Abstract
A clear picture of the mechanisms of action of the anti-epileptic agent gabapentin is far from being accomplished. We have analyzed the effects of gabapentin on ligand- and voltage-gated currents in isolated adult rat cortical neurons. Gabapentin failed to modify glutamate currents and produced a slight reduction of GABA responses. Negligible inhibition of sodium, but consistent inhibition of high-voltage-activated calcium conductance was promoted by gabapentin. In addition, gabapentin reduced calcium current sensitivity to dihydropyridine agonist and antagonists. Interestingly, gabapentin also decreased a not-inactivating, cadmium-sensitive, potassium current. These unconventional effects might underlie its efficacy in a variety of diseases which involve periodic discharge patterns as neuropathic pain or essential tremor.
MeSH terms
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3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / pharmacology
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Acetates / pharmacology*
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Amines*
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Animals
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Anticonvulsants / pharmacology*
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Calcium Channel Agonists / pharmacology
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Calcium Channels / drug effects*
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Calcium Channels / physiology
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Cerebral Cortex / drug effects
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Cerebral Cortex / physiology
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Cyclohexanecarboxylic Acids*
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Gabapentin
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Glutamic Acid / pharmacology
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Male
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Neurons / drug effects*
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Neurons / physiology
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Potassium Channels / drug effects*
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Potassium Channels / physiology
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Pyramidal Cells / drug effects
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Pyramidal Cells / physiology
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Rats
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Rats, Wistar
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Sodium Channels / drug effects*
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Sodium Channels / physiology
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gamma-Aminobutyric Acid / pharmacology
Substances
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Acetates
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Amines
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Anticonvulsants
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Calcium Channel Agonists
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Calcium Channels
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Cyclohexanecarboxylic Acids
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Potassium Channels
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Sodium Channels
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Glutamic Acid
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gamma-Aminobutyric Acid
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Gabapentin
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3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester