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PubMed · 10986733

Pharmacotherapy for obsessive-compulsive disorder.

E Hollander·A Kaplan·A Allen·C Cartwright
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Abstract

SSRIs and the tricyclic antidepressant clomipramine are the first-line therapies for patients with OCD, with the side-effect profile of SSRIs being more favorable than that of clomipramine. As many as 40% to 60% of patients with OCD may not respond to adequate trials of SRIs. Not all patients tolerate SSRIs, and delays in full therapeutic responses often occur. Thus, other pharmacologic approaches to treating patients with OCD have been investigated. Augmentation and monotherapy have been explored with serotonergic enhancers, dopamine and 5-HT antagonists, enhancers of second-messenger systems, and GABAergic agents with varying efficacy.

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Antidepressive Agents, TricyclicHumansMeta-Analysis as TopicMulticenter Studies as TopicObsessive-Compulsive DisorderRandomized Controlled Trials as TopicSelective Serotonin Reuptake InhibitorsJournal ArticleReview

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BibTeXRIS

E Hollander, A Kaplan, A Allen, C Cartwright. 2000. Pharmacotherapy for obsessive-compulsive disorder.. https://doi.org/10.1016/s0193-953x(05)70186-6

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Inhibition of astroglial inwardly rectifying Kir4.1 channels by a tricyclic antidepressant, nortriptyline.

The inwardly rectifying K(+) (Kir) channel Kir4.1 is responsible for astroglial K(+) buffering. We examined the effects of nortriptyline, a tricyclic antidepressant (TCA), on Kir4.1 channel currents heterologously expressed in HEK293T cells, using a whole-cell patch-clamp technique. Nortriptyline (3-300 microM) reversibly inhibited Kir4.1 currents in a concentration-dependent manner, whereas it marginally affected neuronal Kir2.1 currents. The inhibition of Kir4.1 channels by nortriptyline depended on the voltage difference from the K(+) equilibrium potential (E(K)), with greater potency at more positive potentials. Blocking kinetics of the drug could be described by first-order kinetics, where dissociation of the drug slowed down and association accelerated as the membrane was depolarized. The dissociation constant (K(d)) of nortriptyline for Kir4.1 inhibition was 28.1 microM at E(K). Other TCAs, such as amitriptyline, desipramine, and imipramine, also inhibited Kir4.1 currents in a similar voltage-dependent fashion. This study shows for the first time that nortriptyline and related TCAs cause a concentration-, voltage-, and time-dependent inhibition of astroglial K(+)-buffering Kir4.1 channels, which might be involved in therapeutic and/or adverse actions of the drugs.

Antidepressive Agents, Tricyclic↗