GABA affects the glutamate receptor-chloride channel complex in mechanically isolated and internally perfused Aplysia neurons

Abstract

The effects of γ-aminobutyric acid (GABA) on the glutamate receptors chloride ion (Cl −) channel complex were examined in mechanically isolated and internally perfused Aplysia neurons using a concentration clamp technique. GABA at concentrations of 3 × 10 −6 M or more, concentration dependently delayed the recovery of the glutamate response from desensitization. This effect was independent of the GABA response and Cl − redistribution. Muscimol (10 −4 M) mimicked the effect of GABA. However, this was not the case for baclofen (10 −3 M). In some isolated neurons, GABA at concentrations of more than 10 −4 M clearly induced an additional Cl − current, the current kinetics of which were different from those induced by lower concentrations of GABA. Even in the continued presence of 10 −4 M GABA, which desensitized the fast GABA response, higher concentrations of GABA (3 × 10 −4 M to 10 −2 M) elicited the additional current in a concentration-dependent manner. The presence of 10 −4 M glutamate completely abolished this current, indicating cross-desensitization between the glutamate and slow GABA responses. High concentrations of GABA (3 × 10 −2 M) did not activate the glutamate receptor coupled to the large cation channel. The results suggest that, in Aplysia neurons, the glutamate receptor-Cl − channel complex has some similarities to the GABA receptor-Cl − channel complex.