THC has been reported to affect the activity of several neurotransmitter receptor systems. THC, however, does not interact directly with the active site of the receptors, but rather causes an allosteric modification of the receptor, which in turn modifies its response to other agonists and antagonists. After THC administration, the effects of subsequent exposure to the receptor agonists acetylcholine (Domino, 1981; Gessa et al., 1997) and opioids (Vaysse, 1987) and NMDA (Hampson et al., 1998) are decreased, while the effects of catecholamines (Bloom et al., 1978) and GABA are biphasic (Pryor et al., 1977). Bloom and Hillard (1984) concludes that, since THC alters membrane fluidity, its effects on constituent receptors are due to changes in the membrane environment, which in turn, affect membrane receptors. "Although some differences exist in the interactions with specific proteins, the fact remains that psychoactive cannabinoids affect a broad range of membrane-bound receptors, which supports the concept of a direct influence on the membrane lipid bilayer, rather than an embedded receptor specific for A9-THC on each of these very different receptor molecules to neurotransmitters."
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