Short communicationValproate induced changes in GABA metabolism at the subcellular level
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Cited by (117)
An HPLC-based assay for improved measurement of glutamate decarboxylase inhibition/activation
2022, Neurochemistry InternationalCitation Excerpt :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).
Neuroinformatics analyses reveal GABAt and SSADH as major proteins involved in anticonvulsant activity of valproic acid
2016, Biomedicine and PharmacotherapyCitation Excerpt :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
2012, Neurochemistry InternationalCitation Excerpt :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
2011, BoneCitation Excerpt :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.
GABA and valproate modulate trigeminovascular nociceptive transmission in the thalamus
2010, Neurobiology of Disease