PubMed · 8822643
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S K Jindal, D Gupta. Inhalation therapy.. https://pubmed.ncbi.nlm.nih.gov/8822643/
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The goal of this study was to examine the relationship between the presence of subclinical depressive symptoms and physiological and subjective responses to smoked cocaine in humans. Cocaine users without major depression, who participated in various inpatient studies, received a single 0.4 mg/kg of smoked cocaine. When the relationship between the Beck Depression Inventory (BDI) scores and various subjective and physiological responses to cocaine was examined, similar trends were found. Low BDI scores of 0-7 were associated with a smaller physiological and subjective cocaine response. In contrast, BDI ranges of 8-13 were associated with enhanced cocaine response which plateaued or declined in the higher (> 14) BDI group. These group differences were not explained by sex or body weight differences among groups. The implication of these results is that the presence of depressive symptoms may affect cocaine use behavior partly by being associated with an enhanced response to cocaine.
Although the majority of cannabinoid users smoke marijuana, the preponderance of laboratory animal research is based on administration of Delta9-tetrahydrocannabinol (Delta9-THC) or other cannabinoid agents via injection. The aim of the present study was to evaluate the impact of inhaling marijuana, or ethanol-extracted placebo smoke in the mouse model of cannabinoid activity by assessing inhibition of spontaneous activity, antinociception, catalepsy, and body temperature. In order to determine dosimetry, blood levels of Delta9-THC were obtained following either marijuana exposure or intravenous injection of Delta(9)-THC. Inhalation exposure to marijuana produced dose-related increases in antinociception and catalepsy, with estimated ED50 doses of Delta9-THC of 2.4 and 3.8 mg/kg, respectively. However, hypothermia and locomotor depression occurred in both the placebo- and marijuana-exposed mice. The CB1 receptor antagonist, SR 141716A antagonized the antinociceptive effects of marijuana (AD50 = 0.6 mg/kg), but only slightly decreased marijuana-induced catalepsy, and failed to alter either the hypothermic or locomotor depressive effects. In contrast, SR 141716A antagonized the antinociceptive, cataleptic, and hypothermic effects of intravenously administered Delta9-THC in mice that were exposed to air alone, though all subjects exhibited locomotor depression, possibly related to the restraint. In accordance with reports of others, these data suggest that exposure to smoke alone has pharmacological consequences. Our findings also indicate that marijuana-induced antinociception is mediated through a CB1-receptor mechanism of action and are consistent with the notion that Delta9-THC is mainly responsible for this effect.