Effect of adrenocorticotrophic hormone on sodium appetite in mice

Denton, Derek A.; Blair‐West, J. R.; McBurnie, M.; Miller, Julie Ann; Weisinger, R. S.; Williams, Robert

doi:10.1152/ajpregu.1999.277.4.r1033

Cited by 23 publications

(30 citation statements)

References 22 publications

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“…In experimental animals, the development and maintenance of salt appetite is hormonally regulated. Indeed, hypersecretion of endogenous adrenal steroids caused by ACTH administration or stress [1, 2, 3]or high doses of exogenous mineralocorticoids have been shown to stimulate drinking of concentrated NaCl solutions [4, 5]. The role played by the classical mineralocorticoid receptor (MR), the interaction of steroids with vasoactive peptides and enzymes and the neuroanatomical circuitry responsible for this behavior are the subject of continuing investigations in relation to mineralocorticoid-induced salt appetite [6, 7, 8, 9, 10, 11, 12, 13].…”

Section: Introductionmentioning

confidence: 99%

Changes in Fos Expression in Various Brain Regions during Deoxycorticosterone Acetate Treatment: Relation to Salt Appetite, Vasopressin mRNA and the Mineralocorticoid Receptor

Pietranera

Saravia²,

McEwen³

et al. 2001

Neuroendocrinology

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Salt appetite, a conditioning factor for hypertension and cardiovascular diseases, is produced when high doses of mineralocorticoids are given to experimental animals. A commonly used procedure to identify neuronal activation is to determine the number of Fos-immunoreactive cells. In rats with established salt appetite after 8 days of deoxycorticosterone acetate (DOCA) treatment, Fos-positive cells were studied in seven brain areas. Significant increases in Fos activity were recorded in the paraventricular (PVN) and supraoptic (SON) nuclei, median preoptic nucleus (MnPO), organum vasculosum of the lamina terminalis (OVLT), preoptic area (POA), bed nucleus of the stria terminalis (BNST) and amygdala (AMYG). In most of these areas, increased Fos expression was also observed early (2 h) after a single DOCA injection, well before salt appetite develops. Using a mineralocorticoid receptor (MR) antibody, we studied whether Fos-active regions also expressed MR. MR-positive cells were found in the OVLT, MnPO, AMYG and BNST, but not in the POA, PVN and SON. In the PVN and SON, nevertheless, prolonged or single DOCA treatment increased expression of mRNA for arginine vasopressin (AVP). The present demonstration of Fos activation, in conjunction with differential expression of MR and stimulation of AVP mRNA, suggests that a neuroanatomical pathway comprising the AMYG, osmosensitive brain regions and magnocellular nuclei becomes activated during DOCA effects on salt appetite. It is recognized, however, that DOCA effects may also depend on mechanisms and brain structures other than those considered in the present investigation. Since some Fos-positive regions were devoid of MR, a comprehensive view of DOCA-induced salt appetite should consider nongenomic pathways of steroid action, including the role of reduced DOC metabolites binding to GABAergic membrane receptors.

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Section: Introductionmentioning

confidence: 99%

Changes in Fos Expression in Various Brain Regions during Deoxycorticosterone Acetate Treatment: Relation to Salt Appetite, Vasopressin mRNA and the Mineralocorticoid Receptor

Pietranera

Saravia²,

McEwen³

et al. 2001

Neuroendocrinology

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“…A direct stimulatory action of ovine CRF on Na intake of rabbits (20) and mice (9) has been reported. Thus far, however, an action of urocortin on Na intake has not been reported.…”

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confidence: 99%

“…Stress can cause an increase in Na intake (6)(7)(8)(9) and, in some instances, a decrease in food intake (10,11). Corticotropin-releasing factor (CRF), a 41-aa peptide originally isolated from the ovine hypothalamus (12), is one factor involved in the initiation of the various behavioral and physiological responses to stress (1,2,4,5).…”

