Depression of long term potentiation in gerbil hippocampus following postischemic hypothermia

Osamu Miyamoto; Takehiro Nakamura; Shin ich Yamagami; Tetsuro Negi; Masaaki Tokuda; Hideki Matsui; Toshifumi Itano

doi:10.1016/S0006-8993(00)02521-X

Depression of long term potentiation in gerbil hippocampus following postischemic hypothermia

Osamu Miyamoto, Takehiro Nakamura, Shin ich Yamagami, Tetsuro Negi, Masaaki Tokuda, Hideki Matsui, Toshifumi Itano

Graduate School of Medicine Dentistry and Pharmaceutical Sciences

Research output: Contribution to journal › Article › peer-review

6 Citations (Scopus)

Abstract

To investigate the mechanism of chronic cell death following postischemic hypothermia, the change of N-methyl-D-aspartate receptor (NMDAR) were examined by immunohistochemistry of NMDAR1 and long-term potentiation (LTP) in the CA1 subfield of the gerbil hippocampus. At 1 week following postischemic hypothermia (32°Cx4 h), all CA1 neurons survived; however, immunoreactivity of NMDAR1 increased in neuronal perikarya whereas decreased in dendrites in the CA1 neurons. The abnormality was still observed in remaining CA1 neurons at 1 month after hypothermia. LTP was also significantly depressed at 1 week after hypothermia. These results suggest that some abnormalities in the glutamate receptor may be caused by ischemia; such abnormality would persist in spite of hypothermia treatment, resulting in the depression of LTP. Copyright (C) 2000 Elsevier Science B.V.

Original language	English
Pages (from-to)	168-172
Number of pages	5
Journal	Brain Research
Volume	873
Issue number	1
DOIs	https://doi.org/10.1016/S0006-8993(00)02521-X
Publication status	Published - Aug 4 2000

Keywords

Gerbil
Hippocampus
Immunohistochemistry
Long term potentiation
N-Methyl-D-aspartate receptor 1
Postischemic hypothermia

ASJC Scopus subject areas

Neuroscience(all)
Molecular Biology
Clinical Neurology
Developmental Biology

Access to Document

10.1016/S0006-8993(00)02521-X

Fingerprint Dive into the research topics of 'Depression of long term potentiation in gerbil hippocampus following postischemic hypothermia'. Together they form a unique fingerprint.

Cite this

@article{cede243b007b46f7ad48c695c0a907a5,

title = "Depression of long term potentiation in gerbil hippocampus following postischemic hypothermia",

abstract = "To investigate the mechanism of chronic cell death following postischemic hypothermia, the change of N-methyl-D-aspartate receptor (NMDAR) were examined by immunohistochemistry of NMDAR1 and long-term potentiation (LTP) in the CA1 subfield of the gerbil hippocampus. At 1 week following postischemic hypothermia (32°Cx4 h), all CA1 neurons survived; however, immunoreactivity of NMDAR1 increased in neuronal perikarya whereas decreased in dendrites in the CA1 neurons. The abnormality was still observed in remaining CA1 neurons at 1 month after hypothermia. LTP was also significantly depressed at 1 week after hypothermia. These results suggest that some abnormalities in the glutamate receptor may be caused by ischemia; such abnormality would persist in spite of hypothermia treatment, resulting in the depression of LTP. Copyright (C) 2000 Elsevier Science B.V.",

keywords = "Gerbil, Hippocampus, Immunohistochemistry, Long term potentiation, N-Methyl-D-aspartate receptor 1, Postischemic hypothermia",

author = "Osamu Miyamoto and Takehiro Nakamura and Yamagami, {Shin ich} and Tetsuro Negi and Masaaki Tokuda and Hideki Matsui and Toshifumi Itano",

year = "2000",

month = aug,

day = "4",

doi = "10.1016/S0006-8993(00)02521-X",

language = "English",

volume = "873",

pages = "168--172",

journal = "Brain Research",

issn = "0006-8993",

publisher = "Elsevier",

number = "1",

}

TY - JOUR

T1 - Depression of long term potentiation in gerbil hippocampus following postischemic hypothermia

AU - Miyamoto, Osamu

AU - Nakamura, Takehiro

AU - Yamagami, Shin ich

AU - Negi, Tetsuro

AU - Tokuda, Masaaki

AU - Matsui, Hideki

AU - Itano, Toshifumi

PY - 2000/8/4

Y1 - 2000/8/4

N2 - To investigate the mechanism of chronic cell death following postischemic hypothermia, the change of N-methyl-D-aspartate receptor (NMDAR) were examined by immunohistochemistry of NMDAR1 and long-term potentiation (LTP) in the CA1 subfield of the gerbil hippocampus. At 1 week following postischemic hypothermia (32°Cx4 h), all CA1 neurons survived; however, immunoreactivity of NMDAR1 increased in neuronal perikarya whereas decreased in dendrites in the CA1 neurons. The abnormality was still observed in remaining CA1 neurons at 1 month after hypothermia. LTP was also significantly depressed at 1 week after hypothermia. These results suggest that some abnormalities in the glutamate receptor may be caused by ischemia; such abnormality would persist in spite of hypothermia treatment, resulting in the depression of LTP. Copyright (C) 2000 Elsevier Science B.V.

AB - To investigate the mechanism of chronic cell death following postischemic hypothermia, the change of N-methyl-D-aspartate receptor (NMDAR) were examined by immunohistochemistry of NMDAR1 and long-term potentiation (LTP) in the CA1 subfield of the gerbil hippocampus. At 1 week following postischemic hypothermia (32°Cx4 h), all CA1 neurons survived; however, immunoreactivity of NMDAR1 increased in neuronal perikarya whereas decreased in dendrites in the CA1 neurons. The abnormality was still observed in remaining CA1 neurons at 1 month after hypothermia. LTP was also significantly depressed at 1 week after hypothermia. These results suggest that some abnormalities in the glutamate receptor may be caused by ischemia; such abnormality would persist in spite of hypothermia treatment, resulting in the depression of LTP. Copyright (C) 2000 Elsevier Science B.V.

KW - Gerbil

KW - Hippocampus

KW - Immunohistochemistry

KW - Long term potentiation

KW - N-Methyl-D-aspartate receptor 1

KW - Postischemic hypothermia

UR - http://www.scopus.com/inward/record.url?scp=0034604745&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034604745&partnerID=8YFLogxK

U2 - 10.1016/S0006-8993(00)02521-X

DO - 10.1016/S0006-8993(00)02521-X

M3 - Article

C2 - 10915827

AN - SCOPUS:0034604745

VL - 873

SP - 168

EP - 172

JO - Brain Research

JF - Brain Research

SN - 0006-8993

IS - 1

ER -