats. Journal of Comparative Neurology.
Wiley-Blackwell. https://doi.org/10.1002/cne.23774
chicago: Javdani, Fariba, Krisztina Holló, Krisztina Hegedűs, Gréta Kis, Zoltán
Hegyi, Klaudia Dócs, Yu Kasugai, Yugo Fukazawa, Ryuichi Shigemoto, and Miklós
Antal. “Differential Expression Patterns of K+Cl- Cotransporter 2 in Neurons within
the Superficial Spinal Dorsal Horn of Rats.” Journal of Comparative Neurology.
Wiley-Blackwell, 2015. https://doi.org/10.1002/cne.23774.
ieee: F. Javdani et al., “Differential expression patterns of K+Cl- cotransporter
2 in neurons within the superficial spinal dorsal horn of rats,” Journal of
Comparative Neurology, vol. 523, no. 13. Wiley-Blackwell, pp. 1967–1983, 2015.
ista: Javdani F, Holló K, Hegedűs K, Kis G, Hegyi Z, Dócs K, Kasugai Y, Fukazawa
Y, Shigemoto R, Antal M. 2015. Differential expression patterns of K+Cl- cotransporter
2 in neurons within the superficial spinal dorsal horn of rats. Journal of Comparative
Neurology. 523(13), 1967–1983.
mla: Javdani, Fariba, et al. “Differential Expression Patterns of K+Cl- Cotransporter
2 in Neurons within the Superficial Spinal Dorsal Horn of Rats.” Journal of
Comparative Neurology, vol. 523, no. 13, Wiley-Blackwell, 2015, pp. 1967–83,
doi:10.1002/cne.23774.
short: F. Javdani, K. Holló, K. Hegedűs, G. Kis, Z. Hegyi, K. Dócs, Y. Kasugai,
Y. Fukazawa, R. Shigemoto, M. Antal, Journal of Comparative Neurology 523 (2015)
1967–1983.
date_created: 2018-12-11T11:52:42Z
date_published: 2015-09-01T00:00:00Z
date_updated: 2025-09-23T08:26:48Z
day: '01'
department:
- _id: RySh
doi: 10.1002/cne.23774
external_id:
isi:
- '000358228700006'
intvolume: ' 523'
isi: 1
issue: '13'
language:
- iso: eng
month: '09'
oa_version: None
page: 1967 - 1983
publication: Journal of Comparative Neurology
publication_status: published
publisher: Wiley-Blackwell
publist_id: '5614'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Differential expression patterns of K+Cl- cotransporter 2 in neurons within
the superficial spinal dorsal horn of rats
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 523
year: '2015'
...
---
_id: '2241'
abstract:
- lang: eng
text: 'The brain demands high-energy supply and obstruction of blood flow causes
rapid deterioration of the healthiness of brain cells. Two major events occur
upon ischemia: acidosis and liberation of excess glutamate, which leads to excitotoxicity.
However, cellular source of glutamate and its release mechanism upon ischemia
remained unknown. Here we show a causal relationship between glial acidosis and
neuronal excitotoxicity. As the major cation that flows through channelrhodopsin-2
(ChR2) is proton, this could be regarded as an optogenetic tool for instant intracellular
acidification. Optical activation of ChR2 expressed in glial cells led to glial
acidification and to release of glutamate. On the other hand, glial alkalization
via optogenetic activation of a proton pump, archaerhodopsin (ArchT), led to cessation
of glutamate release and to the relief of ischemic brain damage in vivo. Our results
suggest that controlling glial pH may be an effective therapeutic strategy for
intervention of ischemic brain damage.'
article_processing_charge: No
author:
- first_name: Kaoru
full_name: Beppu, Kaoru
last_name: Beppu
- first_name: Takuya
full_name: Sasaki, Takuya
last_name: Sasaki
- first_name: Kenji
full_name: Tanaka, Kenji
last_name: Tanaka
- first_name: Akihiro
full_name: Yamanaka, Akihiro
last_name: Yamanaka
- first_name: Yugo
full_name: Fukazawa, Yugo
last_name: Fukazawa
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Ko
full_name: Matsui, Ko
last_name: Matsui
citation:
ama: Beppu K, Sasaki T, Tanaka K, et al. Optogenetic countering of glial acidosis
suppresses glial glutamate release and ischemic brain damage. Neuron. 2014;81(2):314-320.
doi:10.1016/j.neuron.2013.11.011
apa: Beppu, K., Sasaki, T., Tanaka, K., Yamanaka, A., Fukazawa, Y., Shigemoto, R.,
& Matsui, K. (2014). Optogenetic countering of glial acidosis suppresses glial
glutamate release and ischemic brain damage. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2013.11.011
chicago: Beppu, Kaoru, Takuya Sasaki, Kenji Tanaka, Akihiro Yamanaka, Yugo Fukazawa,
Ryuichi Shigemoto, and Ko Matsui. “Optogenetic Countering of Glial Acidosis Suppresses
Glial Glutamate Release and Ischemic Brain Damage.” Neuron. Elsevier, 2014.
https://doi.org/10.1016/j.neuron.2013.11.011.
ieee: K. Beppu et al., “Optogenetic countering of glial acidosis suppresses
glial glutamate release and ischemic brain damage,” Neuron, vol. 81, no.
2. Elsevier, pp. 314–320, 2014.
ista: Beppu K, Sasaki T, Tanaka K, Yamanaka A, Fukazawa Y, Shigemoto R, Matsui K.
