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 microM), 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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Animals, Newborn
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Benzhydryl Compounds / pharmacology*
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Cells, Cultured
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Drug Interactions
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Glyburide / pharmacology
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Hippocampus / cytology*
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Hypoglycemic Agents / pharmacology
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Membrane Potentials / drug effects*
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Membrane Potentials / physiology
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Membrane Potentials / radiation effects
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Modafinil
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Neuroprotective Agents / pharmacology*
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Patch-Clamp Techniques / methods
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Pyramidal Cells / drug effects*
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Pyramidal Cells / physiology
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Pyramidal Cells / radiation effects
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Rats
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Rats, Sprague-Dawley
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gamma-Aminobutyric Acid / pharmacology*
Substances
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Benzhydryl Compounds
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Hypoglycemic Agents
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Neuroprotective Agents
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gamma-Aminobutyric Acid
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Modafinil
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Glyburide