Abstract
The naturally occurring central nervous system depressant γ-hydroxy-butyrate (GHB) and its lactone precursor, γ-butyrolactone (GBL) cause a marked and selective increase in brain dopamine. Concomitant with the increase in brain dopamine, homovanillic acid, a metabolite of brain dopamine, is decreased. GBL also causes a selective increase in the specific activity of brain dopamine but not of brain norepinephrine when rats are injected with 14C-tyrosine. This is probably the result of a compensatory activation of dopaminergic neurons because of a blockade in dopamine release induced by GHB. When catecholamine biosynthesis is inhibited by administration of α-methyl- p-tyrosine, GBL completely blocks the disappearance of subcortical dopamine but exerts no antagonism on the disappearance of subcortical norepinephrine. These observations are suggestive that GBL increases brain dopamine primarily by selectively blocking the release of this monoamine from dopamine containing neurons. Indirect evidence is also presented which suggests that the central nervous system depressant properties of GHB may be related to this block in the release of brain dopamine.
Published Version
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