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Studies on the biochemical mechanisms of the central effects of gamma-hydroxybutyric acid (1974)

Studies on the biochemical mechanisms of the central effects of gamma-hydroxybutyric acid (1974)

  1. Bajeda
    Biochemical Pharmacology 1974 Feb 15;23(4):879-85

    Menon MK (http://www.ncbi.nlm.nih.gov/sites/e...l.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Fleming RM (http://www.ncbi.nlm.nih.gov/sites/e...l.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Clark WG (http://www.ncbi.nlm.nih.gov/sites/e...l.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus).

    In mice, administration of a 15 mg/kg dose of d-amphetamine sulfate (d-amph), a 10 mg/kg dose ofchloropromazine hydrochloride (CPZ) or a 50 mg/kg dose oftetrabenazine methane sulfonate (TBZ) caused marked elevation of homovanillic acid (HVA) levels in the caudate nucleus. GHB given alone did not change the level of HVA, but blocked the rise caused by d-amph and CPZ. GHB was not only ineffective in blocking the elevation of HVA levels brought about by TBZ, but in TBZ-pretreated mice GHB also failed to block the HVA-elevating effects of d-amph and CPZ. Apparently, GHB blocks the release of dopamine (DA) by acting at the storage granule membrane and, if the functional integrity of these granules is disrupted, as after TBZ, GHB is no longer effective. Using a thin-layer Chromatographie method, it also was shown that GHB does not alter the binding or metabolic pattern of DA by caudate nucleus.

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