Abstract
A transient cerebral ischemia produced in rats by 4-vessel occlusion, produces with a delay of 24 h a fall in the number of somatostatin-containing neurons. In the present study we show that this loss is preceded by a loss of somatostatin mRNA that starts as soon as 30 min after the anoxic episode. By 24 h of revascularization the surviving somatostatinergic hilar cells present a transient recovery of hybridization signal. This effect could be related to a previously reported increase in intracellular calcium.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Base Sequence
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Hippocampus / pathology
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Hippocampus / physiology
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Hippocampus / physiopathology*
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Ischemic Attack, Transient / pathology
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Ischemic Attack, Transient / physiopathology*
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Male
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Molecular Sequence Data
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Neurons / pathology
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Neurons / physiology*
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Oligonucleotide Probes
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RNA, Messenger / genetics*
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RNA, Messenger / metabolism
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Rats
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Rats, Inbred Strains
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Reference Values
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Somatostatin / genetics*
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Time Factors
Substances
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Oligonucleotide Probes
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RNA, Messenger
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Somatostatin