1986
DOI: 10.1016/0378-8741(86)90126-1
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Effects of acute and subchronic Delta 9-tetrahydrocannabinol administration on the plasma catecholamine, beta-endorphin, and corticosterone levels and splenic natural killer cell activity in rats

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Cited by 5 publications
(4 citation statements)
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“…Systemic injections of delta(9)-tetrahydrocannabinol (THC, the main psychoactive component of marijuana) do not alter HPA activity on its own and subchronic THC seems to decrease HPA activity [192]. This may be due, in part, to peripheral effects, as centrally administered THC (intracerebroventricular injections) leads to a marked increase in plasma ACTH and CORT at multiple doses [193].…”
Section: Preclinical Studies Of Drug Administration and Stress Responmentioning
confidence: 99%
“…Systemic injections of delta(9)-tetrahydrocannabinol (THC, the main psychoactive component of marijuana) do not alter HPA activity on its own and subchronic THC seems to decrease HPA activity [192]. This may be due, in part, to peripheral effects, as centrally administered THC (intracerebroventricular injections) leads to a marked increase in plasma ACTH and CORT at multiple doses [193].…”
Section: Preclinical Studies Of Drug Administration and Stress Responmentioning
confidence: 99%
“…In vitro studies on human NK cells demonstrated that cannabinoids can inhibit the constitutive expression of chemokines, IL-8, MIP1-α, MIP-1β, RANTES, phorbol ester stimulated TNF-α, GM-CSF and IFN-gamma. Studies have demonstrated that cannabinoids can suppress NK cell function such as cytolytic activity in rats, mice and humans, which is a cannabinoid receptor-dependent process [7577]. …”
Section: Natural Killer Cells and Neutrophilsmentioning
confidence: 99%
“…Another plausible modality for removing NK inhibitory signals in vivo may be via the modulation of endocannabinoid signaling. Clues for the involvement of endocannabinoids in cancer propagation are evident: the selective inhibition of NK cells by delta-9-tetrahydrocannabinol and marijuana was documented already in the 1980 s [Patel et al, 1985;Specter et al, 1986Specter et al, , 1989Kawakami et al, 1988]. A more recent clue for the anti-cancer potential of augmenting endocannabinoid signaling comes from a demonstration that NK migration is stimulated by the endocannabinoids 2-arachidonoylglycerol, an effect that was blocked by delta-9-tetrahydrocannabinol [Kishimoto et al, 2005].…”
Section: An Endocannabinoid Connection?mentioning
confidence: 95%