Abstract
In this study on guinea pig hippocampal slices, protein kinase C (PKC) involvement in long-term potentiation (LTP) of GABAA and GABAB receptor-mediated fast and slow IPSPs, respectively, was examined. Stimulation of the stratum radiatum induced EPSPs followed by fast and slow IPSPs in the CA1 neurons. Tetanic stimulation of the stratum caused a marginal LTP of the fast IPSP but not of the slow IPSP. When K-252b, a potent inhibitor of PKC, was injected into CA1 neurons, LTP of fast and slow IPSPs was observed. These results indicate that PKC activation in CA1 neurons is involved in minimizing, rather than inducing, LTP of the IPSPs so that the EPSP is not distorted.
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