2014. Optogenetic countering of glial acidosis suppresses glial glutamate release
and ischemic brain damage. Neuron. 81(2), 314–320.
mla: Beppu, Kaoru, et al. “Optogenetic Countering of Glial Acidosis Suppresses Glial
Glutamate Release and Ischemic Brain Damage.” Neuron, vol. 81, no. 2, Elsevier,
2014, pp. 314–20, doi:10.1016/j.neuron.2013.11.011.
short: K. Beppu, T. Sasaki, K. Tanaka, A. Yamanaka, Y. Fukazawa, R. Shigemoto, K.
Matsui, Neuron 81 (2014) 314–320.
date_created: 2018-12-11T11:56:31Z
date_published: 2014-01-22T00:00:00Z
date_updated: 2026-04-16T10:07:56Z
day: '22'
department:
- _id: RySh
doi: 10.1016/j.neuron.2013.11.011
external_id:
isi:
- '000330420700010'
intvolume: ' 81'
isi: 1
issue: '2'
language:
- iso: eng
month: '01'
oa_version: None
page: 314 - 320
publication: Neuron
publication_identifier:
issn:
- 0896-6273
publication_status: published
publisher: Elsevier
publist_id: '4715'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Optogenetic countering of glial acidosis suppresses glial glutamate release
and ischemic brain damage
type: journal_article
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 81
year: '2014'
...
---
_id: '1895'
abstract:
- lang: eng
text: Major histocompatibility complex class I (MHCI) molecules were recently identified
as novel regulators of synaptic plasticity. These molecules are expressed in various
brain areas, especially in regions undergoing activity-dependent synaptic plasticity,
but their role in the nucleus accumbens (NAc) is unknown. In this study, we investigated
the effects of genetic disruption of MHCI function, through deletion of β2-microblobulin,
which causes lack of cell surface expression of MHCI. First, we confirmed that
MHCI molecules are expressed in the NAc core in wild-type mice. Second, we performed
electrophysiological recordings with NAc core slices from wild-type and β2-microglobulin
knock-out mice lacking cell surface expression of MHCI. We found that low frequency
stimulation induced long-term depression in wild-type but not knock-out mice,
whereas high frequency stimulation induced long-term potentiation in both genotypes,
with a larger magnitude in knock-out mice. Furthermore, we demonstrated that knock-out
mice showed more persistent behavioral sensitization to cocaine, which is a NAc-related
behavior. Using this model, we analyzed the density of total AMPA receptors and
their subunits GluR1 and GluR2 in the NAc core, by SDS-digested freeze-fracture
replica labeling. After repeated cocaine exposure, the density of GluR1 was increased,
but there was no change in total AMPA receptors and GluR2 levels in wildtype mice.
In contrast, following repeated cocaine exposure, increased densities of total
AMPA receptors, GluR1 and GluR2 were observed in knock-out mice. These results
indicate that functional deficiency of MHCI enhances synaptic potentiation, induced
by electrical and pharmacological stimulation.
acknowledgement: This work was supported in part by a Grant-in-Aid for Scientific
Research on Innovative Areas (Comprehensive Brain Science Network) and (B) 17330153,
from the Ministry of Education, Culture, Sports, Science and Technology of Japan.
article_number: e107099
article_processing_charge: No
author:
- first_name: Mitsuhiro
full_name: Edamura, Mitsuhiro
last_name: Edamura
- first_name: Gen
full_name: Murakami, Gen
last_name: Murakami
- first_name: Hongrui
full_name: Meng, Hongrui
last_name: Meng
- first_name: Makoto
full_name: Itakura, Makoto
last_name: Itakura
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Atsuo
full_name: Fukuda, Atsuo
last_name: Fukuda
- first_name: Daiichiro
full_name: Nakahara, Daiichiro
last_name: Nakahara
citation:
ama: Edamura M, Murakami G, Meng H, et al. Functional deficiency of MHC class i
enhances LTP and abolishes LTD in the nucleus accumbens of mice. PLoS One.
2014;9(9). doi:10.1371/journal.pone.0107099
apa: Edamura, M., Murakami, G., Meng, H., Itakura, M., Shigemoto, R., Fukuda, A.,
& Nakahara, D. (2014). Functional deficiency of MHC class i enhances LTP and
abolishes LTD in the nucleus accumbens of mice. PLoS One. Public Library
of Science. https://doi.org/10.1371/journal.pone.0107099
chicago: Edamura, Mitsuhiro, Gen Murakami, Hongrui Meng, Makoto Itakura, Ryuichi
Shigemoto, Atsuo Fukuda, and Daiichiro Nakahara. “Functional Deficiency of MHC
Class i Enhances LTP and Abolishes LTD in the Nucleus Accumbens of Mice.” PLoS
One. Public Library of Science, 2014. https://doi.org/10.1371/journal.pone.0107099.
ieee: M. Edamura et al., “Functional deficiency of MHC class i enhances LTP
and abolishes LTD in the nucleus accumbens of mice,” PLoS One, vol. 9,
no. 9. Public Library of Science, 2014.
ista: Edamura M, Murakami G, Meng H, Itakura M, Shigemoto R, Fukuda A, Nakahara
D. 2014. Functional deficiency of MHC class i enhances LTP and abolishes LTD in
the nucleus accumbens of mice. PLoS One. 9(9), e107099.
mla: Edamura, Mitsuhiro, et al. “Functional Deficiency of MHC Class i Enhances LTP
and Abolishes LTD in the Nucleus Accumbens of Mice.” PLoS One, vol. 9,
no. 9, e107099, Public Library of Science, 2014, doi:10.1371/journal.pone.0107099.
short: M. Edamura, G. Murakami, H. Meng, M. Itakura, R. Shigemoto, A. Fukuda, D.
