Inhibition of aldosterone turn-off phenomenon following chronic adrenocorticotropin treatment with in vivo administration of antiglucocorticoid and antioxidants in rats

Ni, Huiping; Mune, Tomoatsu; Morita, Hiroyuki; Daidoh, Hisashi; Hanafusa, Junko; Shibata, Toshiroh; Yamakita, Noriyoshi

doi:10.1530/eje.0.1330578

Cited by 11 publications

(5 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…30 minutes prior to each CSD session and lasted for whole CSD regimen. All The doses of these compounds are chosen on the basis of previous reports (Ratka et al, , Ni et al, , Haller et al, , Macunluoglu et al, ) and our preliminary experiments. All these compounds were purchased from Sigma‐Aldrich (St. Louis, MO).…”

Section: Methodsmentioning

confidence: 99%

Effects of chronic social defeat on expression of dopamine β‐hydroxylase in rat brains

Fan

Chen

Liu

et al. 2013

Synapse

View full text Add to dashboard Cite

It is documented that stress activates the locus coeruleus-norepinephrine system. However, there are far few reports regarding effects of stress on the expression of dopamine β-hydroxylase, a hallmark enzyme of the noradrenergic neuron. In the present study, adult Fischer 344 rats were subjected to chronic social defeat for 4 weeks. Dopamine β-hydroxylase expressional levels in the locus coeruleus and its terminal regions were measured by in situ hybridization and western blotting. The results showed that immediately following chronic social defeat there are significantly increased mRNA and protein levels of dopamine β-hydroxylase in the locus coeruleus, and dopamine β-hydroxylase protein levels in the hippocampus, frontal cortex and amygdala, compared with those in the control. This chronic social defeat-induced upregulation of dopamine β-hydroxylase was completely abolished by adrenalectomy, and/or by treatment with corticosteroid receptor antagonists, mifepristone and spironolactone, either alone or in combination. Furthermore, treatment with desipramine, an antidepressant with specific inhibitory effects on norepinephrine transport, prevented an increased dopamine β-hydroxylase expression by chronic social defeat in the locus coeruleus and its main terminal regions such as the hippocampus, frontal cortex and amygdala. However, treatment with fluoxetine, an antidepressant with specific inhibition for serotonin transport, only selectively blocked increased dopamine β-hydroxylase protein levels in the hippocampus caused by CSD. The present findings indicate that chronic social defeat activates the locus coeruleus-norepinephrine system by upregulating the expression of dopamine β-hydroxylase, which may increase norepinephrine synthesis. This chronic social defeat induced upregulation of DBH expression was mediated through corticosterone and corticosteroid receptors, with possible interference from antidepressants.

show abstract

Section: Methodsmentioning

confidence: 99%

Effects of chronic social defeat on expression of dopamine β‐hydroxylase in rat brains

Fan

Chen

Liu

et al. 2013

Synapse

View full text Add to dashboard Cite

show abstract

“…Therefore, some groups of rats were treated with mifepristone (10 mg/kg, daily, s.c.) or spironolactone (15 mg/kg, daily, s.c.), either alone or in combination. The doses of these antagonists are chosen on the basis of previous reports (Haller et al, 1998; Macunluoglu et al, 2008; Ni et al, 1995; Ratka et al, 1989) and our preliminary experiments. All these compounds were purchased from Sigma-Aldrich (St. Louis, MO, USA).…”

Section: Methodsmentioning

confidence: 99%

Chronic social defeat up-regulates expression of norepinephrine transporter in rat brains

