GABA-ACTIVATED CONDUCTANCE IN CULTURED RAT INFERIOR COLLICULUS NEURONS

With the use of a whole cell voltage-clamp technique and fura-2 fluore scence measurements, the actions of gamma-aminobutyric acid (GABA) on cultured neurons from rat inferior colliculus were investigated. GABA (10-1,000 mu M) induced currents in neurons held under voltage clamp t hat were inhibited by bicuculline (20 mu M). Muscimol (100 mu M) also evoked the currents, whereas baclofen (100 mu M) affected neither the holding currents nor K+ conductance due to depolarizing pulses. The cu rrent density-voltage relation of GABA-induced currents, with equal co ncentrations of Cl- in the internal and external solutions, reversed n ear 0 mV. Reduction of the internal Cl- concentration shifted the reve rsal potential in the negative direction as predicted from the Cl- equ ilibrium potential. Baclofen did not affect Ca2+ conductance due to de polarizing pulses. The extracellular application of 150 mM KCl or 1.0 mM glutamate increased the intracellular Ca2+ concentration ([Ca2+](i) ) a of cultured inferior colliculus neurons only when neurons were bat hed in a Ca2+-containing external solution. However, GABA (1.0 mM) fai led to increase [Ca2+](i) at all concentrations of external Ca2+ used, indicating that GABA neither depolarized the cultured inferior collic ulus neurons sufficiently to activate the voltage-dependent Ca2+ condu ctances nor evoked Ca2+ release from intracellular stores. These resul ts suggest that in cultured rat inferior colliculus neurons, GABA(A) r eceptor channels map be predominantly responsible for the membrane con ductance evoked by GABA and subsequent hyperpolarization of the neuron s.