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PubMed · 12049088

Attention-deficit/hyperactive disorder: making a case for multidisciplinary management.

G Ramanathan·G E White
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Abstract

Attention Deficit/Hyperactivity Disorder (AD/HD) is characterized by a cluster of age-inappropriate behavioral abnormalities comprising inattentivity, hyperactivity and impulsivity. The definition is controversial and without an accurate diagnosis. Therefore, it seems prudent that a multidisciplinary treatment protocol should begin with non-drug psychological and behavioral strategies plus nutritional intervention.

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Antidepressive Agents, TricyclicAttentionAttention Deficit Disorder with HyperactivityBehavior TherapyCentral Nervous System StimulantsChildChild Nutritional Physiological PhenomenaCognitive Behavioral TherapyFatty Acids, EssentialHumansImpulsive BehaviorMotor ActivityPatient Care TeamJournal ArticleReview

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G Ramanathan, G E White. 2001. Attention-deficit/hyperactive disorder: making a case for multidisciplinary management.. https://doi.org/10.17796/jcpd.25.3.gx4131w514x45138

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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↗