GABA-activated conductance in cultured rat inferior colliculus neurons.

With the use of a whole cell voltage-clamp technique and fura-2 fluorescence measurements, the actions of gamma-aminobutyric acid (GABA) on cultured neurons from rat inferior colliculus were investigated. GABA (10-1,000 microM) induced currents in neurons held under voltage clamp that were inhibited by bicuculline (20 microM). Muscimol (100 microM) also evoked the currents, whereas baclofen (100 microM) affected neither the holding currents nor K+ conductance due to depolarizing pulses. The current density-voltage relation of GABA-induced currents, with equal concentrations of Cl- in the internal and external solutions, reversed near 0 mV. Reduction of the internal Cl- concentration shifted the-reversal potential in the negative direction as predicted from the Cl- equilibrium potential. Baclofen did not affect Ca2+ conductance due to depolarizing pulses. The extracellular application of 150 mM.KCl or 1.0 mM glutamate increased the intracellular Ca2+ concentration ([Ca2+]i) of cultured inferior colliculus neurons only when neurons were bathed in a Ca(2+)-containing external solution. However, GABA (1.0 mM) failed to increase [Ca2+]i at all concentrations of external Ca2+ used, indicating that GABA neither depolarized the cultured inferior colliculus neurons sufficiently to activate the voltage-dependent Ca2+ conductances nor evoked Ca2+ release from intracellular stores. These results suggest that in cultured rat inferior colliculus neurons, GABAA receptor channels may be predominantly responsible for the membrane conductance evoked by GABA and subsequent hyperpolarization of the neurons.