Abstract:
:Transient ischemia was produced for 15 min by occlusion of the middle cerebral artery in halothane-anesthetized rats, and changes in the extracellular concentrations of neurotransmitter monoamines and amino acids were examined in the striatum. The occlusion produced marked increases in the extracellular concentrations of both dopamine and glutamate in the striatum in the saline-injected control group, the peak values being 148 and 5.2 times those before ischemia, respectively. Preischemic administration of histamine (200 nmol, i.c.v.) suppressed the increase in dopamine and glutamate levels during ischemia, the peak values being 38% and 40% of those in the control group, respectively. Neither the dopamine nor glutamate level was affected by 6-[2-(4-imidazolyl)ethylamino]-N-(trifluoromethylphenyl)heptanecarboxamide (HTMT), an H(1) agonist (100 nmol, i.c.v.). However, dimaprit, an H(2) agonist (100 nmol, i.c.v.) suppressed the peak values to 42% and 32%, respectively. Most neurons were degenerated 7 days after ischemia in control animals. Histologic outcome was alleviated by either histamine or dimaprit treatment, whereas HTMT did not affect the outcome. Although postischemic administration of mepyramine, an H(1) antagonist (5 nmol, i.c.v.), did not affect the histologic alleviation caused by preischemic treatment with histamine, ranitidine, an H(2) antagonist (30 nmol, i.c.v.), partly abolished the improvement caused by histamine. These results suggest that suppression of ischemic release of excitatory neurotransmitters by histamine H(2) action is a contributing factor in alleviation of histologic outcome.
journal_name
Eur J Pharmacoljournal_title
European journal of pharmacologyauthors
Hamami G,Adachi N,Liu K,Arai Tdoi
10.1016/j.ejphar.2003.11.006keywords:
subject
Has Abstractpub_date
2004-01-26 00:00:00pages
167-73issue
2-3eissn
0014-2999issn
1879-0712pii
S0014299903026347journal_volume
484pub_type
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journal_title:European journal of pharmacology
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