Cerebral infarction was produced by unilateral carotid ligation in the gerbil, and 5HT levels in the cerebral hemispheres were assayed 3.5 hours later. A bilateral fall as confirmed, with the greatest change occurring on the side of carotid ligation in animals showing the clinical sequelae of infarction. Neither absolute levels nor right left differences in 5HT content related directly to the nature or prevalence of neurological morbidity. Neither putative 5HT receptor antagonists nor agents causing increasing brain 5HT levels produced consistent changes in the prevalence of neurological morbidity. It is argued that the fall in 5HT in a cerebral infarct is more likely to be due to reduced synthesis and turnover than to release of the amine into the synaptic cleft. These findings cast doubt on the hypothesis that a significant part of the morbidity and mortality of cerebral infarction is due to the sequelae of 5HT release.
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