Abstract
Membrane potential changes of rat neonatal optic nerves were studied in a sucrose-gap chamber. Nipecotic acid (NPA), which blocks uptake and promotes release of GABA, resulted in a bicuculline-sensitive depolarization (3.08 +/- 0.3 mV, n = 5). Pretreatment of the nerves with the anticonvulsant gabapentin (100 microM for 1 h) resulted in a near doubling of the NPA-induced depolarization (6.64 +/- 0.54 mV, n = 5). Gabapentin itself did not alter membrane potential, nor did brief applications of gabapentin enhance the NPA- or GABA-induced depolarization. Thus, gabapentin appears to enhance the releasable pool of GABA in this CNS neural system. These results have implications for the mechanism of the anticonvulsant properties of gabapentin.
Publication types
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Acetates / pharmacology*
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Action Potentials / drug effects
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Amines*
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Animals
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Animals, Newborn / metabolism*
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Anticonvulsants / pharmacology*
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Bicuculline / pharmacology
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Cyclohexanecarboxylic Acids*
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GABA-A Receptor Antagonists
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Gabapentin
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Membrane Potentials / drug effects
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Neuromuscular Depolarizing Agents / pharmacology*
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Nipecotic Acids / pharmacology
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Optic Nerve / drug effects*
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Proline* / analogs & derivatives*
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Rats
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Rats, Wistar
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Receptors, GABA-A / drug effects
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Receptors, GABA-A / metabolism
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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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Cyclohexanecarboxylic Acids
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GABA-A Receptor Antagonists
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Neuromuscular Depolarizing Agents
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Nipecotic Acids
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Receptors, GABA-A
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nipecotic acid
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gamma-Aminobutyric Acid
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Gabapentin
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Proline
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homoproline
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Bicuculline