Functional deficiency of MHC class I enhances LTP and abolishes LTD in the nucleus accumbens of mice

枝村, 光浩

doi:https://doi.org/10.1371/journal.pone.0107099

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Functional deficiency of MHC class I enhances LTP and abolishes LTD in the nucleus accumbens of mice

http://hdl.handle.net/10271/2878

名前 / ファイル	ライセンス	アクション
論文本文 (1.1 MB)

Item type

学位論文 / Thesis or Dissertation(1)

公開日

2015-08-11

タイトル

Functional deficiency of MHC class I enhances LTP and abolishes LTD in the nucleus accumbens of mice

言語

eng

資源タイプ

資源タイプ識別子

http://purl.org/coar/resource_type/c_db06

資源タイプ

doctoral thesis

アクセス権

open access

アクセス権URI

http://purl.org/coar/access_right/c_abf2

その他のタイトル

主要組織適合遺伝子複合体クラスＩの機能欠損はマウスの側坐核のLTPを亢進しLTDを消失する

著者

枝村, 光浩

書誌情報

en : PLoS ONE

巻 9, 号 9, p. e107099, 発行日 2014-09-30

出版者

PLOS (Public Library of Science)

権利

言語

権利情報

抄録

内容記述タイプ

Abstract

内容記述

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 wild-type 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.

言語

学位名

博士（医学）

学位の区分

内容記述

doctoral

学位の分野

内容記述

医学系研究科

学位授与機関

学位授与機関識別子Scheme

kakenhi

学位授与機関識別子

13802

学位授与機関名

浜松医科大学

学位授与年月日

2014-12-12

学位授与番号

甲第688号

EISSN

収録物識別子タイプ

EISSN

収録物識別子

1932-6203

PubMed番号

識別子タイプ

PMID

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2023-06-20 16:59:19.743420

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Functional deficiency of MHC class I enhances LTP and abolishes LTD in the nucleus accumbens of mice

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