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GABA transaminase inhibitors.

L Ciesielski, S Simler, C Gensburger

    Advances in Experimental Medicine and Biology
    |January 1, 1979
    PubMed
    Summary
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    Branched-chain fatty acids inhibit GABA-T and SSADH enzymes, increasing brain GABA levels. This GABA increase correlates with anticonvulsant effects, suggesting a therapeutic potential for these fatty acids.

    Area of Science:

    • Biochemistry
    • Neuroscience
    • Pharmacology

    Background:

    • Gamma-aminobutyric acid (GABA) is a primary inhibitory neurotransmitter in the central nervous system.
    • Dysregulation of GABAergic signaling is implicated in neurological disorders like epilepsy.
    • Enzymes such as GABA transaminase (GABA-T) and succinate semialdehyde dehydrogenase (SSADH) are key regulators of GABA metabolism.

    Purpose of the Study:

    • To investigate the inhibitory effects of branched-chain fatty acids (BCFAs) on GABA-T and SSADH.
    • To determine if BCFAs can modulate brain GABA levels.
    • To explore the correlation between BCFAs, GABA levels, and anticonvulsant activity.

    Main Methods:

    • Enzyme inhibition assays were performed using purified GABA-T and SSADH.

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  • The effects of various BCFAs on enzyme activity were measured.
  • Brain GABA levels were assessed in response to BCFAs administration.
  • Anticonvulsant activity was evaluated in relevant models.

    • Main Results:

    • Several BCFAs acted as competitive inhibitors of GABA-T.
    • These BCFAs were non-competitive inhibitors of SSADH.
    • BCFAs treatment led to increased brain GABA levels, with regional variations observed for some compounds.
    • Inhibition of SSADH alone did not elevate GABA levels.
    • A correlation was found between elevated brain GABA and the anticonvulsant properties of BCFAs.

    Conclusions:

    • BCFAs modulate GABAergic neurotransmission through dual inhibition of GABA-T and SSADH.
    • The observed increase in brain GABA mediated by BCFAs is linked to their anticonvulsant efficacy.
    • BCFAs represent a potential therapeutic strategy for conditions involving GABAergic deficits.