title: In vivo tryptophan hydroxylase activity in rat major cerebral arteries is decreased by dorsal raphe nucleus lesions.
abstract: The in vivo presence of tryptophan hydroxylase activity in rat major cerebral arteries as well as the possible origin of the structure containing it were explored. Enzyme activity was appraised by accumulation of 5-hydroxytryptophan after inhibition of aromatic L-amino acid decarboxylase. Decarboxylase inhibition evoked a significant increase in 5-hydroxytryptophan levels in rat cerebral arteries, striatum, hippocampus, hypothalamus, and plasma but had no effect on aorta. p-Chlorophenylalanine reduced 5-hydroxytryptophan accumulation in the cerebral vessels and brain nuclei, whereas alpha-methyltyrosine did not modify it except in hypothalamus, where it was enhanced. alpha-Methyltyrosine significantly reduced noradrenaline levels in cerebral arteries and L-dopa accumulation after inhibition of the decarboxylase in striatum. Dorsal raphe nucleus lesioning significantly diminished 5-hydroxytryptophan 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 removal decreased noradrenaline levels in cerebral blood vessels without affecting 5-hydroxytryptophan accumulation. These results indicate the presence of a functionally active tryptophan hydroxylase in rat cerebral arteries associated with fibers originating from dorsal raphe nucleus. This supports that rat major cerebral arteries receive serotonergic innervation from central origin.
authors.affiliation: Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma de Madrid, Spain.
authors.forename: A L
authors.initials: AL
authors.lastname: López de Pablo
authors.forename: M J
authors.initials: MJ
authors.lastname: Moreno
authors.forename: E J
authors.initials: EJ
authors.lastname: Marco
mesh_terms: D006916:5-Hydroxytryptophan / Q000378:metabolism; D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000378:metabolism; D065105:Aromatic Amino Acid Decarboxylase Inhibitors; D002536:Cerebral Arteries / Q000201:enzymology*; D003342:Corpus Striatum / Q000187:drug effects / Q000378:metabolism; D004564:Electrocoagulation; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D010134:Fenclonine / Q000494:pharmacology; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism; D006834:Hydrazines / Q000494:pharmacology*; D007031:Hypothalamus / Q000187:drug effects / Q000378:metabolism; D007980:Levodopa / Q000378:metabolism; D008297:Male; D008781:Methyltyrosines / Q000494:pharmacology; D009638:Norepinephrine / Q000378:metabolism; D011903:Raphe Nuclei / Q000473:pathology* / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014365:Tryptophan Hydroxylase / Q000378:metabolism*; D019805:alpha-Methyltyrosine
chemical_list: D065105:Aromatic Amino Acid Decarboxylase Inhibitors; D004791:Enzyme Inhibitors; D006834:Hydrazines; D008781:Methyltyrosines; D007980:Levodopa; D019805:alpha-Methyltyrosine; C004297:3-hydroxybenzylhydrazine; D006916:5-Hydroxytryptophan; D014365:Tryptophan Hydroxylase; D010134:Fenclonine; D009638:Norepinephrine