Chen

Fan

Liu

et al. 2012

Neurochemistry International

View full text Add to dashboard Cite

Stress has been reported to activate the locus coeruleus (LC)–noradrenergic system. However, the molecular link between chronic stress and noradrenergic neurons remains to be elucidated. In the present study adult Fischer 344 rats were subjected to a regimen of chronic social defeat (CSD) for 4 weeks. Measurements by in situ hybridization and Western blotting showed that CSD significantly increased mRNA and protein levels of the norepinephrine transporter (NET) in the LC region and NET protein levels in the hippocampus, frontal cortex and amygdala. CSD-induced increases in NET expression were abolished by adrenalectomy or treatment with corticosteroid receptor antagonists, suggesting the involvement of corticosterone and corticosteroid receptors in this upregulation. Furthermore, protein levels of protein kinase A (PKA), protein kinase C (PKC), and phosphorylated cAMP-response element binding (pCREB) protein were significantly reduced in the LC and its terminal regions by the CSD paradigm. Similarly, these reduced protein levels caused by CSD were prevented by adrenalectomy. However, effects of corticosteroid receptor antagonists on CSD-induced down-regulation of PKA, PKC, and pCREB proteins were not consistent. While mifeprestone and spironolactone, either alone or in combination, totally abrogate CSD effects on these protein levels of PKA, PKC and pCREB in the LC and those in the hippocampus, frontal cortex and amygdala, their effects on PKA and PKC in the hippocampus, frontal cortex and amygdala were region-dependent. The present findings indicate a correlation between chronic stress and activation of the noradrenergic system. This correlation and CSD-induced alteration in signal transduction molecules may account for their critical effects on the development of symptoms of major depression.

show abstract

“…Chronically, on the other hand, ACTH does not support the glomerulosa cell phenotype, but instead downregulates CYP11B2, induces CYP11B1, and in these and other ways imposes the fasciculata phenotype instead (Aguilera et al, 1981 ; Ho and Vinson, 1993 ; Ni et al, 1995 ; Mitani et al, 1996 ). Though aldosterone secretion is also sensitive to ACTH stimulation (Hattangady et al, 2012 ), MC2R inactivated mice have normal glomerulosa, but greatly involuted fasciculata (Chida et al, 2007 ), whereas POMC knock-out may disrupt the adrenal entirely (see below).…”

Section: Regulation Of Adrenocortical Zonationmentioning

confidence: 99%

Functional Zonation of the Adult Mammalian Adrenal Cortex

Vinson

2016

Front. Neurosci.

View full text Add to dashboard Cite

The standard model of adrenocortical zonation holds that the three main zones, glomerulosa, fasciculata, and reticularis each have a distinct function, producing mineralocorticoids (in fact just aldosterone), glucocorticoids, and androgens respectively. Moreover, each zone has its specific mechanism of regulation, though ACTH has actions throughout. Finally, the cells of the cortex originate from a stem cell population in the outer cortex or capsule, and migrate centripetally, changing their phenotype as they progress through the zones. Recent progress in understanding the development of the gland and the distribution of steroidogenic enzymes, trophic hormone receptors, and other factors suggests that this model needs refinement. Firstly, proliferation can take place throughout the gland, and although the stem cells are certainly located in the periphery, zonal replenishment can take place within zones. Perhaps more importantly, neither the distribution of enzymes nor receptors suggest that the individual zones are necessarily autonomous in their production of steroid. This is particularly true of the glomerulosa, which does not seem to have the full suite of enzymes required for aldosterone biosynthesis. Nor, in the rat anyway, does it express MC2R to account for the response of aldosterone to ACTH. It is known that in development, recruitment of stem cells is stimulated by signals from within the glomerulosa. Furthermore, throughout the cortex local regulatory factors, including cytokines, catecholamines and the tissue renin-angiotensin system, modify and refine the effects of the systemic trophic factors. In these and other ways it more and more appears that the functions of the gland should be viewed as an integrated whole, greater than the sum of its component parts.

show abstract

Inhibition of aldosterone turn-off phenomenon following chronic adrenocorticotropin treatment with in vivo administration of antiglucocorticoid and antioxidants in rats

Cited by 11 publications

References 22 publications

Effects of chronic social defeat on expression of dopamine β‐hydroxylase in rat brains

Effects of chronic social defeat on expression of dopamine β‐hydroxylase in rat brains

Chronic social defeat up-regulates expression of norepinephrine transporter in rat brains

Functional Zonation of the Adult Mammalian Adrenal Cortex

Contact Info

Product

Resources

About