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This Article Full Text Full Text (PDF) All Versions of this Article: 99/4/1596    most recent 01267.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Panek, I. Articles by Torkkeli, P. H. PubMed PubMed Citation Articles by Panek, I. Articles by Torkkeli, P. H.

Contributions of Voltage- and Ca²⁺-Activated Conductances to GABA-Induced Depolarization in Spider Mechanosensory Neurons

Department of Physiology and Biophysics, Dalhousie University, Halifax, Nova Scotia, Canada

Submitted 17 November 2007; accepted in final form 18 January 2008

Activation of ionotropic -aminobutyric acid type A (GABA_A) receptors depolarizes neurons that have high intracellular [Cl^–], causing inhibition or excitation in different cell types. The depolarization often leads to inactivation of voltage-gated Na channels, but additional ionic mechanisms may also be affected. Previously, a simulated model of spider VS-3 mechanosensory neurons suggested that although voltage-activated Na⁺ current is partially inactivated during GABA-induced depolarization, a slowly activating and inactivating component remains and may contribute to the depolarization. Here, we confirmed experimentally, by blocking Na channels prior to GABA application, that Na⁺ current contributes to GABA-induced depolarization in VS-3 neurons. Ratiometric Ca²⁺ imaging experiments combined with intracellular recordings revealed a significant increase in intracellular [Ca²⁺] when GABA_A receptors were activated, synchronous with the depolarization and probably due to Ca²⁺ influx via low-voltage–activated (LVA) Ca channels. In contrast, GABA_B-receptor activation in these neurons was previously shown to inhibit LVA current. Blockade of voltage-gated K channels delayed membrane repolarization, extending GABA-induced depolarization. However, inhibition of Ca channels significantly increased the amplitude of GABA-induced depolarization, indicating that Ca²⁺-activated K⁺ current has an even stronger repolarizing effect. Regulation of intracellular [Ca²⁺] is important for many cellular processes and Ca²⁺ control of K⁺ currents may be particularly important for some functions of mechanosensory neurons, such as frequency tuning. These data show that GABA_A-receptor activation participates in this regulation.