Nongenomic effects of steroids

What's more, activating the aggression system turns on the adrenocortical stress response without actual fighting--or even someone to fight. A hypothetical picture emerges: First, as has long been known, a signal from the nervous system (via pituitary hormone ACTH) signals the adrenals to produce a corticosteroid response that prepares the body for an emergency response, popularly called "fight or flight." Second, in this new finding, the same corticosteroid signal also feeds back to the brain, which lowers attack thresholds and facilitates fighting. Fighting, itself a stressor, then further activates the stress response. And so it goes.

The effects of glucocorticoids are mediated by cytosolic glucocorticoid receptors and result from both genomic and nongenomic mechanisms that also have a role in the therapeutic effects of these agents [ 1-3 ]. The AEs appear to result largely from transactivation that leads to increased expression of regulatory and antiinflammatory proteins [ 2 ]; by contrast, many of the clinically desirable effects appear to result primarily from transrepression, which results in the decreased production of proinflammatory proteins. Nongenomic effects of glucocorticoids include rapid, nonspecific interactions of glucocorticoids with cellular membranes, nongenomic effects medicated by cytosolic glucocorticoid receptors, and specific interactions with membrane-bound glucocorticoid receptors [ 2 ].

Reproductive and Perinatal Effects
Basic science research outstrips clinical research in the complex area of the role endocannabinoids play in all aspects of human reproduction and the impact of exogenous cannabinoids (., the THC and other cannabinoid compounds in marijuana) on reproductive physiology. Animal studies have demonstrated the existence of CB1 receptors, endogenous cannabinoid ligands and the degradation by fatty acid amide hydrolase (FAAH) in sperm, eggs, and preimplantation embryos (Schuel 2006). Studies have found a critical balance between anandamide synthesis and its degradation by FAAH in mouse embryos and oviducts necessary for normal embryo development, oviductal transport, implantation and pregnancy (Wang, Guo et al. 2004; Wang, Xie et al. 2006). As a result, marijuana and THC have been shown in animal models to effect multiple aspects of reproductive physiology, including secretion of gonadotrphic hormones by the pituitary and sex steroids by the gonands, sperm production and capacitation, ovulation, fertilization, early embryonic devepoment, implantation, placental functions, fetal growth, number of pregnancies carried to term, lactation, suckling behavior by newborns and growth of malignant breast and prostate cells (Schuel 2006). The clinical implications of these basic science findings for human reproduction remains unclear despite the fact that animal studies show that exogenous THC can swamp endogenous anadamide signaling systems, thereby affecting multiple physiological processes.

Nongenomic effects of steroids

nongenomic effects of steroids


nongenomic effects of steroidsnongenomic effects of steroidsnongenomic effects of steroidsnongenomic effects of steroidsnongenomic effects of steroids