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Article
May 1991

Desensitization of Terminal 5-HT Autoreceptors by 5-HT Reuptake Blockers

Author Affiliations

Neurobiological Psychiatry Unit Department of Psychiatry McGill University 1033 Pine Ave W Montreal, Quebec, Canada H3A 1A1

Arch Gen Psychiatry. 1991;48(5):483-484. doi:10.1001/archpsyc.1991.01810290095019
Abstract

To the Editor.—  We commend Goodman et al1 for their rigorous study on the effectiveness of fluvoxamine in obsessive-compulsive disorder (OCD) and for the comprehensive and scholarly review on the possible mechanisms of action of 5-hydroxytryptamine (5-HT) reuptake blockers in OCD. We believe, however, that the issue of 5-HT autoreceptor desensitization deserves some clarification. Indeed, these authors stated correctly that long-term administration of 5-HT reuptake blockers leads to an enhanced 5-HT neurotransmission through 5-HT autoreceptor desensitization. However, they failed to specify that both the somatodendritic and terminal 5-HT autoreceptors (Figure) are desensitized following long-term treatment with 5-HT reuptake blockers.2,3 In contrast, long-term treatment with monoamine oxidase (MAO) inhibitors, while inducing desensitization of somatodendritic 5-HT autoreceptors,4 does not modify the function of terminal 5-HT autoreceptors.3,55-HT Neuron Postsynaptic Neuron Somatodendritic 5-HT Autoreceptor Terminal 5-HT Autoreceptor Postsynaptic 5-HT ReceptorSchematic representation of the localization of the different 5-HT

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