GABA actions on the excitability of cultured CNS neurons.

The membrane mechanisms associated with Cl- conductance activated by GABA in spinal and hippocampal neurons cultured from the embryonic mouse and rat have been studied with voltage- and patch-clamp techniques. The elementary mechanism underlying the conductance response is predominantly all-or-none with both similar and different kinetics in different assays. beta-Alanine and glycine also alter conductance via a similar mechanism, but the electrical properties associated with each transmitter are unique. Clinically important drugs modulate GABA-mediated responses by altering the kinetics of ion channel activity. Inhibitory synaptic currents whose time constant of decay coincides with the common, slower phase of channel kinetics in pharmacological experiments are altered in amplitude and/or time course by the same drugs. The results strongly suggest that the synaptic events reflect the activation of 1700 channels whose open-time distribution describes the time constant of decay.