Nakahara, PLoS One 9 (2014).
date_created: 2018-12-11T11:54:35Z
date_published: 2014-09-30T00:00:00Z
date_updated: 2025-09-29T13:04:38Z
day: '30'
ddc:
- '570'
department:
- _id: RySh
doi: 10.1371/journal.pone.0107099
external_id:
isi:
- '000343671700028'
file:
- access_level: open_access
checksum: 1f3be936be93114596d61ba44cacee69
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:09:01Z
date_updated: 2020-07-14T12:45:20Z
file_id: '4724'
file_name: IST-2016-439-v1+1_journal.pone.0107099.pdf
file_size: 6262085
relation: main_file
file_date_updated: 2020-07-14T12:45:20Z
has_accepted_license: '1'
intvolume: ' 9'
isi: 1
issue: '9'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
publication: PLoS One
publication_status: published
publisher: Public Library of Science
publist_id: '5200'
pubrep_id: '439'
scopus_import: '1'
status: public
title: Functional deficiency of MHC class i enhances LTP and abolishes LTD in the
nucleus accumbens of mice
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: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 9
year: '2014'
...
---
_id: '1898'
abstract:
- lang: eng
text: Fast synaptic transmission is important for rapid information processing.
To explore the maximal rate of neuronal signaling and to analyze the presynaptic
mechanisms, we focused on the input layer of the cerebellar cortex, where exceptionally
high action potential (AP) frequencies have been reported invivo. With paired
recordings between presynaptic cerebellar mossy fiber boutons and postsynaptic
granule cells, we demonstrate reliable neurotransmission upto ~1 kHz. Presynaptic
APs are ultrafast, with ~100μs half-duration. Both Kv1 and Kv3 potassium channels
mediate the fast repolarization, rapidly inactivating sodium channels ensure metabolic
efficiency, and little AP broadening occurs during bursts of up to 1.5 kHz. Presynaptic
Cav2.1 (P/Q-type) calcium channels open efficiently during ultrafast APs. Furthermore,
a subset of synaptic vesicles is tightly coupled to Ca2+ channels, and vesicles
are rapidly recruited to the release site. These data reveal mechanisms of presynaptic
AP generation and transmitter release underlying neuronal kHz signaling.
article_processing_charge: No
author:
- first_name: Andreas
full_name: Ritzau Jost, Andreas
last_name: Ritzau Jost
- first_name: Igor
full_name: Delvendahl, Igor
last_name: Delvendahl
- first_name: Annika
full_name: Rings, Annika
last_name: Rings
- first_name: Niklas
full_name: Byczkowicz, Niklas
last_name: Byczkowicz
- first_name: Harumi
full_name: Harada, Harumi
id: 2E55CDF2-F248-11E8-B48F-1D18A9856A87
last_name: Harada
orcid: 0000-0001-7429-7896
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Johannes
full_name: Hirrlinger, Johannes
last_name: Hirrlinger
- first_name: Jens
full_name: Eilers, Jens
last_name: Eilers
- first_name: Stefan
full_name: Hallermann, Stefan
last_name: Hallermann
citation:
ama: Ritzau Jost A, Delvendahl I, Rings A, et al. Ultrafast action potentials mediate
kilohertz signaling at a central synapse. Neuron. 2014;84(1):152-163. doi:10.1016/j.neuron.2014.08.036
apa: Ritzau Jost, A., Delvendahl, I., Rings, A., Byczkowicz, N., Harada, H., Shigemoto,
R., … Hallermann, S. (2014). Ultrafast action potentials mediate kilohertz signaling
at a central synapse. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2014.08.036
chicago: Ritzau Jost, Andreas, Igor Delvendahl, Annika Rings, Niklas Byczkowicz,
Harumi Harada, Ryuichi Shigemoto, Johannes Hirrlinger, Jens Eilers, and Stefan
Hallermann. “Ultrafast Action Potentials Mediate Kilohertz Signaling at a Central
Synapse.” Neuron. Elsevier, 2014. https://doi.org/10.1016/j.neuron.2014.08.036.
ieee: A. Ritzau Jost et al., “Ultrafast action potentials mediate kilohertz
signaling at a central synapse,” Neuron, vol. 84, no. 1. Elsevier, pp.
152–163, 2014.
ista: Ritzau Jost A, Delvendahl I, Rings A, Byczkowicz N, Harada H, Shigemoto R,
Hirrlinger J, Eilers J, Hallermann S. 2014. Ultrafast action potentials mediate
kilohertz signaling at a central synapse. Neuron. 84(1), 152–163.
mla: Ritzau Jost, Andreas, et al. “Ultrafast Action Potentials Mediate Kilohertz
Signaling at a Central Synapse.” Neuron, vol. 84, no. 1, Elsevier, 2014,
pp. 152–63, doi:10.1016/j.neuron.2014.08.036.
short: A. Ritzau Jost, I. Delvendahl, A. Rings, N. Byczkowicz, H. Harada, R. Shigemoto,
J. Hirrlinger, J. Eilers, S. Hallermann, Neuron 84 (2014) 152–163.
date_created: 2018-12-11T11:54:36Z
date_published: 2014-10-01T00:00:00Z
date_updated: 2025-09-29T13:03:03Z
day: '01'
department:
- _id: RySh
doi: 10.1016/j.neuron.2014.08.036
external_id:
isi:
- '000342502800017'
intvolume: ' 84'
isi: 1
issue: '1'
language:
- iso: eng
month: '10'
oa_version: None
page: 152 - 163
publication: Neuron
publication_status: published
publisher: Elsevier
publist_id: '5197'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Ultrafast action potentials mediate kilohertz signaling at a central synapse
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 84
year: '2014'
...
