Abstract

Excitatory postsynaptic potentials (termed U 1 and U 2) were extracellularly recorded from the frog optic tectum in vitro following electrical stimulation of the contralateral optic nerve. γ-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 glycerine 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 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 U 2 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.

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