Abstract
Gabapentin was developed as an anticonvulsant, but has also been used to alleviate hyperalgesia in neuropathic pain. In this study, the protective effect of gabapentin against N-methyl-D-aspartate (NMDA)-induced excitotoxicity in rat hippocampal CA1 neurons was investigated. Pre-treatment with gabapentin reduced the degree of neuronal damage induced by NMDA exposure in cultured hippocampal slices. Patch-clamp studies revealed that gabapentin significantly inhibited the NMDA receptor-activated ion current in dissociated hippocampal CA1 neurons, resulting in suppression of glutamate-induced neuronal injury. These results show that gabapentin may exert protective effects against glutamate-induced neuronal injury at least in part by inhibiting the NMDA receptor-activated ion current.
MeSH terms
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Amines / pharmacology*
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Animals
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Animals, Newborn
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Anticonvulsants / pharmacology
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Cyclohexanecarboxylic Acids / pharmacology*
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Dose-Response Relationship, Drug
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Excitatory Amino Acid Agonists / toxicity
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Gabapentin
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Hippocampus / cytology
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Ion Channels / physiology
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Membrane Potentials / drug effects
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N-Methylaspartate / toxicity*
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Neurons / cytology
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Neurons / drug effects*
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Neurons / physiology
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Neuroprotective Agents / pharmacology*
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Patch-Clamp Techniques / methods
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Pyramidal Cells / cytology
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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, Sprague-Dawley
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Receptors, N-Methyl-D-Aspartate / physiology
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gamma-Aminobutyric Acid / pharmacology*
Substances
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Amines
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Anticonvulsants
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Cyclohexanecarboxylic Acids
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Excitatory Amino Acid Agonists
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Ion Channels
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Neuroprotective Agents
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Receptors, N-Methyl-D-Aspartate
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gamma-Aminobutyric Acid
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N-Methylaspartate
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Gabapentin