---
_id: '1919'
abstract:
- lang: eng
text: Long-lasting memories are formed when the stimulus is temporally distributed
(spacing effect). However, the synaptic mechanisms underlying this robust phenomenon
and the precise time course of the synaptic modifications that occur during learning
remain unclear. Here we examined the adaptation of horizontal optokinetic response
in mice that underwent 1 h of massed and spaced training at varying intervals.
Despite similar acquisition by all training protocols, 1 h of spacing produced
the highest memory retention at 24 h, which lasted for 1 mo. The distinct kinetics
of memory are strongly correlated with the reduction of floccular parallel fiber-Purkinje
cell synapses but not with AMPA receptor (AMPAR) number and synapse size. After
the spaced training, we observed 25%, 23%, and 12% reduction in AMPAR density,
synapse size, and synapse number, respectively. Four hours after the spaced training,
half of the synapses and Purkinje cell spines had been eliminated, whereas AMPAR
density and synapse size were recovered in remaining synapses. Surprisingly, massed
training also produced long-term memory and halving of synapses; however, this
occurred slowly over days, and the memory lasted for only 1 wk. This distinct
kinetics of structural plasticity may serve as a basis for unique temporal profiles
in the formation and decay of memory with or without intervals.
acknowledgement: his work was supported by Solution Oriented Research for Science
and Technology (R.S.), Core Research for Evolutional Science and Technology, Japan
Science and Technology Agency (Y.F.), and Grants-in-Aid for Scientific Research
on Priority Areas-Molecular Brain Sciences 16300114 (to R.S.) and 18022043 (to Y.F.).
article_processing_charge: No
author:
- first_name: Wajeeha
full_name: Aziz, Wajeeha
last_name: Aziz
- first_name: Wen
full_name: Wang, Wen
last_name: Wang
- first_name: Sebnem
full_name: Kesaf, Sebnem
id: 401AB46C-F248-11E8-B48F-1D18A9856A87
last_name: Kesaf
- first_name: Alsayed
full_name: Mohamed, Alsayed
last_name: Mohamed
- first_name: Yugo
full_name: Fukazawa, Yugo
last_name: Fukazawa
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
citation:
ama: Aziz W, Wang W, Kesaf S, Mohamed A, Fukazawa Y, Shigemoto R. Distinct kinetics
of synaptic structural plasticity, memory formation, and memory decay in massed
and spaced learning. PNAS. 2014;111(1):E194-E202. doi:10.1073/pnas.1303317110
apa: Aziz, W., Wang, W., Kesaf, S., Mohamed, A., Fukazawa, Y., & Shigemoto,
R. (2014). Distinct kinetics of synaptic structural plasticity, memory formation,
and memory decay in massed and spaced learning. PNAS. National Academy
of Sciences. https://doi.org/10.1073/pnas.1303317110
chicago: Aziz, Wajeeha, Wen Wang, Sebnem Kesaf, Alsayed Mohamed, Yugo Fukazawa,
and Ryuichi Shigemoto. “Distinct Kinetics of Synaptic Structural Plasticity, Memory
Formation, and Memory Decay in Massed and Spaced Learning.” PNAS. National
Academy of Sciences, 2014. https://doi.org/10.1073/pnas.1303317110.
ieee: W. Aziz, W. Wang, S. Kesaf, A. Mohamed, Y. Fukazawa, and R. Shigemoto, “Distinct
kinetics of synaptic structural plasticity, memory formation, and memory decay
in massed and spaced learning,” PNAS, vol. 111, no. 1. National Academy
of Sciences, pp. E194–E202, 2014.
ista: Aziz W, Wang W, Kesaf S, Mohamed A, Fukazawa Y, Shigemoto R. 2014. Distinct
kinetics of synaptic structural plasticity, memory formation, and memory decay
in massed and spaced learning. PNAS. 111(1), E194–E202.
mla: Aziz, Wajeeha, et al. “Distinct Kinetics of Synaptic Structural Plasticity,
Memory Formation, and Memory Decay in Massed and Spaced Learning.” PNAS,
vol. 111, no. 1, National Academy of Sciences, 2014, pp. E194–202, doi:10.1073/pnas.1303317110.
short: W. Aziz, W. Wang, S. Kesaf, A. Mohamed, Y. Fukazawa, R. Shigemoto, PNAS 111
(2014) E194–E202.
corr_author: '1'
date_created: 2018-12-11T11:54:43Z
date_published: 2014-01-07T00:00:00Z
date_updated: 2025-09-29T12:19:01Z
day: '07'
department:
- _id: RySh
doi: 10.1073/pnas.1303317110
external_id:
isi:
- '000329350700025'
intvolume: ' 111'
isi: 1
issue: '1'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3890840/
month: '01'
oa: 1
oa_version: Submitted Version
page: E194 - E202
publication: PNAS
publication_status: published
publisher: National Academy of Sciences
publist_id: '5175'
scopus_import: '1'
status: public
title: Distinct kinetics of synaptic structural plasticity, memory formation, and
memory decay in massed and spaced learning
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 111
year: '2014'
...
