The effect of GABA on the frog optic tectum is sensitive to ammonium and to penicillin.

Excitatory postsynaptic potentials (termed U1 and U2) were extracellularly recorded from the frog optic tectum in vitro following electrical stimulation of the contralateral optic nerve. Gamma-Aminobutyric acid (GABA) and glycine elicited a large and sustained enhancement of these synaptic waves. In the presence of the Cl- transport inhibitor ammonium (NH+4) the effects of GABA or glycine were progressively reduced to about 50% of their initial action without changes in the control synaptic waves. In 50% Cl- media the depression of GABA and glycine responses by NH+4 was more intense. Other Cl- transport inhibitors such as bumetanide, piretanide and 4-acetamido-4'-isothiocyanatostilbene-2,2'-disulphonate (SITS) were inactive against responses to GABA or glycine. Penicillin, a Cl- channel blocker, antagonized the action of GABA and glycine, while increasing the amplitude of the U2 waveform. The present results provide pharmacological evidence in support of the Cl- dependence of the unusual action of GABA or glycine in facilitating excitatory synaptic transmission in the optic tectum.