Effect of acute adrenalectomy on rat liver glucocorticoid receptor

Isenović, Esma R.; Radojčić, Marija B.; Žakula, Zorica; Korićanac, Goran; Ribarac-Stepic, Nevena

doi:10.2298/abs0603153i

Cited by 3 publications

(2 citation statements)

References 24 publications

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“…Upregulated GR expression could be a protective response to hypocortisolemia, as some degree of GR activity may be critical for survival ( Cole et al, 1995 ), and the initial hypocortisolemia could result from stress-induced synaptic plasticity that promotes CRH cell suppression. Indeed, GR expression generally increases following adrenalectomy ( Olpe and McEwen, 1976 ; Svec et al, 1989 ; Isenovic et al, 2006 ).…”

Section: Perspectives and Outlookmentioning

confidence: 99%

Synaptic regulation of the hypothalamic–pituitary–adrenal axis and its modulation by glucocorticoids and stress

Levy¹,

Tasker²

2012

Front. Cell. Neurosci.

118

104

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Dysregulation of the hypothalamic–pituitary–adrenal (HPA) axis has been implicated in a range of affective and stress-related disorders. The regulatory systems that control HPA activity are subject to modulation by environmental influences, and stressful life events or circumstances can promote subsequent HPA dysregulation. The brain is a major regulator of the HPA axis, and stress-induced plasticity of the neural circuitry involved in HPA regulation might constitute an etiological link between stress and the development of HPA dysregulation. This review focuses on the synaptic regulation of neuroendocrine corticotropin-releasing hormone (CRH) neurons of the hypothalamic paraventricular nucleus, which are the cells through which the brain predominantly exerts its influence on the HPA axis. CRH neuronal activity is largely orchestrated by three neurotransmitters: GABA, glutamate, and norepinephrine. We discuss our current understanding of the neural circuitry through which these neurotransmitters regulate CRH cell activity, as well as the plastic changes in this circuitry induced by acute and chronic stress and the resultant changes in HPA function.

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Section: Perspectives and Outlookmentioning

confidence: 99%

Synaptic regulation of the hypothalamic–pituitary–adrenal axis and its modulation by glucocorticoids and stress

Levy¹,

Tasker²

2012

Front. Cell. Neurosci.

118

104

View full text Add to dashboard Cite

show abstract

“…One of these forms can be extracted with salt (0. , 2006a;Isenović et al, 2006b;Žakulaet al, 2005). The function of either cytoplasmatic or nuclear receptor association with the matrix is still unresolved, and the physiological significance of these cytoplasmic and nuclear estrogen binding sites remains speculative, although it is apparent from published studies that levels of nuclear binding sites in the rat uterus are increased by the hormone, i.e., after E2 administration (M a r k a v e r i c h and C l a r c, 1979; H a l a c h m i et H t u n et al, 1999;Andersonet al, 1975).…”

Section: Introductionmentioning

confidence: 99%

Estrogen-induced modification of uterine RNA polymerase activity depends on localization of the estrogen receptor

Žakula¹,

Isenović²,

Stojiljković³

et al. 2007

ARCH BIOL SCI BELGRA

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The aim of this study was to examine the effects of estradiol (E2) on activity of RNA polymerase I and RNA polymerase II in uterine nuclei of ovariectomized (OVX) female rats. The obtained results show that estrogen-receptor (E-R) complexes in 30 min induced an increase of polymerase II activity. A second increase of polymerase II activity was observed after 3 h-incubation of nuclei with the E-R complex formed in the cytosol fraction. However, activity of polymerase I was increased 2 h after the start of incubation, with highest activity detected at 3 h in nuclei incubated with E-R complexes. On the contrary, no stimulatory effect on either polymerase I or polymerase II activity was observed in nuclei incubated with E2 alone. These results indicate that E2 stimulates the cytosolic estrogen receptor (ER), which in turn causes uterotrophic responses in OVX rats. In addition, they suggest that in order to provoke uterotrophic responses E-R complexes formed in the cytosol need to be retained in the nucleus for a longer period of time.

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Comparative analysis of tryptophan oxygenase activity and glucocorticoid receptor under the influence of insulin

Er¹,

Žakula²,

Korićanac³

et al. 2008

Physiol Res

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This investigation addresses the interaction of insulin (INS) and glucocorticoid (GC) signaling in the hepatic regulation of tryptophan oxygenase (TO) enzyme activity in the rat. Male Wistar rats (200-250 g b.w) received an injection of the different doses of INS (10, 25, 50, 70 and 100 μg/200 g b.w., i.p.) and were used for experiments 3 h and 18 h after INS administration. This study shows that maximum of TO activity was found at dose of 50 μg of INS with peak increases observed at 3 h and 18 h after injection of INS, while INS had no effect on TO activity in adrenalectomized rats. The analysis of INS effects on glucocorticoid receptor-complex (GC/GR complex) stability shows that complexes from INS-treated rats are less stable than those from control animals. In addition, INS-stimulated stability of glucocorticoid receptor (GR) protein was significantly increased from the controls. Furthermore, the results show that GC/GR complexes from INS-treated rats could be activated and accumulated at higher rate in cell nuclei of control animals. These data support the involvement of INS in modulation of GC signaling pathway which mediates, in part, the activity of TO.

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Effect of acute adrenalectomy on rat liver glucocorticoid receptor

Cited by 3 publications

References 24 publications

Synaptic regulation of the hypothalamic–pituitary–adrenal axis and its modulation by glucocorticoids and stress

Synaptic regulation of the hypothalamic–pituitary–adrenal axis and its modulation by glucocorticoids and stress

Estrogen-induced modification of uterine RNA polymerase activity depends on localization of the estrogen receptor

Comparative analysis of tryptophan oxygenase activity and glucocorticoid receptor under the influence of insulin

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