The Journal of Neurophysiology Vol. 77 No. 2 February 1997, pp. 994-1002
Copyright ©1997 The American Physiological Society

GABA-Activated Conductance in Cultured Rat Inferior Colliculus Neurons

Hidenobu Hosomi¹, Masahiro Mori¹, Mutsuo Amatsu², and Yasuhiro Okada¹

Departments of ¹ Physiology and ² Otorhinolaryngology, Kobe University, School of Medicine, Kobe 650, Japan

Hosomi, Hidenobu, Masahiro Mori, Mutsuo Amatsu, and Yasuhiro Okada. GABA-activated conductance in cultured rat inferior colliculus neurons. J. Neurophysiol. 77: 994-1002, 1997. With the use of a whole cell voltage-clamp technique and fura-2 fluorescence measurements, the actions of -aminobutyric acid (GABA) on cultured neurons from rat inferior colliculus were investigated. GABA (10-1,000 µM) induced currents in neurons held under voltage clamp that were inhibited by bicuculline (20 µM). Muscimol (100 µM) also evoked the currents, whereas baclofen (100 µM) 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 Ca²⁺-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, GABA_A receptor channels may be predominantly responsible for the membrane conductance evoked by GABA and subsequent hyperpolarization of the neurons.

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