Relationship between NaCl rewarded bar-pressing and duration of sodium deficiency

McCutcheon, Bruce; Levy, Carolyn J.

doi:10.1016/0031-9384(72)90108-4

Cited by 17 publications

(7 citation statements)

References 7 publications

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“…The conclusion reached by Breslin et al (1993) appears most tenable: The hedonic valence of NaCl is altered-it doesn't taste different, it tastes better. The alteration in the hedonic, reinforcing qualities of NaCl is also consistent with behavioral experiments in which lever pressing, rather than lick rate, is measured (Quartermain et al 1967;Krieckhaus and Wolf 1968;McCutcheon and Levy 1972;Clark and Bernstein 2006;Starr and Rowland 2006), and those in which oromotor behaviors ("taste reactivity"), considered by some researchers to reflect hedonic evaluation, are measured (Berridge et al 1984;Na et al 2012). Finally, this idea is consistent with the effect of sodium depletion on central reward circuits (Clark and Bernstein 2004;Tindell et al 2006;Na et al 2012).…”

Section: Discussionsupporting

confidence: 77%

The Perceptual Characteristics of Sodium Chloride to Sodium-Depleted Rats

John

2016

CHEMSE

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Three experiments assessed potential changes in the rat's perception of sodium chloride (NaCl) during a state of sodium appetite. In Experiment 1, sodium-sufficient rats licking a range of NaCl concentrations (0.028-0.89 M) in 15 s trials showed an inverted U-shaped concentration response function peaking at 0.281 M. Depleted rats (furosemide) showed an identical function, merely elevated, suggesting altered qualitative or hedonic perception but no change in perceived intensity. In Experiment 2, sodium-depleted rats were tested with NaCl, sodium gluconate, and potassium chloride (KCl; 0.028-0.89 M) similar to Experiment 1. KCl was licked at the same rate as water except for a slight elevation at 0.158; sodium gluconate and NaCl were treated similarly, but rats showed more licking for hypertonic sodium gluconate than hypertonic NaCl. Sodium-depleted rats were also tested with NaCl mixed in amiloride (10-300 μM). Amiloride reduced licking but did not alter the shape of the concentration-response function. Collectively, these results suggest that transduction of sodium by epithelial sodium channels (which are blocked by amiloride and are more dominant in sodium gluconate than NaCl transduction) is crucial for the perception of sodium during physiological sodium depletion. In Experiment 3, sodium-deplete rats were tested with NaCl as in Experiment 1 but after taste aversion conditioning to 0.3 M NaCl or sucrose. Rats conditioned to avoid NaCl but not sucrose failed to express a sodium appetite, strongly suggesting that NaCl does not undergo a change in taste quality during sodium appetite-rats show no confusion between sucrose and NaCl in this paradigm.

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Section: Discussionsupporting

confidence: 77%

The Perceptual Characteristics of Sodium Chloride to Sodium-Depleted Rats

John

2016

CHEMSE

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“…Sodium appetite is a highly motivated behavioural state. Sodium‐deprived rats will perform increased amounts of work (bar pressing) for a salty reward (Wagman, 1963; Quartermain et al 1967; McCutcheon & Levy, 1972). They will also sprint significantly faster down a runway leading to a tube of saline when they are salt‐hungry (Zhang et al 1984; Schulkin et al 1985).…”

Section: What Is Sodium Appetite and Why Is It Important?mentioning

confidence: 99%

“…However, changes in gustatory processing alone cannot explain the motivated salt‐seeking behaviour exhibited during sodium deficiency. For example, sodium‐deficient animals will trek extended distances to locate and ingest salt (Blair‐West et al 1968; Denton, 1982) and will perform increased amounts of work to obtain it (Wagman, 1963; Quartermain et al 1967; McCutcheon & Levy, 1972). Such motivational changes are more likely to be driven by sites in the forebrain that integrate multiple signals associated with sodium homeostasis.…”

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confidence: 99%

Central regulation of sodium appetite

Geerling

Loewy

2008

Experimental Physiology

238

197

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Sodium appetite, the behavioural drive to ingest salt, is stimulated by prolonged physiological sodium deficiency in many animal species. The same neural mechanisms that are responsible for sodium appetite in laboratory animals may influence human behaviour as well, with particular relevance to the dietary salt intake of patients with diseases such as heart failure, renal failure, liver failure and salt-sensitive hypertension. Since the original experimental work of Curt Richter in the 1930s, much has been learned about the regulation of salt-ingestive behaviour. Here, we review data from physiology, pharmacology, neuroanatomy and neurobehavioural investigations into the stimulatory and inhibitory signals that regulate sodium appetite. A rudimentary framework is proposed for the brain circuits that integrate peripheral information representing the need for sodium with neural signals for the gustatory detection of salt in order to drive a motivated ingestive response. Based on this model, areas of remaining uncertainty are highlighted where future information would allow a more detailed understanding of the neural circuitry responsible for sodium appetite.

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“…The results of the present PR experiment, as well as a few literature reports, are consistent with this perspective. Thus, McCutcheon and Levy (24) found that formalin-treated rats bar pressing in a variable interval 20-s schedule Table 4. Plasma parameters of furosemide-treated rats taken either before (pre) or after (post) satiation in the plasma renin protocol.…”

Section: Discussionmentioning

confidence: 99%

Matching salt intake to physiological need in rats using foraging protocols

Ne¹

2007

Braz J Med Biol Res

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Several studies of the quantitative relationship between sodium need and sodium intake in rats are reviewed. Using acute diuretic treatment 24 h beforehand, intake matches need fairly accurately when intake is spread out in time by using a hypotonic solution of NaCl. In contrast, using a hypertonic solution, intake is typically double the need. Using the same diuretic treatment, although the natriuresis occurs within ~1 h, the appetite appears only slowly over 24 h. Increased plasma levels of aldosterone parallel the increased intake; however, treatment with metyrapone blocks the rise in aldosterone but has no effect on appetite. Satiation of sodium appetite was studied in rats using sodium loss induced by chronic diuretic treatment and daily salt consumption sessions. When a simulated foraging cost was imposed on NaCl access in the form of a progressive ratio lever press task, rats showed satiation for NaCl (break point) after consuming an amount close to their estimated deficit. The chronic diuretic regimen produced hypovolemia and large increases in plasma aldosterone concentration and renin activity. These parameters were reversed to or toward nondepleted control values at the time of behavioral satiation in the progressive ratio protocol. Satiation mechanisms for sodium appetite thus do appear to exist. However, they do not operate quantitatively when concentrated salt is available at no effort, but instead allow overconsumption. There are reasons to believe that such a bias toward overconsumption may have been beneficial over evolutionary time, but such biasing for salt and other commodities is maladaptive in a resource-rich environment.

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Relationship between NaCl rewarded bar-pressing and duration of sodium deficiency

Cited by 17 publications

References 7 publications

The Perceptual Characteristics of Sodium Chloride to Sodium-Depleted Rats

The Perceptual Characteristics of Sodium Chloride to Sodium-Depleted Rats

Central regulation of sodium appetite

Matching salt intake to physiological need in rats using foraging protocols

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