---
_id: '1920'
abstract:
- lang: eng
text: Cerebellar motor learning is suggested to be caused by long-term plasticity
of excitatory parallel fiber-Purkinje cell (PF-PC) synapses associated with changes
in the number of synaptic AMPA-type glutamate receptors (AMPARs). However, whether
the AMPARs decrease or increase in individual PF-PC synapses occurs in physiological
motor learning and accounts for memory that lasts over days remains elusive. We
combined quantitative SDS-digested freeze-fracture replica labeling for AMPAR
and physical dissector electron microscopy with a simple model of cerebellar motor
learning, adaptation of horizontal optokinetic response (HOKR) in mouse. After
1-h training of HOKR, short-term adaptation (STA) was accompanied with transient
decrease in AMPARs by 28% in target PF-PC synapses. STA was well correlated with
AMPAR decrease in individual animals and both STA and AMPAR decrease recovered
to basal levels within 24 h. Surprisingly, long-termadaptation (LTA) after five
consecutive daily trainings of 1-h HOKR did not alter the number of AMPARs in
PF-PC synapses but caused gradual and persistent synapse elimination by 45%, with
corresponding PC spine loss by the fifth training day. Furthermore, recovery of
LTA after 2 wk was well correlated with increase of PF-PC synapses to the control
level. Our findings indicate that the AMPARs decrease in PF-PC synapses and the
elimination of these synapses are in vivo engrams in short- and long-term motor
learning, respectively, showing a unique type of synaptic plasticity that may
contribute to memory consolidation.
acknowledgement: This work was supported by Solution-Oriented Research for Science
and Technology from the Japan Science and Technology Agency; Ministry of Education,
Culture, Sports, Science and Technology of Japan Grant 16300114 (to R.S.).
article_processing_charge: No
author:
- first_name: Wen
full_name: Wang, Wen
last_name: Wang
- first_name: Kazuhiko
full_name: Nakadate, Kazuhiko
last_name: Nakadate
- first_name: Miwako
full_name: Masugi Tokita, Miwako
last_name: Masugi Tokita
- first_name: Fumihiro
full_name: Shutoh, Fumihiro
last_name: Shutoh
- first_name: Wajeeha
full_name: Aziz, Wajeeha
last_name: Aziz
- first_name: Etsuko
full_name: Tarusawa, Etsuko
last_name: Tarusawa
- first_name: Andrea
full_name: Lörincz, Andrea
last_name: Lörincz
- first_name: Elek
full_name: Molnár, Elek
last_name: Molnár
- first_name: Sebnem
full_name: Kesaf, Sebnem
id: 401AB46C-F248-11E8-B48F-1D18A9856A87
last_name: Kesaf
- first_name: Yunqing
full_name: Li, Yunqing
last_name: Li
- first_name: Yugo
full_name: Fukazawa, Yugo
last_name: Fukazawa
- first_name: Soichi
full_name: Nagao, Soichi
last_name: Nagao
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
citation:
ama: Wang W, Nakadate K, Masugi Tokita M, et al. Distinct cerebellar engrams in
short-term and long-term motor learning. PNAS. 2014;111(1):E188-E193. doi:10.1073/pnas.1315541111
apa: Wang, W., Nakadate, K., Masugi Tokita, M., Shutoh, F., Aziz, W., Tarusawa,
E., … Shigemoto, R. (2014). Distinct cerebellar engrams in short-term and long-term
motor learning. PNAS. National Academy of Sciences. https://doi.org/10.1073/pnas.1315541111
chicago: Wang, Wen, Kazuhiko Nakadate, Miwako Masugi Tokita, Fumihiro Shutoh, Wajeeha
Aziz, Etsuko Tarusawa, Andrea Lörincz, et al. “Distinct Cerebellar Engrams in
Short-Term and Long-Term Motor Learning.” PNAS. National Academy of Sciences,
2014. https://doi.org/10.1073/pnas.1315541111.
ieee: W. Wang et al., “Distinct cerebellar engrams in short-term and long-term
motor learning,” PNAS, vol. 111, no. 1. National Academy of Sciences, pp.
E188–E193, 2014.
ista: Wang W, Nakadate K, Masugi Tokita M, Shutoh F, Aziz W, Tarusawa E, Lörincz
A, Molnár E, Kesaf S, Li Y, Fukazawa Y, Nagao S, Shigemoto R. 2014. Distinct cerebellar
engrams in short-term and long-term motor learning. PNAS. 111(1), E188–E193.
mla: Wang, Wen, et al. “Distinct Cerebellar Engrams in Short-Term and Long-Term
Motor Learning.” PNAS, vol. 111, no. 1, National Academy of Sciences, 2014,
pp. E188–93, doi:10.1073/pnas.1315541111.
short: W. Wang, K. Nakadate, M. Masugi Tokita, F. Shutoh, W. Aziz, E. Tarusawa,
A. Lörincz, E. Molnár, S. Kesaf, Y. Li, Y. Fukazawa, S. Nagao, R. Shigemoto, PNAS
111 (2014) E188–E193.
corr_author: '1'
date_created: 2018-12-11T11:54:43Z
date_published: 2014-01-07T00:00:00Z
date_updated: 2025-09-29T12:18:06Z
day: '07'
department:
- _id: RySh
doi: 10.1073/pnas.1315541111
external_id:
isi:
- '000329350700024'
intvolume: ' 111'
isi: 1
issue: '1'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3890858/
month: '01'
oa: 1
oa_version: Submitted Version
page: E188 - E193
publication: PNAS
publication_status: published
publisher: National Academy of Sciences
publist_id: '5174'
scopus_import: '1'
status: public
title: Distinct cerebellar engrams in short-term and long-term motor learning
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 111
year: '2014'
...
