Abstract

The sustained effects of gamma-aminobutyric acid (GABA) on voltage-gated conductances, and excitatory and inhibitory postsynaptic currents (EPSC and IPSC, respectively) in crayfish opener muscle fibers were analyzed using the two-electrode voltage-clamp technique. GABA (1.0 mM) was applied for 1-2 min and measurements were performed 30 min after restoring control Ringer solution. The L-type Ca2+ current (ICa) was reduced by > 33%. The ICa conductance (gCa) was reduced and the activation and inactivation were slowed down by GABA. The ICa regulation outlasted GABA superfusion (150 min). A small decrease (< 19%) of the Ca2+-activated K+ current (IKCa), due to the ICa reduction, was also recorded. The leak (IL), the delayed-rectifier (IK) and the hyperpolarization-activated (IAB) currents were not affected. Picrotoxin (0.5 mM) and bicuculline (0.2 mM) blocked the ICa reduction. Neither the GABAB antagonist saclofen (1.0 mM) nor the agonist baclofen (1.0 mM) had any effect. Therefore, the ICa regulation was probably mediated through GABAA receptors. EPSCs, but not IPSCs, were reduced (30%) for prolonged periods (> 100 min.) after GABA application. We describe a new, potentially functional, role for GABA receptors in the mediation of a sustained reduction of presynaptic and postsynaptic excitability in crustacean muscle.

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