Background: The purpose of this study was to investigate the effect of potassium, bicuculline (BIC) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) on epileptiform activity induced by pilocarpine in the rat visual cortex slices. Methods: In the rat visual cortex slices, we observed the change of pilocarpine-induced epileptiform discharges using extracellular recordings during perfusion of artificial cerebro-spinal fluid (ACSF) with various potassium concentrations ([K+], 2.5, 5, 7.5 and 10 mM) and ACSF with 10 μM BIC and 20 μM CNQX under 7.5 mM [K+]. Results: Spontaneous interictal epileptiform activity induced by pilocarpine was observed in 5 mM or higher [K+] and ictal discharge was only detected in 7.5 mM [K+]. Increase of [K+] from 2.5 to 7.5 mM not only resulted in the increase of frequency and amplitude of epileptiform activity but also favored the transformation of pilocarpine-induced interictal activity into ictal activity in the rat visual cortex. However, in 10 mM [K+], the ictal discharge was unprovoked and interictal activity was provoked with decreased frequency and amplitude. The spontaneous ictal discharge was blocked but interictal activity was maintained with increased frequency and amplitude by BIC. Interictal and ictal activities were completely blocked by CNQX. Conclusions: These results suggested that the extracellular potassium concentration, GABA system, and non- NMDA mechanism seemed to be involved in the development and maintenance of pilocarpine-induced epileptiform activity in the rat visual cortex.

Background: The purpose of this study was to investigate the effect of potassium, bicuculline (BIC) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) on epileptiform activity induced by pilocarpine in the rat visual cortex slices. Methods: In the rat visual cortex slices, we observed the change of pilocarpine-induced epileptiform discharges using extracellular recordings during perfusion of artificial cerebro-spinal fluid (ACSF) with various potassium concentrations ([K+], 2.5, 5, 7.5 and 10 mM) and ACSF with 10 μM BIC and 20 μM CNQX under 7.5 mM [K+]. Results: Spontaneous interictal epileptiform activity induced by pilocarpine was observed in 5 mM or higher [K+] and ictal discharge was only detected in 7.5 mM [K+]. Increase of [K+] from 2.5 to 7.5 mM not only resulted in the increase of frequency and amplitude of epileptiform activity but also favored the transformation of pilocarpine-induced interictal activity into ictal activity in the rat visual cortex. However, in 10 mM [K+], the ictal discharge was unprovoked and interictal activity was provoked with decreased frequency and amplitude. The spontaneous ictal discharge was blocked but interictal activity was maintained with increased frequency and amplitude by BIC. Interictal and ictal activities were completely blocked by CNQX. Conclusions: These results suggested that the extracellular potassium concentration, GABA system, and non- NMDA mechanism seemed to be involved in the development and maintenance of pilocarpine-induced epileptiform activity in the rat visual cortex.

Pilocarpine, Potassium, Bicuculline, CNQX, Epileptiform activity, Epileptogenesis