Expressions of nerve growth factor and p75 low affinity receptor after transient forebrain ischemia in gerbil hippocampal CA1 neurons

T. H. Lee, Koji Abe, K. Kogure, Y. Itoyama

Research output: Contribution to journalArticle

43 Citations (Scopus)

Abstract

Expressions of nerve growth factor (NGF) and low affinity p75 NGF receptor (p75 NGFR) in gerbil hippocampal neurons after 3.5-min transient forebrain ischemia were studied. Most hippocampal CA1 neurons were lost (neuronal density = 44 ± 12/mm) at 7 days after recirculation, while no cell death was found in the sham-control neurons (220 ± 27/mm). NGF immunoreactivity was normally present in the sham-control hippocampal neurons. However, it decreased in hippocampal CA1 neurons, and slightly decreased in the neurons of CA3 and dentate gyrus areas from 3 hr after recirculation. By 7 days, NGF immunoreactivity returned almost completely to the sham-control level in the CA3 and dentate gyrus neurons but decreased markedly in the CA1 neurons. In contrast, p75 NGFR immunoreactivity was scarcely present in the sham-control hippocampal neurons but was induced from 1 hr after recirculation in the CA1 and CA3 neurons and from 3 hr in the dentate gyrus. At 7 days, p75 NGFR immunoreactivity was expressed greatly in the surviving CA1 neurons and the reactive astrocytes but was not seen in the other hippocampal neurons. The markedly decreased NGF and greatly induced p75 NGFR immunoreactivity found in the CA1 neurons after transient forebrain ischemia suggests that NGF and p75 NGFR may be involved in the mechanism of delayed neuronal death.

Original languageEnglish
Pages (from-to)684-695
Number of pages12
JournalJournal of Neuroscience Research
Volume41
Issue number5
DOIs
Publication statusPublished - 1995
Externally publishedYes

Fingerprint

Nerve Growth Factor Receptor
Gerbillinae
Prosencephalon
Ischemia
Neurons
Nerve Growth Factor
Dentate Gyrus
Astrocytes

Keywords

  • hippocampus
  • ischemia
  • NGF
  • p75 NGFR

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Expressions of nerve growth factor and p75 low affinity receptor after transient forebrain ischemia in gerbil hippocampal CA1 neurons. / Lee, T. H.; Abe, Koji; Kogure, K.; Itoyama, Y.

In: Journal of Neuroscience Research, Vol. 41, No. 5, 1995, p. 684-695.

Research output: Contribution to journalArticle

@article{47f697ffbb6a49e695ac9fdd331e644b,
title = "Expressions of nerve growth factor and p75 low affinity receptor after transient forebrain ischemia in gerbil hippocampal CA1 neurons",
abstract = "Expressions of nerve growth factor (NGF) and low affinity p75 NGF receptor (p75 NGFR) in gerbil hippocampal neurons after 3.5-min transient forebrain ischemia were studied. Most hippocampal CA1 neurons were lost (neuronal density = 44 ± 12/mm) at 7 days after recirculation, while no cell death was found in the sham-control neurons (220 ± 27/mm). NGF immunoreactivity was normally present in the sham-control hippocampal neurons. However, it decreased in hippocampal CA1 neurons, and slightly decreased in the neurons of CA3 and dentate gyrus areas from 3 hr after recirculation. By 7 days, NGF immunoreactivity returned almost completely to the sham-control level in the CA3 and dentate gyrus neurons but decreased markedly in the CA1 neurons. In contrast, p75 NGFR immunoreactivity was scarcely present in the sham-control hippocampal neurons but was induced from 1 hr after recirculation in the CA1 and CA3 neurons and from 3 hr in the dentate gyrus. At 7 days, p75 NGFR immunoreactivity was expressed greatly in the surviving CA1 neurons and the reactive astrocytes but was not seen in the other hippocampal neurons. The markedly decreased NGF and greatly induced p75 NGFR immunoreactivity found in the CA1 neurons after transient forebrain ischemia suggests that NGF and p75 NGFR may be involved in the mechanism of delayed neuronal death.",
keywords = "hippocampus, ischemia, NGF, p75 NGFR",
author = "Lee, {T. H.} and Koji Abe and K. Kogure and Y. Itoyama",
year = "1995",
doi = "10.1002/jnr.490410515",
language = "English",
volume = "41",
pages = "684--695",
journal = "Journal of Neuroscience Research",
issn = "0360-4012",
publisher = "Wiley-Liss Inc.",
number = "5",

