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Characterization and Pharmacology of the GHB Receptor

Radioligand binding using [3H]NCS‐382, an antagonist of the GHB receptor, revealed specific binding sites in the rat cerebrocortical and hippocampal membranes. Scatchard analysis of saturation isotherms revealed two different populations of binding sites. NCS‐382 was about 10 times more potent than GHB in inhibiting [3H]NCS‐382 binding. A variety of ligands for other receptors did not affect [3H]NCS‐382 binding. Quantitative autoradiographic analysis of [3H]NCS‐382 binding revealed similar characteristics. Thus [3H]NCS‐382, being more potent and selective, offers advantage over [3H]GHB as a radioligand. Unlike GHB, several analogues of GHB such as UMB68 (a tertiary alcohol analogue of GHB), UMB86 (4‐hydroxy‐4‐napthylbutanoic acid, sodium salt), UMB72 [4‐(3‐phenylpropyloxy)butyric acid, sodium salt], UMB73 (4‐benzyloxybutyric acid, sodium salt), UMB66 (3‐chloropropanoic acid), gamma‐hydroxyvaleric acid (that is, GHV, a 4‐methyl‐substituted analogue of GHB), 3‐HPA (3‐hydroxyphenylacetic acid), and ethers of 3‐hydroxyphenylacetic acid (UMB108, UMB109, and UMB119) displaced [3H]NCS‐382 without affecting [3H]GABA binding to GABAB receptor. Thus these compounds offer an advantage over GHB as an experimental tool. Our study, aimed at exploring the potential involvement of the GHB receptor in the pharmacology of ethanol, indicated that ethanol does not affect [3H]NCS‐382 binding in the rat brain, thereby suggesting that ethanol does not interact directly with the GHB receptor. Our study, aimed at exploring the involvement of the GHB receptor in the pathology of succinate semialdehyde dehydrogenase deficiency, which is known to cause elevation of GHB levels, revealed no change in the affinity, receptor density or displacement potency as determined by using [3H]NCS‐382 as a radioligand in Aldh5a1−/− vs. Aldh5a1+/+ mouse brain.