---
_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
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: 2021-01-12T06:53:54Z
day: '30'
ddc:
- '570'
department:
- _id: RySh
doi: 10.1371/journal.pone.0107099
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'
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: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 9
year: '2014'
...