POTASSIUM-evoked H-3-serotonin (5-HT) release from rat cerebrocortical
synaptosomes was performed after peripheral inoculation with fixed ra
bies virus CVS (challenge virus strain). At the onset of clinical symp
toms, the rats were sacrificed, synaptosomes were prepared from dissec
ted cortices and assayed for K+ evoked 5-HT release. The results show
a decrease in evoked 5-HT release from virus-infected synaptosomes. Al
terations in serotoninergic transmission in rabies virus infected brai
n cortex indicate a possible involvement in the triggering of pathogen
etic mechanisms relating to the clinicopathological manifestations of
the viral disease.