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confidence: 99%

The inhibitory effect of hormones associated with stress on Na appetite of sheep

Weisinger

Blair‐West

Burns

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

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Stress is a large stimulus of Na appetite in rabbits, rats, and mice. This study investigated the influence of some peptides implicated in stress, i.e., adrenocorticotropin (ACTH), corticotropin-releasing factor (CRF), and the recently discovered member of the CRF family, urocortin, on the ingestive behavior of sheep. Intracerebroventricular infusion of these peptides over 4 days decreased the need-free Na intake of Na-repleted sheep. Intracerebroventricular infusion of urocortin, however, did not alter Na intake of Na-depleted sheep. Systemic infusion of ACTH increased, whereas systemic infusion of either urocortin or CRF decreased, Na intake of Na-repleted sheep. The increase in Na intake caused by the peripheral infusion of ACTH was blocked by concurrent i.v. infusion of urocortin, substantiating the inhibitory role of this peptide on Na appetite. Central administration of all peptides and i.v. administration of urocortin or urocortin and ACTH combined decreased food intake. Water intake was not directly influenced by the peptides. Rather, decreased water intake, when observed, was secondary to decreased food intake, as determined by pair-feeding experiments. Whereas systemic infusion of ACTH mimics the increase in Na intake observed in several different stressful situations, CRF and urocortin actually inhibit Na intake, indicating a direct central action overriding any effect of these peptides on ACTH release. Indeed, the inhibition of Na intake by urocortin occurred despite its stimulation of ACTH release and the subsequent increase in peripheral level of cortisol. Thus it would appear that hormones associated with stress have both excitatory and inhibitory influences on Na intake. Presumably, other physiological processes entrained by stress also will be important in determining the quantitative outcome on Na appetite.

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“…Furthermore, sodium-deficient mice develop an avid, specific sodium appetite. Like other species, mice will rapidly gratify appetite over 10 min if presented with sodium solution (5,11). Chronic administration of ACTH (5, 11) also produces a robust sodium appetite.…”

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confidence: 99%

Relation of addiction genes to hypothalamic gene changes subserving genesis and gratification of a classic instinct, sodium appetite

Liedtke

McKinley

Walker

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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Sodium appetite is an instinct that involves avid specific intention. It is elicited by sodium deficiency, stress-evoked adrenocorticotropic hormone (ACTH), and reproduction. Genome-wide microarrays in sodium-deficient mice or after ACTH infusion showed up-regulation of hypothalamic genes, including dopamine-and cAMP-regulated neuronal phosphoprotein 32 kDa (DARPP-32), dopamine receptors-1 and -2, α-2C-adrenoceptor, and striatally enriched protein tyrosine phosphatase (STEP). Both DARPP-32 and neural plasticity regulator activity-regulated cytoskeleton associated protein (ARC) were upregulated in lateral hypothalamic orexinergic neurons by sodium deficiency. Administration of dopamine D1 (SCH23390) and D2 receptor (raclopride) antagonists reduced gratification of sodium appetite triggered by sodium deficiency. SCH23390 was specific, having no effect on osmotic-induced water drinking, whereas raclopride also reduced water intake. D1 receptor KO mice had normal sodium appetite, indicating compensatory regulation. Appetite was insensitive to SCH23390, confirming the absence of off-target effects. Bilateral microinjection of SCH23390 (100 nM in 200 nL) into rats' lateral hypothalamus greatly reduced sodium appetite. Gene set enrichment analysis in hypothalami of mice with sodium appetite showed significant enrichment of gene sets previously linked to addiction (opiates and cocaine). This finding of concerted gene regulation was attenuated on gratification with perplexingly rapid kinetics of only 10 min, anteceding significant absorption of salt from the gut. Salt appetite and hedonic liking of salt taste have evolved over >100 million y (e.g., being present in Metatheria). Drugs causing pleasure and addiction are comparatively recent and likely reflect usurping of evolutionary ancient systems with high survival value by the gratification of contemporary hedonic indulgences. Our findings outline a molecular logic for instinctive behavior encoded by the brain with possible important translational-medical implications.

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Effect of adrenocorticotrophic hormone on sodium appetite in mice

Cited by 23 publications

References 22 publications

Changes in Fos Expression in Various Brain Regions during Deoxycorticosterone Acetate Treatment: Relation to Salt Appetite, Vasopressin mRNA and the Mineralocorticoid Receptor

Changes in Fos Expression in Various Brain Regions during Deoxycorticosterone Acetate Treatment: Relation to Salt Appetite, Vasopressin mRNA and the Mineralocorticoid Receptor

The inhibitory effect of hormones associated with stress on Na appetite of sheep

Relation of addiction genes to hypothalamic gene changes subserving genesis and gratification of a classic instinct, sodium appetite

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