Effects of combined administration of L-tryptophan and tricyclic antidepressants on α2- and β-adrenoceptors and monoamine levels in rat brain

Date
1985, 1985
Authors
Russell V.A.
Lamm M.C.L.
De Villiers A.S.
Russell V.A.
Lamm M.C.L.
De Villiers A.S.
Journal Title
Journal ISSN
Volume Title
Publisher
Abstract
In order to test whether co-administration of a serotonin precursor with antidepressant drugs could potentiate the effects of the antidepressants on monoamines or adrenoceptors in rat brain, L-tryptophan (20 mg/kg) was administered to rats daily for 7 or 15 days, either alone or in combination with desipramine (10 mg/kg) or amitriptyline (10 mg/kg). After treatment with L-tryptophan for 7 days, increases were observed in rat hypothalamic and frontal cortex 5-hydroxy-3-indoleacetic acid levels as well as in hypothalamic dopamine and nucleus accumbens 3,4-dihydroxyphenylacetic acid levels. After 15 days, hippocampal β-adrenoceptor density was found to be decreased. There was no evidence of potentiation of desipramine or amitriptyline action when L-tryptophan was administered in combination with the antidepressants. On the contrary, the antidepressants appeared to interact with L-tryptophan to reduce its effects.
In order to test whether co-administration of a serotonin precursor with antidepressant drugs could potentiate the effects of the antidepressants on monoamines or adrenoceptors in rat brain, L-tryptophan (20 mg/kg) was administered to rats daily for 7 or 15 days, either alone or in combination with desipramine (10 mg/kg) or amitriptyline (10 mg/kg). After treatment with L-tryptophan for 7 days, increases were observed in rat hypothalamic and frontal cortex 5-hydroxy-3-indoleacetic acid levels as well as in hypothalamic dopamine and nucleus accumbens 3,4-dihydroxyphenylacetic acid levels. After 15 days, hippocampal β-adrenoceptor density was found to be decreased. There was no evidence of potentiation of desipramine or amitriptyline action when L-tryptophan was administered in combination with the antidepressants. On the contrary, the antidepressants appeared to interact with L-tryptophan to reduce its effects.
Description
Keywords
alpha 2 adrenergic receptor; amitriptyline; beta adrenergic receptor; desipramine; monoamine; radioisotope; tricyclic antidepressant agent; tryptophan; 4 aminoclonidine h 3; animal cell; animal experiment; brain; central nervous system; dihydroalprenolol h 3; dopamine brain level; dose response; drug comparison; drug interaction; drug potentiation; drug receptor binding; drug response; intraperitoneal drug administration; nonhuman; pharmacokinetics; priority journal; rat; Amitriptyline; Animal; Antidepressive Agents, Tricyclic; Brain Chemistry; Catecholamines; Desipramine; Drug Combinations; Kinetics; Male; Rats; Rats, Inbred Strains; Receptors, Adrenergic, alpha; Receptors, Adrenergic, beta; Support, Non-U.S. Gov't; Time Factors; Tryptophan, alpha 2 adrenergic receptor, amitriptyline, beta adrenergic receptor, desipramine, monoamine, radioisotope, tricyclic antidepressant agent, tryptophan, 4 aminoclonidine h 3, animal cell, animal experiment, brain, central nervous system, dihydroalprenolol h 3, dopamine brain level, dose response, drug comparison, drug interaction, drug potentiation, drug receptor binding, drug response, intraperitoneal drug administration, nonhuman, pharmacokinetics, priority journal, rat, Amitriptyline, Animal, Antidepressive Agents, Tricyclic, Brain Chemistry, Catecholamines, Desipramine, Drug Combinations, Kinetics, Male, Rats, Rats, Inbred Strains, Receptors, Adrenergic, alpha, Receptors, Adrenergic, beta, Support, Non-U.S. Gov't, Time Factors, Tryptophan
Citation
Neurochemical Research
10
12
Neurochemical Research
10
12