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PubMed · 7037102

Side effects and placebo amplification.

R Thomson
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Abstract

A sample of placebo-controlled tricyclic antidepressant studies was examined retrospectively to determine whether there was any difference in the relative efficacy of the tricyclic when it was compared against an inert placebo as against an active (atropine) placebo with anticholinergic side effects. Fewer studies showed a significant difference between atropine placebo and drug than between inert placebo and drug. The possibilities that atropine has a specific antidepressant effect, or that side effects amplify placebo responses are considered.

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Antidepressive Agents, TricyclicAtropineClinical Trials as TopicDouble-Blind MethodHumansPlacebosRetrospective StudiesClinical TrialComparative StudyJournal Article

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R Thomson. 1982. Side effects and placebo amplification.. https://doi.org/10.1192/bjp.140.1.64

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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↗