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PubMed · 7130580

Treating geriatric depression: a 26-week interim analysis.

Abstract

Two concurrent studies of geriatric outpatients who received diagnoses of depression were conducted. In the first, patients were treated with one of two tricyclic antidepressants or with a placebo. In the second, patients were assigned to groups receiving either psychodynamic group therapy or cognitive-behavioral group therapy. Patients in the placebo group showed the least improvement; most patients receiving group psychotherapy showed some improvement, but only 12% had full remissions; by contrast, 45% of patients receiving imipramine or doxepin had full remissions, while 36% of them experienced little or no benefit. An early response to tricyclic antidepressant drugs was a reliable predictor of continued improvement.

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BibTeXRIS

L F Jarvik, J Mintz, J Steuer, R Gerner. 1982. Treating geriatric depression: a 26-week interim analysis.. https://doi.org/10.1111/j.1532-5415.1982.tb01987.x

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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.

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