PubMed · 11658102
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
1996. Voluntary euthanasia.. https://pubmed.ncbi.nlm.nih.gov/11658102/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Chronic cocaine administration produces alterations in mu and kappa opioid receptor density as well as striatal and accumbens opioid-regulated adenylyl cyclase activity, suggesting a psychostimulant responsive interaction between opioidergic and dopaminergic systems. Stimulation of G-protein-coupled opioid receptors inhibits adenylyl cyclase production of cyclic AMP. The present study employed in situ [(35)S]GTPgammaS binding to measure opioid receptor-stimulated activation of G-proteins in response to acute and chronic cocaine exposure. Male Fischer rats received acute (1 or 3 days) or chronic (14 days) binge pattern cocaine administration. Three and 14 days of cocaine injections resulted in greater increases in the ability of the mu receptor agonist DAMGO to stimulate [(35)S]GTPgammaS binding in both the core and the shell of the nucleus accumbens, all regions of the caudate putamen and the cingulate cortex compared with saline-matched controls. The greatest increases in DAMGO-stimulated [(35)S]GTPgammaS binding were observed in the dorsal areas of the caudate putamen in animals that received 14 days of cocaine. No significant changes in delta (DPDPE), or kappa (dynorphin A(1-17)) receptor-stimulated [(35)S]GTPgammaS binding were found in any brain region in response to cocaine administration. These results demonstrate that binge pattern cocaine administration induce changes in mu but not delta or kappa opioid receptor-mediated G-protein activity. This study provides support for the hypothesis that the addictive properties of both psychostimulants and opiates may share common neurochemical signaling substrates.
In the present study we investigated the development of tolerance to an antinociceptive effect after intrathecal administration of endomorphin-1, endomorphin-2 and morphine in tail-flick and paw pressure tests. We also assessed cross-tolerance between the antinociceptive effects of the two endogenous mu-opioid receptor agonists - endomorphins and morphine. The tolerance developed on day 3 after i.th. injection of both endomorphins, endomorphin-2 (18, 36 nmol), endomorphin-1 (16 nmol). After morphine (30 nmol) the tolerance developed on day 6. Our study described the cross-tolerance between morphine and endomorphin-1, but not endomorphin-2. In comparison with naive rats, morphine had a weaker antinociceptive effect in rats tolerant to endomorphin-1. In contrast, no cross-tolerance was observed after administration of endomorphin-2 in rats tolerant to endomorphin-1. In rats tolerant to endomorphin-2, the antinociceptive effect of morphine and endomorphin-1 was attenuated in both the tests used. Our results suggest that the three ligands of mu-opioid receptors probably act via different subtypes of the mu-opioid receptor.
Morphine is frequently used for cancer patient's terminal medical care to relieve cancer pain. In the present study, we examined the inhibitory effect of morphine on experimental lung metastasis and invasion of colon 26-L5 cells. Morphine was found to significantly reduce the number of tumor colonies and the weight of the tumor-containing lung. Morphine inhibited the adhesion and migration of colon 26-L5 cells to extracellular matrix components and invasion into reconstituted basement membrane Matrigel, without affecting the cell proliferation in vitro. Notably, naloxone, an antagonist of morphine, abrogated morphine-induced inhibition of tumor cell adhesion, but did not affect the inhibitory effect on the production of matrix metalloproteinases (MMPs) from tumor cells. These results suggest that morphine inhibited the adhesive and invasive properties of tumor cells by different inhibitory mechanisms that involved the mediation of an opioid receptor.