Regular ArticleTumor Suppressor p53 Induction and DNA Damage in Hippocampal Granule Cells after Adrenalectomy
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NMDA receptor antagonist prevents cell death in the hippocampal dentate gyrus induced by hyponatremia accompanying adrenal insufficiency in rats
2017, Experimental NeurologyCitation Excerpt :One of the reasons for the lack of such studies is the lack of appropriate animal models of adrenal insufficiency accompanied by relatively chronic hyponatremia. Although many studies on cell degradation or apoptosis in the hippocampus following bilateral adrenalectomy (ADX) have been reported (Cameron and Gould, 1996; Gould et al., 1990; Hu et al., 1997; Jaarsma et al., 1992; Krugers et al., 1994; Schreiber et al., 1994; Sloviter et al., 1993a; Sloviter et al., 1993b; Sloviter et al., 1989), animals in those studies were given saline after ADX to avoid decreases in serum [Na+] and death; in those previous studies; adrenalectomized rats without saline administration died several days after ADX. Sloviter et al. reported the selective loss of granule cells in the hippocampal DG of rats that were given free access to food and saline solution for three or four months after ADX (Sloviter et al., 1989).
The neuronal mineralocorticoid receptor: From cell survival to neurogenesis
2014, SteroidsCitation Excerpt :Decades ago, it has been reported that in rats, 3 days after adrenalectomy when plasma corticosterone was undetectable, the granule cells of the dentate gyrus in the hippocampus exhibited many signs of apoptosis [69]. Later on, it was established that this phenomenon was linked to the increase of p53 expression, a major cell cycle regulator but was reversed by a daily corticosterone administration [70]. Conversely, long-lasting high levels of glucocorticoids such as found under stress, lead to neuronal loss often associated with increased deleterious effects of neurotoxic molecules such as NMDA and kainic acid [71,72].
Glucocorticoid signaling and exercise-induced downregulation of the mineralocorticoid receptor in the induction of adult mouse dentate neurogenesis by treadmill running
2008, PsychoneuroendocrinologyCitation Excerpt :Furthermore, reduction of GCs by adrenalectomy (ADX) or inhibition of the hypothalamus-pituitary-adrenal (HPA) axis has been shown to promote neurogenesis (Gould et al., 1992; Cameron and Gould, 1994; Cameron and McKay, 1999). However, it has also been reported that lack of GCs enhances neuronal apoptosis (Sloviter et al., 1989; Schreiber et al., 1994) and that slight elevation of serum GC concentrations lead to neuroprotection from excitotoxic insults (Abraham et al., 1997), suggesting that GCs play a biphasic role in neural development. These observations led to a “narrow concentration-window hypothesis of GCs” that fine tuning of GC action is essential for neural development, particularly for the control of cellular differentiation and the maintenance of neural integrity and function in adult brain (Abraham et al., 2001).
Neuronal actions of glucocorticoids: Focus on depression
2008, Journal of Steroid Biochemistry and Molecular BiologyGlucocorticoid regulation of glial responses during hippocampal neurodegeneration and regeneration
2005, Brain Research ReviewsCitation Excerpt :However, sometimes, increased p53 expression can result in apoptosis by increasing Bax and caspases (reviewed in [50]). We previously found that p53 mRNA was increased 5-fold in cells after adrenalectomy [116]. Sakhi et al. [107] showed that the number of dying cells was decreased by 75% in heterozygous and homozygous p53 knockout mice after adrenalectomy, indicating that p53 was involved in the apoptotic pathway.
Involvement of DNA damage and repair systems in neurodegenerative process
2003, Toxicology Letters