Kindling suppresses primed-burst-induced long-term potentiation in hippocampal CA1.

In a previous study, we showed that partial hippocampal kindling in rats, a model of temporal lobe epilepsy, reduced the efficacy of presynaptic GABA(B) receptors in the CA1 area of hippocampal slices. In this study, we show that long-term potentiation (LTP) induced by theta-frequency primed bursts was suppressed in kindled as compared to control rats, but not in the presence of the GABA(B) receptor antagonists CGP35348 or CGP55845A. This is original evidence that LTP is suppressed by pathophysiological downregulation of GABA(B) autoreceptors. Control of postsynaptic inhibition by presynaptic GABA(B) receptors may provide a compensatory mechanism for controlling paroxysmal activity, with a side effect of blocking synaptic plasticity.