The findings suggested that the active ingredient in cannabis, THC binds to cannabinoid receptors in the brain called CB1s, which inhibits chemical signals that tell us not to eat, New Scientist reported.
According to researchers at INSERM, the CB1 receptor in particular nerve cells within the olfactory system plays a central role in stimulating feeding.
Cannabinoids act via a specific receptor (i.e., CB1) to alter central physiological processes such as cognition, locomotion, appetite, and pain (Iversen 2003).
Little information is available on the expression and function of CB1 in the CeA.
In the hippocampus, CB1 ligands close a family of potassium channels (i.e., M-channels) also affected by alcohol (Moore et al.
The neuroadaptation to chronic alcohol exposure has been shown to involve changes in the CB 1 system, including alterations in the synthesis of eCBs and their precursors, as well as a decrease in the number of CB1 receptors (Basavarajappa and Hungund 2002; Gonzalez et al.
The eCBs acting at CB1 modulate alcohol consumption in rats, perhaps by affecting the activity of brain reward systems.
These results suggest that CB1 helps to regulate alcohol's effects in CeA neurons.
(1) Blockade of CB1 drastically diminishes alcohol preference, suggesting that endogenous CB1 ligands reinforce the preference for alcohol; (2) chronic alcohol exposure increases the levels of eCBs; (3) CB1 may play a critical role in stress-stimulated alcohol use; (4) CB1 antagonists suppress alcohol self-administration but only in alcohol-dependent animals; and (5) chronic alcohol downregulates CB1 and increases eCB levels.
Behavioral evidence supporting interactions of opioid and cannabinoid systems in drug addiction includes (1) the blockade of some effects of the psychoactive compound [DELTA]-9-tetrahydrocannabinol (THC) by opioid antagonists, (2) suppression of opioid withdrawal signs by cannabinoids and induction of withdrawal symptoms in morphine-dependent rats by CB1 antagonists, (3) precipitation of abstinence symptoms in THC-tolerant animals by naloxone, and (4) involvement of the cannabinoid and opioid systems in mechanisms underlying relapse (Cichewicz 2004b; Fattore et al.
In various studies, chronic morphine produced divergent effects as well as brain region--dependent effects on CB1 binding and expression levels.