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PubMed · 15768687

Separation anxiety disorder.

Nichole Jurbergs·Deborah Roth Ledley
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Abstract

SAD is a disorder that can cause a great deal of distress and impairment. Children with the disorder often miss school, as well as many other important social opportunities like playing with friends and participating in extracurricular activities. It is quite likely that, if untreated, SAD can lead to numerous negative psychosocial outcomes. Luckily, effective treatments for SAD are available, including CBT and SSRI pharmacotherapy. Pediatricians can play an important role in identifying SAD and other anxiety disorders and providing parents with information about appropriate treatments.

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Antidepressive Agents, TricyclicAnxiety, SeparationBenzodiazepinesChildCognitive Behavioral TherapyHumansParent-Child RelationsPrevalencePsychiatric Status Rating ScalesReinforcement, PsychologySelective Serotonin Reuptake InhibitorsJournal ArticleReview

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BibTeXRIS

Nichole Jurbergs, Deborah Roth Ledley. 2005. Separation anxiety disorder.. https://doi.org/10.3928/0090-4481-20050201-09

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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↗