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

Research output: Contribution to journalArticle

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 languageEnglish
Pages (from-to)168-172
Number of pages5
JournalBrain Research
Volume873
Issue number1
DOIs
Publication statusPublished - Aug 4 2000

Fingerprint

Gerbillinae
Long-Term Potentiation
Hypothermia
Hippocampus
Neurons
Glutamate Receptors
Dendrites
N-Methyl-D-Aspartate Receptors
Cell Death
Ischemia
Immunohistochemistry
NMDA receptor A1

Keywords

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

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Miyamoto, O., Nakamura, T., Yamagami, S. I., Negi, T., Tokuda, M., Matsui, H., & Itano, T. (2000). Depression of long term potentiation in gerbil hippocampus following postischemic hypothermia. Brain Research, 873(1), 168-172. https://doi.org/10.1016/S0006-8993(00)02521-X

Depression of long term potentiation in gerbil hippocampus following postischemic hypothermia. / Miyamoto, Osamu; Nakamura, Takehiro; Yamagami, Shin ich; Negi, Tetsuro; Tokuda, Masaaki; Matsui, Hideki; Itano, Toshifumi.

In: Brain Research, Vol. 873, No. 1, 04.08.2000, p. 168-172.

Research output: Contribution to journalArticle

Miyamoto, O, Nakamura, T, Yamagami, SI, Negi, T, Tokuda, M, Matsui, H & Itano, T 2000, 'Depression of long term potentiation in gerbil hippocampus following postischemic hypothermia', Brain Research, vol. 873, no. 1, pp. 168-172. https://doi.org/10.1016/S0006-8993(00)02521-X
Miyamoto O, Nakamura T, Yamagami SI, Negi T, Tokuda M, Matsui H et al. Depression of long term potentiation in gerbil hippocampus following postischemic hypothermia. Brain Research. 2000 Aug 4;873(1):168-172. https://doi.org/10.1016/S0006-8993(00)02521-X
Miyamoto, Osamu ; Nakamura, Takehiro ; Yamagami, Shin ich ; Negi, Tetsuro ; Tokuda, Masaaki ; Matsui, Hideki ; Itano, Toshifumi. / Depression of long term potentiation in gerbil hippocampus following postischemic hypothermia. In: Brain Research. 2000 ; Vol. 873, No. 1. pp. 168-172.
@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 = "8",
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 -