GABA-induced chloride current in catfish horizontal cells mediated by non-GABAA receptor channels.

GABA-induced currents were recorded in cone-driven horizontal cells dissociated from the catfish, using the patch clamp technique in the whole-cell configuration. GABA-induced current consisted of two components; approximately 80% of the current was blocked by 100 microM picrotoxin (PTX), and the remaining 20% of the current was blocked when extracellular Na+ was replaced with Li+ or choline. The PTX-sensitive current was carried by Cl-. When methanesulfonate was substituted for the intrapipette Cl-, the reversal potentials of the PTX-sensitive current shifted to a more negative potential close to the Cl- equilibrium potential. The PTX-sensitive current was unaffected either by bicuculline (up to 500 microM), pentobarbital (100 microM), or diazepam (100 microM). These observations suggest that the PTX-sensitive current is not mediated via GABAA receptors. Baclofen, a GABAB receptor agonist, had no effect, suggesting the absence of GABAB receptors. Cis- or trans-4-aminocrotonic acid (CACA and TACA), GABAC receptor agonists, evoked currents in a dose-dependent manner. The potency sequence was TACA > GABA > muscimol > CACA. These observations suggest that the PTX-sensitive current of cone-driven horizontal cells is carried via the GABAC receptor channel. The Cl- equilibrium potential in intact cells was estimated to be approximately -30 mV by recording the GABA-induced voltage response of dissociated cells with a conventional intracellular microelectrode. The intracellular Cl- concentration seemed to be approximately 40 mM. From these results, it is suggested that GABAC receptor channels shape the kinetics of light-induced responses of horizontal cells, and mediate a chemical coupling between neighboring horizontal cells.