Reduced hedonic behavior and altered cardiovascular function induced by mild sodium depletion in rats.

Grippo, Angela J.; Moffitt, Julia A.; Beltz, Terry G.; Johnson, Alan Kim

doi:10.1037/0735-7044.120.5.1133

Cited by 31 publications

(37 citation statements)

References 59 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In rats, hedonic behaviors, such as sucrose ingestion and rewarding self-brain stimulation, are blunted by sodium depletion or chronic mineralocorticoid administration (77,124). Humans, similarly, report pronounced gustatory anhedonia during chronic sodium deprivation (119).…”

Section: Neurons Forming a Small Subpopulation Of The Nts Are Aldostementioning

confidence: 98%

Aldosterone in the brain

Geerling¹,

Loewy²

2009

American Journal of Physiology-Renal Physiology

160

151

View full text Add to dashboard Cite

Pharmacological and physiological phenomena suggest that cells somewhere inside the central nervous system are responsive to aldosterone. Here, we present the fundamental physiological limitations for aldosterone action in the brain, including its limited blood-brain barrier penetration and its substantial competition from glucocorticoids. Recently, a small group of neurons with unusual sensitivity to circulating aldosterone were identified in the nucleus of the solitary tract. We review the discovery and characterization of these neurons, which express the enzyme 11beta-hydroxysteroid dehydrogenase type 2, and consider alternative proposals regarding sites and mechanisms for mineralocorticoid action within the brain.

show abstract

Section: Neurons Forming a Small Subpopulation Of The Nts Are Aldostementioning

confidence: 98%

Aldosterone in the brain

Geerling¹,

Loewy²

2009

American Journal of Physiology-Renal Physiology

160

151

View full text Add to dashboard Cite

show abstract

“…The sodium recovery value was not significantly different from either the baseline value or the sodium depletion value. (Reprinted from [19] with permission. )…”

Section: Discussionmentioning

confidence: 99%

“…Our laboratory has recently discovered that two models of sodium appetite induction in rats, DOCA-induced and diuretic-induced sodium appetite, produce decreases in reward sensitivity in animals that are denied saline access [18,19] (Figures 7 & 8). Koob and colleagues have reported analogous findings following withdrawal from cocaine, morphine, and nicotine in rats [197][198][199].…”

Section: Discussionmentioning

confidence: 99%

“…We have also found that a similar treatment protocol (daily DOCA treatment, 10 mg/kg, for 4 weeks) actually increases voluntary running wheel activity (unpublished observations). A second experiment found that furosemide-induced sodium depletion also produced a decrease in sensitivity to LHSS reward when the animals were denied saline for 48 hours and that the presence of saline or subsequent repletion prevented or reversed, respectively, the rightward shifts in the midpoint (ECu 50 ) of LHSS current-response functions [19] (Figure 8). Sodium depleted rats that were denied access to saline also exhibited decreased heart rate variability compared to rats provided saline.…”

Section: Hedonic and Mood-related Effects Of Sodium Deficiencymentioning

confidence: 99%

See 1 more Smart Citation

Salt craving: The psychobiology of pathogenic sodium intake

Morris

Johnson

2008

Physiology & Behavior

Self Cite

113

View full text Add to dashboard Cite

Ionic sodium, obtained from dietary sources usually in the form of sodium chloride (NaCl, common table salt) is essential to physiological function, and in humans salt is generally regarded as highly palatable. This marriage of pleasant taste and physiological utility might appear fortunate -an appealing taste helps to ensure that such a vital substance is ingested. However, the powerful mechanisms governing sodium retention and sodium balance are unfortunately best adapted for an environment in which few humans still exist. Our physiological and behavioral means for maintaining body sodium and fluid homeostasis evolved in hot climates where sources of dietary sodium were scarce. For many reasons, contemporary diets are high in salt and daily sodium intakes are excessive. High sodium consumption can have pathological consequences. Although there are a number of obstacles to limiting salt ingestion, high sodium intake, like smoking, is a modifiable behavioral risk factor for many cardiovascular diseases. This review discusses the psychobiological mechanisms that promote and maintain excessive dietary sodium intake. Of particular importance are experiencedependent processes including the sensitization of the neural systems underlying sodium appetite and the effects of sodium balance on hedonic state and mood. Accumulating evidence suggests that plasticity within the central nervous system as a result of experience with high salt intake, sodium depletion, or a chronic unresolved sodium appetite fosters enduring changes in sodium related appetitive and consummatory behaviors.

show abstract

“…Patients with a decreased sense of well-being and chronic fatigue responded favorably to ␤-antagonists or mineralocorticoid administration along with increased dietary sodium (41). Furthermore, several animal studies report that reduced body sodium is associated with anhedonia (inability to derive pleasure from normally enjoyable activities), anxiety, decreased physical activity, and abnormal cardiovascular parameters such as increased resting heart rate, reduced heart rate variability, and exaggerated cardiovascular response to stressors (115,118,195).…”

Section: Autonomic Nervous System Activitymentioning

confidence: 99%