---
_id: '1933'
abstract:
- lang: eng
text: The development of the vertebrate brain requires an exquisite balance between
proliferation and differentiation of neural progenitors. Notch signaling plays
a pivotal role in regulating this balance, yet the interaction between signaling
and receiving cells remains poorly understood. We have found that numerous nascent
neurons and/or intermediate neurogenic progenitors expressing the ligand of Notch
retain apical endfeet transiently at the ventricular lumen that form adherens
junctions (AJs) with the endfeet of progenitors. Forced detachment of the apical
endfeet of those differentiating cells by disrupting AJs resulted in precocious
neurogenesis that was preceded by the downregulation of Notch signaling. Both
Notch1 and its ligand Dll1 are distributed around AJs in the apical endfeet, and
these proteins physically interact with ZO-1, a constituent of the AJ. Furthermore,
live imaging of a fluorescently tagged Notch1 demonstrated its trafficking from
the apical endfoot to the nucleus upon cleavage. Our results identified the apical
endfoot as the central site of active Notch signaling to securely prohibit inappropriate
differentiation of neural progenitors.
article_processing_charge: No
author:
- first_name: Jun
full_name: Hatakeyama, Jun
last_name: Hatakeyama
- first_name: Yoshio
full_name: Wakamatsu, Yoshio
last_name: Wakamatsu
- first_name: Akira
full_name: Nagafuchi, Akira
last_name: Nagafuchi
- first_name: Ryoichiro
full_name: Kageyama, Ryoichiro
last_name: Kageyama
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Kenji
full_name: Shimamura, Kenji
last_name: Shimamura
citation:
ama: Hatakeyama J, Wakamatsu Y, Nagafuchi A, Kageyama R, Shigemoto R, Shimamura
K. Cadherin-based adhesions in the apical endfoot are required for active Notch
signaling to control neurogenesis in vertebrates. Development. 2014;141(8):1671-1682.
doi:10.1242/dev.102988
apa: Hatakeyama, J., Wakamatsu, Y., Nagafuchi, A., Kageyama, R., Shigemoto, R.,
& Shimamura, K. (2014). Cadherin-based adhesions in the apical endfoot are
required for active Notch signaling to control neurogenesis in vertebrates. Development.
Company of Biologists. https://doi.org/10.1242/dev.102988
chicago: Hatakeyama, Jun, Yoshio Wakamatsu, Akira Nagafuchi, Ryoichiro Kageyama,
Ryuichi Shigemoto, and Kenji Shimamura. “Cadherin-Based Adhesions in the Apical
Endfoot Are Required for Active Notch Signaling to Control Neurogenesis in Vertebrates.”
Development. Company of Biologists, 2014. https://doi.org/10.1242/dev.102988.
ieee: J. Hatakeyama, Y. Wakamatsu, A. Nagafuchi, R. Kageyama, R. Shigemoto, and
K. Shimamura, “Cadherin-based adhesions in the apical endfoot are required for
active Notch signaling to control neurogenesis in vertebrates,” Development,
vol. 141, no. 8. Company of Biologists, pp. 1671–1682, 2014.
ista: Hatakeyama J, Wakamatsu Y, Nagafuchi A, Kageyama R, Shigemoto R, Shimamura
K. 2014. Cadherin-based adhesions in the apical endfoot are required for active
Notch signaling to control neurogenesis in vertebrates. Development. 141(8), 1671–1682.
mla: Hatakeyama, Jun, et al. “Cadherin-Based Adhesions in the Apical Endfoot Are
Required for Active Notch Signaling to Control Neurogenesis in Vertebrates.” Development,
vol. 141, no. 8, Company of Biologists, 2014, pp. 1671–82, doi:10.1242/dev.102988.
short: J. Hatakeyama, Y. Wakamatsu, A. Nagafuchi, R. Kageyama, R. Shigemoto, K.
Shimamura, Development 141 (2014) 1671–1682.
date_created: 2018-12-11T11:54:47Z
date_published: 2014-04-01T00:00:00Z
date_updated: 2025-09-29T12:10:15Z
day: '01'
department:
- _id: RySh
doi: 10.1242/dev.102988
external_id:
isi:
- '000334347900007'
intvolume: ' 141'
isi: 1
issue: '8'
language:
- iso: eng
month: '04'
oa_version: None
page: 1671 - 1682
publication: Development
publication_status: published
publisher: Company of Biologists
publist_id: '5161'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Cadherin-based adhesions in the apical endfoot are required for active Notch
signaling to control neurogenesis in vertebrates
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 141
year: '2014'
...
