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Delayed increase in neuronal nitric oxide synthase immunoreactivity in thalamus and other brain regions after hypoxic-ischemic injury in neonatal rats.

Abstract：

:We examined the response of neuronal nitric oxide synthase (nNOS)-containing CNS neurons in rats exposed to a unilateral hypoxic-ischemic insult at 7 days of age. Animals were sacrificed at several time points after the injury, up to and including 7 days (Postnatal Day 14). Brain regions ipsilateral to the injury (including cerebral cortex, caudate-putamen, and thalamus) exhibited delayed, focal increases in nNOS immunoreactivity. The increase in nNOS immunoreactive fiber staining was prominent in areas adjacent to severe neuronal damage, especially in the cortex and the thalamus, regions that are also heavily and focally injured in term human neonates with hypoxic-ischemic encephalopathy. In cerebral cortex, these increases occurred despite modest declines in nNOS catalytic activity and protein levels. Proliferation of surviving nNOS immunoreactive fibers highlights regions of selective vulnerability to hypoxic-ischemic insult in the neonatal brain and may also contribute to plasticity of neuronal circuitry during recovery.

journal_name

Exp Neurol

journal_title

Experimental neurology

authors

Ishida A,Ishiwa S,Trescher WH,Nakajima W,Lange MS,Blue ME,Johnston MV

doi

10.1006/exnr.2000.7606

keywords:

subject

Has Abstract

pub_date

2001-04-01 00:00:00

pages

323-33

issue

2

eissn

0014-4886

issn

1090-2430

pii

S0014-4886(00)97606-4

journal_volume

168

pub_type

杂志文章

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