Differential effects of nialamide and clomipramine on serotonin efflux and autoreceptors
Autor: | Steve J. Offord, Robert O. Warwick |
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Rok vydání: | 1987 |
Předmět: |
Nialamide
Male Clomipramine medicine.medical_specialty Serotonin medicine.drug_class Clinical Biochemistry Hypothalamus Neurotransmission Pharmacology In Vitro Techniques Toxicology Serotonergic Biochemistry 5-Methoxytryptamine Behavioral Neuroscience Internal medicine Medicine Animals Biological Psychiatry Monoamine oxidase inhibitor business.industry Rats Inbred Strains Hydroxyindoleacetic Acid Rats Endocrinology Receptors Serotonin Autoreceptor Antidepressant Stereotyped Behavior business medicine.drug |
Zdroj: | Pharmacology, biochemistry, and behavior. 26(3) |
ISSN: | 0091-3057 |
Popis: | Serotonin (5-HT) activity in vivo and in vitro was evaluated in rats following acute and chronic administration of the antidepressants nialamide (NMD) and clomipramine (CMI). The 5-HT motor syndrome was used as an index of in vivo serotonergic function. In vitro , 3 H-5-HT uptake, potassium-evoked 3 H-5-HT release and 5-HT autoreceptor activity were evaluated as measures of presynaptic function. Repeated injections of NMD abolished the 5-methoxy-N, N-dimethyltryptamine (5-MeODMT)-induced motor syndrome and the ability of 5-methoxytryptamine (5-MEOT) to attenuate the potassium-evoked release of 3 H-5-HT. Autoreceptor subsensitivity was associated with a marked increase in basal and potassium-evoked 3 H-5-HT release. In contrast, acute NMD, and acute and chronic CMI did not affect the expression of the motor syndrome or alter 3 H-5-HT release or autoreceptor activity. Acute and chronic injections of NMD enhanced 3 H-5-HT uptake. The results suggest that the antidepressant efficacy of monoamine oxidase inhibitor (MAOI) antidepressant may be related to their ability to increase endogenous levels of 5-HT and thereby produce a subsensitivity of 5-HT 1 type receptors. This subsensitivity is reflected both by attenuation of the motor syndrome and enhanced 5-HT neurotransmission resulting in part from autoreceptor down-regulation. |
Databáze: | OpenAIRE |
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