---
_id: '2018'
abstract:
- lang: eng
text: Synaptic cell adhesion molecules are increasingly gaining attention for conferring
specific properties to individual synapses. Netrin-G1 and netrin-G2 are trans-synaptic
adhesion molecules that distribute on distinct axons, and their presence restricts
the expression of their cognate receptors, NGL1 and NGL2, respectively, to specific
subdendritic segments of target neurons. However, the neural circuits and functional
roles of netrin-G isoform complexes remain unclear. Here, we use netrin-G-KO and
NGL-KO mice to reveal that netrin-G1/NGL1 and netrin-G2/NGL2 interactions specify
excitatory synapses in independent hippocampal pathways. In the hippocampal CA1
area, netrin-G1/NGL1 and netrin-G2/NGL2 were expressed in the temporoammonic and
Schaffer collateral pathways, respectively. The lack of presynaptic netrin-Gs
led to the dispersion of NGLs from postsynaptic membranes. In accord, netrin-G
mutant synapses displayed opposing phenotypes in long-term and short-term plasticity
through discrete biochemical pathways. The plasticity phenotypes in netrin-G-KOs
were phenocopied in NGL-KOs, with a corresponding loss of netrin-Gs from presynaptic
membranes. Our findings show that netrin-G/NGL interactions differentially control
synaptic plasticity in distinct circuits via retrograde signaling mechanisms and
explain how synaptic inputs are diversified to control neuronal activity.
acknowledgement: This work was supported by “Funding Program for World-Leading Innovative
R&D on Science and Technology (FIRST Program)” initiated by the Council for Science
and Technology Policy.
article_processing_charge: No
article_type: original
author:
- first_name: Hiroshi
full_name: Matsukawa, Hiroshi
last_name: Matsukawa
- first_name: Sachiko
full_name: Akiyoshi Nishimura, Sachiko
last_name: Akiyoshi Nishimura
- first_name: Qi
full_name: Zhang, Qi
last_name: Zhang
- first_name: Rafael
full_name: Luján, Rafael
last_name: Luján
- first_name: Kazuhiko
full_name: Yamaguchi, Kazuhiko
last_name: Yamaguchi
- first_name: Hiromichi
full_name: Goto, Hiromichi
last_name: Goto
- first_name: Kunio
full_name: Yaguchi, Kunio
last_name: Yaguchi
- first_name: Tsutomu
full_name: Hashikawa, Tsutomu
last_name: Hashikawa
- first_name: Chie
full_name: Sano, Chie
last_name: Sano
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Toshiaki
full_name: Nakashiba, Toshiaki
last_name: Nakashiba
- first_name: Shigeyoshi
full_name: Itohara, Shigeyoshi
last_name: Itohara
citation:
ama: Matsukawa H, Akiyoshi Nishimura S, Zhang Q, et al. Netrin-G/NGL complexes encode
functional synaptic diversification. Journal of Neuroscience. 2014;34(47):15779-15792.
doi:10.1523/JNEUROSCI.1141-14.2014
apa: Matsukawa, H., Akiyoshi Nishimura, S., Zhang, Q., Luján, R., Yamaguchi, K.,
Goto, H., … Itohara, S. (2014). Netrin-G/NGL complexes encode functional synaptic
diversification. Journal of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.1141-14.2014
chicago: Matsukawa, Hiroshi, Sachiko Akiyoshi Nishimura, Qi Zhang, Rafael Luján,
Kazuhiko Yamaguchi, Hiromichi Goto, Kunio Yaguchi, et al. “Netrin-G/NGL Complexes
Encode Functional Synaptic Diversification.” Journal of Neuroscience. Society
for Neuroscience, 2014. https://doi.org/10.1523/JNEUROSCI.1141-14.2014.
ieee: H. Matsukawa et al., “Netrin-G/NGL complexes encode functional synaptic
diversification,” Journal of Neuroscience, vol. 34, no. 47. Society for
Neuroscience, pp. 15779–15792, 2014.
ista: Matsukawa H, Akiyoshi Nishimura S, Zhang Q, Luján R, Yamaguchi K, Goto H,
Yaguchi K, Hashikawa T, Sano C, Shigemoto R, Nakashiba T, Itohara S. 2014. Netrin-G/NGL
complexes encode functional synaptic diversification. Journal of Neuroscience.
34(47), 15779–15792.
mla: Matsukawa, Hiroshi, et al. “Netrin-G/NGL Complexes Encode Functional Synaptic
Diversification.” Journal of Neuroscience, vol. 34, no. 47, Society for
Neuroscience, 2014, pp. 15779–92, doi:10.1523/JNEUROSCI.1141-14.2014.
short: H. Matsukawa, S. Akiyoshi Nishimura, Q. Zhang, R. Luján, K. Yamaguchi, H.
Goto, K. Yaguchi, T. Hashikawa, C. Sano, R. Shigemoto, T. Nakashiba, S. Itohara,
Journal of Neuroscience 34 (2014) 15779–15792.
date_created: 2018-12-11T11:55:14Z
date_published: 2014-11-19T00:00:00Z
date_updated: 2025-09-29T12:00:37Z
day: '19'
ddc:
- '570'
department:
- _id: RySh
doi: 10.1523/JNEUROSCI.1141-14.2014
external_id:
isi:
- '000345907500026'
pmid:
- '25411505'
file:
- access_level: open_access
checksum: 6913e9bc26e9fc1c0441a739a4199229
content_type: application/pdf
creator: dernst
date_created: 2022-05-24T08:41:41Z
date_updated: 2022-05-24T08:41:41Z
file_id: '11410'
file_name: 2014_JournNeuroscience_Matsukawa.pdf
file_size: 3963728
relation: main_file
success: 1
file_date_updated: 2022-05-24T08:41:41Z
has_accepted_license: '1'
intvolume: ' 34'
isi: 1
issue: '47'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
page: 15779 - 15792
pmid: 1
publication: Journal of Neuroscience
publication_identifier:
eissn:
- 1529-2401
issn:
- 0270-6474
publication_status: published
publisher: Society for Neuroscience
publist_id: '5054'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Netrin-G/NGL complexes encode functional synaptic diversification
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 34
year: '2014'
...
