cannabinoid receptor

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cannabinoid receptor

THC receptor, see there.
References in periodicals archive ?
Antagonists for the CB1 receptor also have neural actions, and there is increasing evidence of the therapeutic usefulness of these compounds.
Blockade of these receptors by selective CB1 receptor antagonists causes weight loss and ameliorates risk factors for obesity related disorders such as cardiovascular disease and type II diabetes.
The key classes of mechanism of action include combination therapies, CETP inhibitors, MTP inhibitors, PPAR agonists, thyroid hormone receptor modulators, gene therapies, nicotinic acid receptor agonists, AMPK modulators, enzyme inhibitors, cholesterol absorption inhibitors, farsenyl X receptor agonists, prostacyclin release stimulators, CB1 receptor agonists, A1 adenosine receptor agonists and omega-3 fatty acid derivatives.
This compound, through its high level of observed selectivity for the CB2 receptor versus the CB1 receptor, is designed to provide pain relief without psychotropic effects or the potential for dependence or abuse.
Pregnenolone prevents THC, the main active principle in cannabis, from fully activating its brain receptor, the CB1 receptor, that when overstimulated by THC causes the intoxicating effects of cannabis.
For example, cannabinoid antagonists targeting the CB1 receptor, such as agents being developed to treat obesity, have been associated with such central side effects as negative mood and depression.
The drug was designed to act selectively in peripheral tissues and organs, in contrast with the first generation of CB1 receptor blockers, which also significantly affected the brain.
The CB1 receptor is predominantly expressed in the central nervous system and plays a key role in regulating appetite and other reward-based behaviors.
MDA19 was designed to have a much stronger effect on the CB2 receptor than on the CB1 receptor.
Researchers investigated this by studying mice that lacked the CB1 receptor.
Cannabinoid CB1 receptor stimulation affords neuroprotection in MPTP-induced neurotoxicity by attenuating S1 00B up-regulation in vitro.
Cannabinoid CB1 receptor knockout mice exhibit markedly reduced voluntary alcohol consumption and lack alcohol-induced dopamine release in the nucleus accumbens.