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 CAI 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/min). NGF immunoreactivity was normally present in the sham‐control hippocampal neurons. However, it decreased in hippocampal CAI 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 CAI 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 CAI and CA3 neurons and from 3 hr in the dentate gyrus. At 7 days, p75 NGFR immunoreactivity was expressed greatly in the surviving CAI 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 CAI neurons after transient forebrain ischemia suggests that NGF and p75 NGFR may be involved in the mechanism of delayed neuronal death. © 1995 Wiley‐Liss, Inc.
- p75 NGFR
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience