IN-VIVO TRYPTOPHAN-HYDROXYLASE ACTIVITY IN RAT MAJOR CEREBRAL-ARTERIES IS DECREASED BY DORSAL RAPHE NUCLEUS LESIONS

The in vivo presence of tryptophan hydroxylase activity in rat major c erebral arteries as well as the possible origin of the structure conta ining it were explored. Enzyme activity was appraised by accumulation of 5-hydroxytryptophan after inhibition of aromatic L-amino acid decar boxylase. Decarboxylase inhibition evoked a significant increase in 5- hydroxytryptophan levels in rat cerebral arteries, striatum, hippocamp us, hypothalamus, and plasma but had no effect on aorta. p-Chloropheny lalanine reduced 5-hydroxytryptophan accumulation in the cerebral vess els and brain nuclei, whereas alpha-methyltyrosine did not modify it e xcept in hypothalamus, where it was enhanced. alpha-Methyltyrosine sig nificantly reduced noradrenaline levels in cerebral arteries and L-dop a accumulation after inhibition of the decarboxylase in striatum. Dors al raphe nucleus lesioning significantly diminished 5-hydroxytryptopha n formation in cerebral arteries, striatum, and hypothalamus, without affecting it in hippocampus. Lesion of median raphe nucleus reduced 5- hydroxytryptophan accumulation in hippocampus and in hypothalamus but not in cerebral blood vessels or striatum. Superior cervical ganglia r emoval decreased noradrenaline levels in cerebral blood vessels withou t affecting 5-hydroxytryptophan accumulation. These results indicate t he presence of a functionally active tryptophan hydroxylase in rat cer ebral arteries associated with fibers originating from dorsal raphe nu cleus. This supports that rat major cerebral arteries receive serotone rgic innervation from central origin.