---
_id: '2064'
abstract:
- lang: eng
text: We examined the synaptic structure, quantity, and distribution of α-amino-3-hydroxy-5-methylisoxazole-4-propionic
acid (AMPA)- and N-methyl-D-aspartate (NMDA)-type glutamate receptors (AMPARs
and NMDARs, respectively) in rat cochlear nuclei by a highly sensitive freeze-fracture
replica labeling technique. Four excitatory synapses formed by two distinct inputs,
auditory nerve (AN) and parallel fibers (PF), on different cell types were analyzed.
These excitatory synapse types included AN synapses on bushy cells (AN-BC synapses)
and fusiform cells (AN-FC synapses) and PF synapses on FC (PF-FC synapses) and
cartwheel cell spines (PF-CwC synapses). Immunogold labeling revealed differences
in synaptic structure as well as AMPAR and NMDAR number and/or density in both
AN and PF synapses, indicating a target-dependent organization. The immunogold
receptor labeling also identified differences in the synaptic organization of
FCs based on AN or PF connections, indicating an input-dependent organization
in FCs. Among the four excitatory synapse types, the AN-BC synapses were the smallest
and had the most densely packed intramembrane particles (IMPs), whereas the PF-CwC
synapses were the largest and had sparsely packed IMPs. All four synapse types
showed positive correlations between the IMP-cluster area and the AMPAR number,
indicating a common intrasynapse-type relationship for glutamatergic synapses.
Immunogold particles for AMPARs were distributed over the entire area of individual
AN synapses; PF synapses often showed synaptic areas devoid of labeling. The gold-labeling
for NMDARs occurred in a mosaic fashion, with less positive correlations between
the IMP-cluster area and the NMDAR number. Our observations reveal target- and
input-dependent features in the structure, number, and organization of AMPARs
and NMDARs in AN and PF synapses.
acknowledgement: "National Institutes of Health (NIH) Grant Number: 1R01DC013048‐0;
Biotechnology and Biological Sciences Research Council, UK Grant Number: BB/J015938/1\r\n"
article_processing_charge: No
author:
- first_name: Maía
full_name: Rubio, Maía
last_name: Rubio
- first_name: Yugo
full_name: Fukazawa, Yugo
last_name: Fukazawa
- first_name: Naomi
full_name: Kamasawa, Naomi
last_name: Kamasawa
- first_name: Cheryl
full_name: Clarkson, Cheryl
last_name: Clarkson
- first_name: Elek
full_name: Molnár, Elek
last_name: Molnár
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
citation:
ama: Rubio M, Fukazawa Y, Kamasawa N, Clarkson C, Molnár E, Shigemoto R. Target-
and input-dependent organization of AMPA and NMDA receptors in synaptic connections
of the cochlear nucleus. Journal of Comparative Neurology. 2014;522(18):4023-4042.
doi:10.1002/cne.23654
apa: Rubio, M., Fukazawa, Y., Kamasawa, N., Clarkson, C., Molnár, E., & Shigemoto,
R. (2014). Target- and input-dependent organization of AMPA and NMDA receptors
in synaptic connections of the cochlear nucleus. Journal of Comparative Neurology.
Wiley-Blackwell. https://doi.org/10.1002/cne.23654
chicago: Rubio, Maía, Yugo Fukazawa, Naomi Kamasawa, Cheryl Clarkson, Elek Molnár,
and Ryuichi Shigemoto. “Target- and Input-Dependent Organization of AMPA and NMDA
Receptors in Synaptic Connections of the Cochlear Nucleus.” Journal of Comparative
Neurology. Wiley-Blackwell, 2014. https://doi.org/10.1002/cne.23654.
ieee: M. Rubio, Y. Fukazawa, N. Kamasawa, C. Clarkson, E. Molnár, and R. Shigemoto,
“Target- and input-dependent organization of AMPA and NMDA receptors in synaptic
connections of the cochlear nucleus,” Journal of Comparative Neurology,
vol. 522, no. 18. Wiley-Blackwell, pp. 4023–4042, 2014.
ista: Rubio M, Fukazawa Y, Kamasawa N, Clarkson C, Molnár E, Shigemoto R. 2014.
Target- and input-dependent organization of AMPA and NMDA receptors in synaptic
connections of the cochlear nucleus. Journal of Comparative Neurology. 522(18),
4023–4042.
mla: Rubio, Maía, et al. “Target- and Input-Dependent Organization of AMPA and NMDA
Receptors in Synaptic Connections of the Cochlear Nucleus.” Journal of Comparative
Neurology, vol. 522, no. 18, Wiley-Blackwell, 2014, pp. 4023–42, doi:10.1002/cne.23654.
short: M. Rubio, Y. Fukazawa, N. Kamasawa, C. Clarkson, E. Molnár, R. Shigemoto,
Journal of Comparative Neurology 522 (2014) 4023–4042.
date_created: 2018-12-11T11:55:30Z
date_published: 2014-07-29T00:00:00Z
date_updated: 2025-09-29T11:47:23Z
day: '29'
department:
- _id: RySh
doi: 10.1002/cne.23654
external_id:
isi:
- '000343973100005'
intvolume: ' 522'
isi: 1
issue: '18'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4198489/
month: '07'
oa: 1
oa_version: Submitted Version
page: 4023 - 4042
publication: Journal of Comparative Neurology
publication_status: published
publisher: Wiley-Blackwell
publist_id: '4974'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Target- and input-dependent organization of AMPA and NMDA receptors in synaptic
connections of the cochlear nucleus
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 522
year: '2014'
...