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Claude de Montigny, MD, PhD; Pierre Blier, MD, PhD
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.

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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.^3,5

5-HT Neuron Postsynaptic Neuron Somatodendritic 5-HT Autoreceptor Terminal 5-HT Autoreceptor Postsynaptic 5-HT Receptor

Schematic representation of the localization of the different 5-HT . . . [Full Text PDF of this Article]

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