Voltage-clamp characterization of Cl^- conductance gated by GABA and L-glutamate in single neurons of aplysia

1. Cl^- conductance gated by γ-aminobutyric acid (GABA) and L-glutamate in the medial pleural neurons of Aplysia was studied using conventional two-electrode voltage-clamp techniques and a continuous microperfusion system that allowed rapid and uniform agonist application. 2. Both GABA and glutamate elicited current responses that rapidly activated and then decayed (desensitized) during maintained presence of agonist. 3. Recovery from desensitization was rapid for both agonists. For intermediate concentrations of each agonist, recovery was ~90% complete with 1 min. 4. Dose-response experiments at a holding potential of -45 mV showed that 1) maximal peak responses to glutamate were on the average ~40% of those to GABA, 2) the dose-peak response curve for glutamate was steeper than that for GABA, and 3) time-to-peak (risetime) and desentitization half-time decreased monotonically with dose for GABA but were relatively insensitive to dose and more variable for glutamate. 5. Peak conductances elicited by GABA were voltage dependent, increasing with depolarization, whereas the Cl^- conductance elicited by glutamate was voltage dependent. Risetime and desensitization kinetics were insensitive to voltage for both agonists. 6. Lowering the temperature of the perfusion medium by 10°C slowed activation and desensitization for both 0.1 mM GABA and 2 mM glutamate. The responses to the two agonists differed, however, in that the peak response to glutamate increased, whereas that to GABA decreased in amplitude. 7. Since previous studies on crustacean muscle as well as on the medial pleural neurons of Aplysia have shown cross-desensitization between Cl^--mediated responses to GABA and glutamate, the differences in kinetic properties of the responses may reflect agonist-specific influences on a common channel.