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Mild hypothermia ameliorates ubiquitin synthesis and prevents delayed neuronal death in the gerbil hippocampus.

Abstract：

BACKGROUND AND PURPOSE:The purpose of the present study is to determine the effect of mild hypothermia on the synthesis of ubiquitin, an important protein for maintenance of cell viability, in the hippocampal neurons following transient cerebral ischemia. METHODS:Transient ischemia was induced by occluding both common carotid arteries for 5 minutes. In experiment 1, the animals were divided into four groups according to the rectal and scalp temperatures during ischemia: the normothermia group and the graded hypothermia A, B, and C groups (n = 9 per group). CA1 neuronal density was assessed at 7 days after ischemia. In experiment 2, the animals were divided into two groups designated the normothermia and the hypothermia groups (n = 6 per group). The presence of ubiquitin was examined by immunohistochemistry at 6, 24, and 48 hours after transient ischemia in various regions of the hippocampus. RESULTS:In experiment 1, the mean +/- SEM neuronal density per millimeter was 12 +/- 1 in the normothermia group and 126 +/- 25, 225 +/- 10, and 214 +/- 9 in hypothermia groups A, B, and C, respectively. Mild hypothermia in groups B and C, in which the brain temperature was below 33 degrees C, ameliorated markedly the extent of ischemic neuronal damage in the CA1 sector (p less than 0.01). In experiment 2, ubiquitin immunoreactivity had disappeared in all regions of the hippocampus at 6 hours after ischemia and showed no subsequent recovery in the CA1 pyramidal neurons under normothermic conditions. Under hypothermic conditions, however, it had recovered significantly in the CA1 pyramidal neurons at 24 and 48 hours after ischemia (p less than 0.01). CONCLUSIONS:We conclude that mild hypothermia, in which the brain temperature is below 33 degrees C, markedly improves the ischemic delayed neuronal damage in the CA1 sector, and that increased ubiquitin synthesis and protein ubiquitination could be one essential part of the protective mechanism afforded by mild hypothermia against delayed neuronal death.

journal_name

Stroke

journal_title

Stroke

authors

Yamashita K,Eguchi Y,Kajiwara K,Ito H

doi

10.1161/01.str.22.12.1574

subject

Has Abstract

pub_date

1991-12-01 00:00:00

pages

1574-81

issue

eissn

0039-2499

issn

1524-4628

journal_volume

pub_type

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Mild hypothermia ameliorates ubiquitin synthesis and prevents delayed neuronal death in the gerbil hippocampus.