Abstract
Stereotaxic injection of kainic acid into rat striatum produces neuronal degeneration and neurochemical alterations resembling Huntington's disease (HD). Since correction of the deficiency in gamma-aminobutyric acid (GABA) in HD may be of therapeutic value, the efficacy of drugs that inhibit the GABA-degrading enzyme (GABA-T) in elevating the levels of GABA has been examined in the animal model for HD. High doses of di-N-propylacetic acid only partially correct the GABA deficiency in the striatum, whereas low doses of gamma-acetylenic GABA, a specific irreversible inhibitor of GABA-T, completely restore the levels of GABA in striatum and substantia nigra.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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4-Aminobutyrate Transaminase / antagonists & inhibitors*
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Alkynes / pharmacology
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Aminocaproates / pharmacology*
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Aminocaproic Acid / pharmacology
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Animals
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Caudate Nucleus / enzymology
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Glutamate Decarboxylase / metabolism
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Huntington Disease / chemically induced
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Huntington Disease / enzymology*
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Kainic Acid / pharmacology
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Male
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Nerve Degeneration / drug effects
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Rats
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Substantia Nigra / enzymology
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Transaminases / antagonists & inhibitors*
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Valproic Acid / pharmacology
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gamma-Aminobutyric Acid / metabolism*
Substances
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Alkynes
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Aminocaproates
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gamma-Aminobutyric Acid
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Valproic Acid
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Transaminases
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4-Aminobutyrate Transaminase
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Glutamate Decarboxylase
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Kainic Acid
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Aminocaproic Acid