Impact of protein kinase C activation on epileptiform activity in the hippocampal slice.

Epilepsy Research
Michaelangelo G FuortesL R Merlin

Abstract

There is evidence suggesting that protein kinase C (PKC) activation can prevent the enhanced network excitability associated with status epilepticus and group I metabotropic glutamate receptor (mGluR)-induced epileptogenesis. However, we observed no suppression of mGluR-induced burst prolongation in the guinea pig hippocampal slice when applied in the presence of the PKC activator phorbol-12,13-dibutyrate (PDBu). Furthermore, PDBu alone converted picrotoxin-induced interictal bursts into ictal-length discharges ranging from 2 to 6s in length. This effect could not be elicited by the inactive analog 4-alpha-PDBu and was suppressed with the PKC inhibitor chelerythrine, indicating PKC dependence. PKC activation can enhance neurotransmitter release, and both glutamate and acetylcholine are capable of eliciting similar prolonged synchronized discharges. However, neither mGluR1 nor NMDA receptor antagonist suppressed PDBu-driven burst prolongation, suggesting that increased glutamate release alone is unlikely to account for the PKC-induced expression of ictaform discharges. Similarly, atropine, a broad-spectrum muscarinic receptor antagonist, had no effect on PKC-induced burst prolongation. By contrast, AMPA/kainate receptor antagoni...Continue Reading

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Citations

May 28, 2010·Journal of Neurotrauma·Lie YangDouglas S F Ling
Nov 19, 2014·Journal of Psychiatric Practice·Jonathan T Stewart, David A Kahn
Jul 31, 2020·The International Journal of Neuroscience·Maria V TurovskayaEgor A Turovsky

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