1. Electrophysiological recordings were obtained from neurons in the amphibian intact retina and retinal slice preparations. The effects of gamma-aminobutyric acid (GABA) were evaluated in the presence of bicuculline or SR95531, which block the GABAA receptor, and baclofen, which saturates the GABAB receptor. 2. Under these conditions, GABA preferentially reduced ON light responses in amacrine and ganglion cells, apparently through a presynaptic mechanism that reduced bipolar cell input. GABA also produced a small hyperpolarization in the resting membrane potential of ganglion cells. 3. Picrotoxin blocked these effects of GABA. The action of GABA was duplicated by muscimol and by trans-aminocrotonic acid. Cis-aminocrotonic acid was neither a potent nor selective agonist. This pharmacology is indicative of the GABAC receptor. 4. In voltage-clamp recordings of ganglion cells in the slice preparation, GABA produced a large chloride conductance that was blocked by bicuculline or SR95531, and a smaller chloride conductance that was not blocked by these GABAA receptor antagonists, but was blocked by picrotoxin. This indicates that ganglion cells possess both GABAA and GABAC receptors. 5. The GABAC receptor current was relatively nondesensitized. Consequently, whereas the peak GABAA receptor current was more than fivefold larger than the GABAC receptor current, after desensitization the latter current was larger. Both currents reversed near the chloride equilibrium potential.
GABAA receptor-mediated increase in membrane chloride conductance in rat paratracheal neurones