Abstract
Modafinil is a well-known psychoactive drug used to treat narcolepsy, hypoglycemia, cerebral ischemia and Parkinson's disease. Previous studies showed that ATP-sensitive potassium channels (K ATP) play a key role in response to cerebral ischemia, hypoglycemia or metabolic inhibition. Modafinil (0.01–1 mM) dose-dependently decreased the GABA-activated currents (I GABA). Pretreatment with the K ATP channel blocker, glibenclamide (10 μM), significantly reduced the decrease of I GABA caused by modafinil. Thus, the inhibitory effect of modafinil on the I GABA is indirect by modulating K ATP channel activation, at least in part mediated by K ATP channel.
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