}

TY - JOUR

T1 - Expressions of nerve growth factor and p75 low affinity receptor after transient forebrain ischemia in gerbil hippocampal CA1 neurons

AU - Lee, T. H.

AU - Abe, Koji

AU - Kogure, K.

AU - Itoyama, Y.

PY - 1995

Y1 - 1995

N2 - Expressions of nerve growth factor (NGF) and low affinity p75 NGF receptor (p75 NGFR) in gerbil hippocampal neurons after 3.5-min transient forebrain ischemia were studied. Most hippocampal CA1 neurons were lost (neuronal density = 44 ± 12/mm) at 7 days after recirculation, while no cell death was found in the sham-control neurons (220 ± 27/mm). NGF immunoreactivity was normally present in the sham-control hippocampal neurons. However, it decreased in hippocampal CA1 neurons, and slightly decreased in the neurons of CA3 and dentate gyrus areas from 3 hr after recirculation. By 7 days, NGF immunoreactivity returned almost completely to the sham-control level in the CA3 and dentate gyrus neurons but decreased markedly in the CA1 neurons. In contrast, p75 NGFR immunoreactivity was scarcely present in the sham-control hippocampal neurons but was induced from 1 hr after recirculation in the CA1 and CA3 neurons and from 3 hr in the dentate gyrus. At 7 days, p75 NGFR immunoreactivity was expressed greatly in the surviving CA1 neurons and the reactive astrocytes but was not seen in the other hippocampal neurons. The markedly decreased NGF and greatly induced p75 NGFR immunoreactivity found in the CA1 neurons after transient forebrain ischemia suggests that NGF and p75 NGFR may be involved in the mechanism of delayed neuronal death.

AB - Expressions of nerve growth factor (NGF) and low affinity p75 NGF receptor (p75 NGFR) in gerbil hippocampal neurons after 3.5-min transient forebrain ischemia were studied. Most hippocampal CA1 neurons were lost (neuronal density = 44 ± 12/mm) at 7 days after recirculation, while no cell death was found in the sham-control neurons (220 ± 27/mm). NGF immunoreactivity was normally present in the sham-control hippocampal neurons. However, it decreased in hippocampal CA1 neurons, and slightly decreased in the neurons of CA3 and dentate gyrus areas from 3 hr after recirculation. By 7 days, NGF immunoreactivity returned almost completely to the sham-control level in the CA3 and dentate gyrus neurons but decreased markedly in the CA1 neurons. In contrast, p75 NGFR immunoreactivity was scarcely present in the sham-control hippocampal neurons but was induced from 1 hr after recirculation in the CA1 and CA3 neurons and from 3 hr in the dentate gyrus. At 7 days, p75 NGFR immunoreactivity was expressed greatly in the surviving CA1 neurons and the reactive astrocytes but was not seen in the other hippocampal neurons. The markedly decreased NGF and greatly induced p75 NGFR immunoreactivity found in the CA1 neurons after transient forebrain ischemia suggests that NGF and p75 NGFR may be involved in the mechanism of delayed neuronal death.

KW - hippocampus

KW - ischemia

KW - NGF

KW - p75 NGFR

UR - http://www.scopus.com/inward/record.url?scp=0029154564&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029154564&partnerID=8YFLogxK

U2 - 10.1002/jnr.490410515

DO - 10.1002/jnr.490410515

M3 - Article

VL - 41

SP - 684

EP - 695

JO - Journal of Neuroscience Research

JF - Journal of Neuroscience Research

SN - 0360-4012

IS - 5

ER -