Baclofen increases transient light responses of amacrine and ganglion cells despite acting as a classical inhibitory transmitter to both hyperpolarize and shunt these cells. 2. This effect seems to occur at the level of the inner retina and appears not to be due to an additional input from bipolar cells. 3. In some transient cells baclofen increases the total amplitude of the light response but does not change the peak potential of the light evoked EPSP. In these cells, the baclofen-induced enhancement can be accounted for by an increase in driving force of the excitatory postsynaptic potential (EPSP) resulting from the hyperpolarization. 4. However, in other cells the peak of the light response after baclofen application is greater, which cannot be accounted for by a change in driving force. This effect of baclofen can be mimicked by a blockers of gamma-aminobutyric acid (GABA) and glycine, suggesting that in these cells baclofen's enhancement is due in part to network effects resulting in a removal of sustained inhibition. 5. Therefore, the paradoxical effect of an inhibitory transmitter producing an enhancement of synaptic responses seems due to at least two mechanisms. 6. The results indicate that some transient cells receive significant tonic inhibition which limits their response amplitude in a push-pull type mechanism, but other cells are not under this inhibitory control process.
