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EFFECTS OF LESIONS AND DRUGS ON BRAIN TRYPTAMINE
Author(s) -
Marsden C. A.,
Curzon G.
Publication year - 1974
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1974.tb12214.x
Subject(s) - tryptamine , reserpine , monoamine oxidase , chemistry , serotonin , dopamine , tryptophan , monoamine oxidase inhibitor , monoamine neurotransmitter , endocrinology , amphetamine , medicine , pharmacology , phenelzine , monoamine oxidase b , striatum , biochemistry , biology , enzyme , receptor , amino acid
— The effects of various drugs and lesions on rat brain 5‐hydroxytryptamine and tryptamine were determined. Monoamine oxidase inhibition caused a proportionately greater increase in tryptamine than in 5‐hydroxytryptamine, reserpine depleted 5‐hydroxytryptamine but had no effect on tryptamine while p ‐chlorophenylalanine lowered 5‐hydroxytryptamine but increased tryptamine. α‐Methyl‐ p ‐tyrosine reduced striatal dopamine with no effect on either 5‐hydroxytryptamine or tryptamine. Increasing brain tryptophan by amphetamine administration. 24 h food deprivation or giving L‐tryptophan did not increase brain tryptamine. However a high dose of L ‐tryptophan (100 or 200mg/kg) together with a monoamine oxidase inhibitor caused a proportionately much greater increase in tryptamine than in 5‐hydroxytryptamine. Raphe lesions reduced 5‐hydroxytryptamine by 64 per cent and tryptamine by only 29 per cent while intraventricular 6‐hydroxydopamine lowered striatal dopamine (56 per cent), had no effect on 5‐hydroxytryptamine but reduced tryptamine by 24 per cent, suggesting that tryptamine can be formed in both 5‐HT and catecholaminergic neurones. The results are discussed in relation to the formation, distribution, storage and possible transmitter function of tryptamine in rat brain.