Chloride conductances in central neurons.

Two types of chloride conductances--gamma-aminobutyric acid (GABA)-activated and Ca2+-voltage dependent--were studied in tissue-cultured central neurons. Cultured hippocampal neurons contain identified GABA-mediated perisomatic synaptic connections. Activation of these synapses evokes, in voltage-clamped neurons, an inhibitory postsynaptic current (IPSC) that rises within 3 to 5 msec and decays exponentially with a time constant of 15 to 20 msec. The decay of the IPSC is voltage-dependent, and is altered by drugs known to act on GABA receptors. The kinetics of the IPSC appears to be determined by that of the GABA-activated Cl- ion channel. Ca2+ and voltage-dependent Cl- conductance is best seen in cells where K conductances are blocked. It usually follows a Ca spike and is blocked by Ca antagonists. Analysis of tail currents in voltage clamped hippocampal, hypothalamic and spinal cord neurons indicates that the current decays slowly (200 msec) and passively and reverses a function of [E]C1 (equilibrium potential for Cl-). Chloride conductance functions to suppress excitability of these neurons. The pharmacological and physiological properties of this conductance in vivo are not as yet known.