GABAA receptors in plasma membranes of neurons are integral oligomers which form chloride channels. The binding of GABA molecules at recognition sites for channel opening triggers a transient increase in transmembrane chloride ion flux. The multiplicity and drug specificity of GABAA receptor, kinetics of channel opening, and desensitization of GABAA receptor and its short‐ and long‐term regulation have been investigated by the use of tracer amounts of the radioactive chloride isotope, 36Cl− ion. Results and new insights from 36Cl− ion flux measurements have been reviewed. © 1993 Wiley‐Liss, Inc.
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience