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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.

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