Sodium deficient rats are unmotivated by sodium chloride solutions mixed with the sodium channel blocker amiloride.

McCutcheon, N. Bruce

doi:10.1037/0735-7044.105.5.764

Cited by 44 publications

(26 citation statements)

References 9 publications

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“…The taste quality of minerals is thought to be determined primarily by their cation [41,42], and rats deprived of sodium and calcium show appetites for multiple compounds that contain whichever cation is needed [2,20,43]. Furthermore, sodium-deprived rats showed a blunted appetite for NaCl when it is mixed with amiloride, which is thought to interfere with the passage of sodium cations into taste receptor cells [44][45][46]. Nevertheless, anions do exert some influence on perceived taste quality in humans [47] and on taste preferences for minerals in rodents.…”

Section: Appetite Specificitymentioning

confidence: 99%

Licking for taste solutions by potassium-deprived rats: Specificity and mechanisms

Guenthner

McCaughey

Tordoff

et al. 2008

Physiology & Behavior

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There has been little work on the specificity and mechanisms underlying the appetite of potassium (K + ) deprived rats, and there are conflicting results. To investigate the contribution of oral factors to changes in intake induced by K + deficiency, we conducted two experiments using 20-s "brief access" tests. In Experiment 1, K + -deprived rats licked less for water than did replete rats. After adjusting for this difference, K + -deprived rats exhibited increased licking for 100 mM CaCl 2 , 100 mM MgCl 2 , and 100 mM FeCl 2 compared with K + -replete rats. In Experiment 2, which used larger rats, the K + -deprived and replete groups licked equally for water, 500 mM Na·Gluconate, 350 mM KCl, 500 mM KHCO 3 , and 1 mM quinine·HCl, but the K + -deprived rats licked more for 500 mM KCl, 500 mM CsCl, and 500 mM NaCl than did the replete rats. Licking was unaffected by addition to NaCl of 200 μM amiloride, an epithelial Na + channel (ENaC) blocker, or 100 μM ruthenium red, a vanilloid receptor 1 (VR-1) antagonist, or by addition to KCl of 50 μM 4-aminopyridine, a K + channel blocker. These findings suggest that K + -deprivation produces a non-specific appetite that is guided by oral factors. We found no evidence that this response was mediated by ENaC, VR-1, or K + channels in taste receptor cells.

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Section: Appetite Specificitymentioning

confidence: 99%

Licking for taste solutions by potassium-deprived rats: Specificity and mechanisms

Guenthner

McCaughey

Tordoff

et al. 2008

Physiology & Behavior

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“…The transduction of sodium involves increasing intracellular Na + by entry of the cation through epithelial type sodium channels (ENac) to depolarize the receptor and a subsequent increase in intracellular Na + and Ca 2+ [90]. Inhibiting the depolarization of sodium taste receptors by blocking sodium channels with amiloride produces a significant impairment of sodium ingestion in depleted rats [91][92][93] and also reduces responsivity to NaCl in sodium replete rats in the CT and GSP nerves [94]. This effect is compounded when combined with a CT transection or a CT plus GSP transection [92,95].…”

Section: Taste and Sodium Appetitementioning

confidence: 99%

Salt craving: The psychobiology of pathogenic sodium intake

Morris

Johnson

2008

Physiology & Behavior

114

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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.

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“…The ability of rats to recognize the taste of sodium when in a sodium-depleted state appears to depend on taste receptor cells in the oral cavity that contain passive ion channels selective for sodium and lithium ions (Bernstein & Hennessy, 1987;McCutcheon, 1991;Roitman & Bernstein, 1999). The sodium-selective ion channels, or epithelial sodium channels (ENaCs), expressed by these cells can be blocked with the drug amiloride (see Brand, Teeter, & Silver, 1985;DeSimone & Ferrell, 1985;Doolin & Gilbertson, 1993;Heck, Mierson, & DeSimone, 1984;Schiffman, Lockhead, & Maes, 1983).…”

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confidence: 99%

Anion Size Does Not Compromise Sodium Recognition by Rats After Acute Sodium Depletion.

Geran¹,

Spector²

2004

Behavioral Neuroscience

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Amiloride-insensitive sodium taste transduction is severely limited by large anions (i.e., gluconate). We found that in a brief-access taste test, sodium-depleted rats exhibited similar levels of increased licking to several sodium salts regardless of anion but did not increase licking to nonsodium salts compared with water. The enhanced licking of sodium salts was abolished in the presence of amiloride. These results suggest that the amiloride-sensitive taste transduction pathway is not only necessary but that it is also sufficient for sodium identification in rats. Sodium-depleted rats tested with amiloride initiated significantly more trials than nondepleted rats; hence, appetitive behavior was mildly potentiated by depletion, even in the absence of a sodium taste cue. Overall, these findings provide compelling support for the primacy of the amiloride-sensitive taste transduction mechanism and its associated neural pathway in the recognition of the sodium cation.

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Sodium deficient rats are unmotivated by sodium chloride solutions mixed with the sodium channel blocker amiloride.

Cited by 44 publications

References 9 publications

Licking for taste solutions by potassium-deprived rats: Specificity and mechanisms

Licking for taste solutions by potassium-deprived rats: Specificity and mechanisms

Salt craving: The psychobiology of pathogenic sodium intake

Anion Size Does Not Compromise Sodium Recognition by Rats After Acute Sodium Depletion.

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