This study addresses how
gamma-aminobutyric acid-A(GABAA) and
GABAC receptors confer distinct temporal properties to neuronal synaptic responses. The retina is a model system for the study of postsynaptic contributions to synaptic responses because GABAergic amacrine cells synapse onto neurons, which have different combinations of GABAA and
GABAC receptors. It is not known, however, how GABAA versus
GABAC receptors influence the time course of
retinal synaptic responses or what proportion of inhibitory input is mediated by each receptor type. We examined the time courses of synaptic responses mediated by
GABA receptors in
ganglion and bipolar cells by recording currents evoked by activating amacrine cells with a stimulating
electrode in the salamander
retinal slice. The pharmacologically isolated, GABAergic synaptic currents were long-lasting in bipolar cells and relatively brief in
ganglion cells. The receptors that mediated these temporally distinct synaptic responses exhibited different pharmacological properties. In
ganglion cells, GABAergic synaptic currents were abolished by the GABAA receptor antagonists
bicuculline or SR95531. In bipolar cells, the GABAC receptor antagonist 3-aminopropyl[methyl]
phosphonic acid (3-APMPA) largely blocked GABAergic synaptic responses; the remaining response was blocked by
bicuculline or SR95531. The GABAA receptor component of the bipolar cell response was relatively brief compared with the GABAC receptor component. Puffing
GABA onto
ganglion cell dendrites or bipolar cell terminals yielded similar pharmacological and kinetic results, indicating that transmitter release differences did not determine the response time courses. Moreover, the
GABAC receptors on bipolar cells may be different from those reported in rat or fish retina because
imidazole-4-acetic acid (I4AA), which acts as an antagonist in these preparations, acts as an agonist in salamander. Our data show that the prolonged synaptic responses in bipolar cells were mediated predominantly by
GABAC receptors, whereas transient synaptic responses in
ganglion cells were mediated by GABAA receptors.