Distribution of indoleamines and [3H]paroxetine binding in rat brain regions following acute or perinatal ?9-tetrahydrocannabinol treatments

Reflection impulsivity in adolescent cannabis users: a comparison with alcohol-using and non-substance-using adolescents

“…Cannabinoids have been shown to interact with 5-HT receptors (Kelaï et al 2006;Kimura et al 1998) and evidence from preclinical studies suggests the involvement of cannabinoid receptors (CB1) in the regulation of serotonergic responses (Lau and Schloss 2008;Mato et al 2007), whereby stimulation of CB1 receptors reduces (Balazsa et al 2008) and inhibits (Best and Regehr 2008;Nakazi et al 2000) 5-HT release. Administration of THC has been shown to decrease serotonergic activity in various brain regions in animal studies (Molina-Holgado et al 1993;Moranta et al 2004;Sagredo et al 2006). Chronic exposure to cannabinoids during adolescence has similarly been shown to attenuate serotonergic activity (Bambico et al 2010) and differentially affect 5-HT1A receptor binding and mRNA expression in adult versus adolescent brains (Zavitsanou et al 2010).…”

The antinociceptive effect of acetylsalicylic acid is differently affected by a CB1 agonist or antagonist and involves the serotonergic system in rats

“…Finally, several studies suggest a possible interaction between the cannabinoid and serotonin neurotransmitter systems in discrete rat brain areas (Molina-Holgado et al 1993) including the prefrontal cortex (Marsicano and Lutz 1999). Other evidence suggests that central 5-HT 2 receptor activation promotes the release of endocannabinoids, which, in turn, activate CB 1 receptors throughout the CNS (Freund et al 2003).…”

The Potent Emetogenic Effects of the Endocannabinoid, 2-AG (2-Arachidonoylglycerol) Are Blocked by Δ9-Tetrahydrocannabinol and Other Cannnabinoids

“…Larger doses of SR 141716A (Darmani, 2001a) probably produce emesis by the release of emetic neurotransmitters such as acetylcholine (Pertwee, 2001) or serotonin (Darmani and Pandya, 2000) either by inverse agonism or an as yet unknown mechanism. Indeed, cannabinoid agonists not only decrease the release and turnover of the latter emetogenic neurotransmitters Molina-Holgado et al, 1993;Pertwee, 2001) but also block intestinal contractions produced by serotonin (Pertwee, 2001). However, most cannabinoid studies classify WIN 55,212-2 and CP 55,940 as fully efficacious cannabinoids (Pertwee, 1999), which argues against the discussed partial agonist theory.…”