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Anandamide (AEA) and Δ⁹-tetrahydrocannabinol (THC) are endogenous and exogenous ligands, respectively, for cannabinoid receptors. Whereas most of the pharmacological actions of cannabinoids are mediated by CB1 receptors, there is also evidence that these compounds can produce effects that are not mediated by the activation of identified cannabinoid receptors. Here, we report that THC and AEA, in a CB1 receptor-independent manner, cause a significant potentiation of the amplitudes of glycine-activated currents (I_Gly) in acutely isolated neurons from rat ventral tegmental area (VTA) and in Xenopus laevis oocytes expressing human homomeric (α1) and heteromeric (α1β1) subunits of glycine receptors (GlyRs). The potentiation of I_Gly by THC and AEA is concentration-dependent, with respective EC₅₀ values of 86 ± 9 and 319 ± 31 nM for α1 homomeric receptors, 73 ± 8 and 318 ± 24 nM for α1β1 …