PMC:3951193 / 21204-25861
Annnotations
{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/3951193","sourcedb":"PMC","sourceid":"3951193","source_url":"http://www.ncbi.nlm.nih.gov/pmc/3951193","text":"Opiates\nNaloxone, a μ-opioid receptor antagonist, inhibited THC-induced Fos immunoreactivity in several regions of the rat central nervous system, including the ventral tegmental area, hypothalamus, caudate-putamen, and periaqueductal grey. Conversely, naloxone and THC had an additive effect on Fos immunoreactivity in the amygdala, stria terminalis, insular cortex, and paraventricular nucleus of the thalamus [63].\nShort-term co-administration of morphine with THC caused an upregulation of CB1 protein in the spinal column of rats, far greater than THC or morphine given alone [64]. A rodent study of chronic but voluntary intake of opiates (rats self-administering heroin) enhanced [3H]CP55,940 binding in the amygdala and ventral tegmental area, plus a marked increase in cannabinoid-stimulated [35S]GTPγS binding in the nucleus accumbens, caudate putamen, and amygdala [65]. Superperfusion of ex vivo rat nucleus accumbens slices with 4-aminopyridine and NMDA released glutamate and GABA, respectively, and either morphine or the CB1 agonist HU210 predictably inhibited these responses. Combining HU210 and morphine caused a synergistic inhibition of GABA release, but a non-additive response in glutamate release [66].\nChronic morphine exposure in rats caused a reduction in hippocampal and cerebellar CB1 density measured with [3H]CP55,940, and a strong reduction in CP55,940-stimulated [35S]GTPγS binding; 2-AG contents were also reduced [67]. Another rat study showed that chronic morphine exposure caused variable, regionally-specific modulations in [3H]CP55,940 binding and CB1 mRNA levels; CB1 upregulated in some regions and dowregulated in other regions [68]. In human CB1-transfected HEK293 cells, morphine induced a desensitization of the μ-opioid receptor and heterologous desensitization of CB1, demonstrated by a reduction in WIN55212-2-induced [Ca2+]i release [69]. μ-opioid receptor knockout mice showed a dramatic reduction in WIN55212-2-stimulated [35S]GTPγS binding [70]. In human SH-SY5Y neuroblastoma cells, sequential activation of CB1 and δ-opioid receptor produced synergistic elevations of intracellular Ca2+, a response that each receptor alone did not trigger in an efficacious way [71].\nIn behavioral studies, heroin reinstated “drug-seeking” behavior for WIN55,212-2 in rats [72]. Morphine did the same for THC in monkeys [73]. The rewarding effects of THC, measured by conditioned place-preference, were reversed by naloxone in rats [74]. In rats trained to discriminate THC, morphine administration markedly potentiated the THC discriminative stimulus [75]. Morphine or codeine potentiated THC-induced antinociception and analgesia in mice and rats [76]–[79]; inactive doses of the drugs in combination produce potent, synergistic analgesia [80]. Synergistic analgesia was confirmed in an isobolographic analysis [64]. Historically this is the first isobolographic analysis of a cannabinoid since the days Walter Siegfried Loewe, who invented the isobologram to test drug combinations for synergy [81]. Loewe demonstrated synergy generated by cannabis extracts combined with other drugs [82], [83], as well as synergy generated amongst the individual components within cannabis itself [84], [85].\nNormal men subjected to a thermal pain stimulus did not experience analgesia from a low dose of nabilone (a synthetic THC analogue), or a low dose of morphine. But co-administration of the drugs produced an analgesic effect [86].\nEndorphins (endogenous opioids) enhance the effects of cannabinoids: Administering a low dose of THC to rats produced an anxiolytic response in the light-dark box test, which was abolished by beta-funaltrexamine, a μ-opioid receptor antagonist [87]. In rats trained to discriminate THC, microinjection of β-endorphin into the ventral tegmental area potentiated the THC discriminative stimulus [75]. Enkephalins (endogenous opioids) also enhance the effects of THC: the inhibition of encephalin-degrading enzymes augmented THC-induced antinociception in mice, an effect blocked by either rimonabant or naloxone [88]. Naltrexone, a μ- and κ-opioid receptor antagonist, significantly increased many of the “positive” subjective effects of oral THC [89] and smoked cannabis [90] in marijuana smokers. These results suggest that endogenous opioids contribute to the effects of cannabis.\nIn 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 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