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or synergy. Loewe demonstrated synergy generated by cannabis extracts combined Systematic Review of eCB Modulation assay; result compared to unsupplemented controls1 in vivo piglets, whole brain homogenates; qAEA, <2-AG in vivo mice, whole brain homogenates; qAEA in vivo mice, whole brain homogenates; Q2-AG in vivo mice, whole brain homogenates; q2-AG in vitro mouse 3T3-F442A adipocytes; Q2-AG, QAEA in vitro mouse 3T3-F442A adipocytes; q2-AG in vivo rats, whole brain homogenates; PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/19631915 by either rimonabant or naloxone. Naltrexone, a m- and k-opioid receptor antagonist, significantly increased many of the “positive”subjective effects of oral THC and smoked cannabis in marijuana smokers. These results suggest that endogenous opioids contribute to the effects of cannabis. In summary, preclinical studies and clinical trials indicate that acute opiate administration enhances the activity of eCBs, phytocannabinoids, and synthetic cannabinoids. Acute opiates may also upregulate CB1 expression. Chronic opiate administration, however, may have a deleterious effect on the eCB system. Antidepressant drugs. Serotonin selective uptake inhibitors, tricyclic antidepressants and monoamine oxidase inhibitors are the most commonly prescribed antidepressant drugs. Treatment with fluoxetine, the archetypal SSRI, potentiated THC-induced hypothermia in rats, but did not change THC-induced behavioral effects–freezing behavior, social interaction or exploration, and preference for outer or inner zones. Fluoxetine increased CB1 Debio 1347 binding density in the prefrontal cortex, without altering AEA or 2-AG levels in rat brains. Chronic fluoxetine also increased WIN55212-2-stimulated GTPcS binding in the rat prefrontal cortex. Conversely, treatment with citalopram reduced HU210-stimulated GTPcS binding in the rat hypothalamus and hippocampus. Treatment with fluoxetine prevented synaptic defects in mice induced by PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/19631704 chronic unpredictable stress, and CUS preserved eCB- and WIN55,212-2-stimulated CB1 signaling. In the hands of Mato et al., fluoxetine in rats enhanced the inhibition of adenylyl cyclase by WIN55212-2, but did not alter WIN55212-2-stimulated GTPcS binding or CB1 d