Elsevier

Biochemical Pharmacology

Volume 30, Issue 11, 1 June 1981, Pages 1364-1366
Biochemical Pharmacology

Short communication
Valproate induced changes in GABA metabolism at the subcellular level

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References (28)

  • W. Löscher

    Biochem. Pharmac.

    (1979)
  • S. Simler et al.

    Biochem. Pharmac.

    (1973)
  • P.K.P. Harvey et al.

    FEBS Lett.

    (1975)
  • G. Anlezark et al.

    Biochem. Pharmac.

    (1976)
  • C.W. Cotman
  • R.A. Salvador et al.

    J. biol. Chem.

    (1959)
  • O.H. Lowry et al.

    J. biol. Chem.

    (1951)
  • M.A.K. Markwell et al.

    Analyt. Biochem.

    (1978)
  • R.M. Pinder et al.

    Drugs

    (1977)
  • M.J. Ladarola et al.

    J. Neurochem.

    (1979)
  • W. Löscher et al.

    Arzneim.-Forsch.

    (1977)
  • W. Löscher et al.

    Naunyn-Schmiedeberg's Arch. Pharmac.

    (1977)
  • W.D. Lust et al.
  • S. Simler et al.

    Commun. Psychopharmac.

    (1978)
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      It was found that valproic acid manifested potentiating effect at the lower tested concentration (15.2 ± 4.1% of activation) and an opposite effect (19.4 ± 4.4% of inhibition) at the higher concentration. In previous studies of the effect of valproic acid on GAD enzyme, somewhat inconsistent results were obtained (Löscher, 1981; Sethi et al., 1987; Wikinski et al., 1996). However, these studies differed significantly in terms of whether they employed in vivo or in vitro models, the enzyme origin (rats or Escherichiacoli), and the method used for determining enzyme activity (radiometric or fluorometric).

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      The inhibition elevates the level of SSA which results in increase in GABA level in turn, due to the reversible nature of transamination reaction of GABAt contributing majorly towards the anti-convulsion activity of VPA. The findings are in good accordance with earlier postulates of Löscher [11,14,16] describing GABAergic mode of VPA action. α-KGDH being the another proposed site of action of VPA (Fig. 1) was also investigated in present study.

    • Dietary supplementation with acetyl-l-carnitine in seizure treatment of pentylenetetrazole kindled mice

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      The latter did, however, increase the amount of glutathione. A major metabolic effect of valproate is potentiation of GABAerigc metabolism (Loscher, 1981, 1999, 2002) and ALCAR may be preferentially metabolized in GABAerig neurons (Scafidi et al., 2010). PTZ, on the other hand, diminishes GABAergic inhibition through binding to the GABA-A receptor.

    • Suberoylanilide hydroxamic acid (SAHA; vorinostat) causes bone loss by inhibiting immature osteoblasts

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      The mechanisms behind valproate's induction of bone loss in vivo are unclear due to conflicting reports of its effects on bone formation and bone resorption [35,36,40–42]. Furthermore, valproate can inhibit other enzymes (e.g., succinate semialdehyde-dehydrogenase and -reductase) [43,44], thus it is uncertain that its capacity to stimulate bone loss in vivo is specific to deacetylase inhibition. In this study we sought to determine the consequences of another clinically-relevant histone deacetylase inhibitor, SAHA (vorinostat or Zolinza™), on bone mass and bone turnover in vivo.

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