The effects on GABA metabolism of an anticonvulsant drug, di‐ n ‐propylacetate (DPA), were studied. Given intraperitoneally DPA increases the brain GABA content and does not change its biosynthesis from glutamic acid. However, it inhibits in vitro both glutamate decarboxylase and aminobutyrate transaminase (GABA‐T) activities. The inhibition is more pronounced on the GABA‐T and this observation might explain the increase of GABA level.
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Godin et al. (1969) studied this question.
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