Acquisition of sodium by rats: Interaction of innate mechanisms and latent learning.

Krieckhaus, E. E.; Wolf, George

doi:10.1037/h0025547

Cited by 140 publications

(83 citation statements)

References 6 publications

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“…Several other studies have demonstrated an increase in the motivational value of sodium when animals are depleted. Rats treated with furosemide showed enhanced operant responding to gain access to sodium chloride solutions (Krieckhaus and Wolf, 1968;Quartermain et al, 1967;Weisinger et al, 1970). In addition, breakpoint in a progressive ratio task for access to 3% NaCl is increased in rats with a history of sodium depletions (Clark and Bernstein, 2006).…”

Section: Discussionmentioning

confidence: 99%

The neural substrates of enhanced salt appetite after repeated sodium depletions

Morris

Johnson

et al. 2007

Brain Research

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Sodium appetite is associated with a form of behavioral plasticity in which animals experimentally depleted of sodium progressively increase their intake of hypertonic NaCl over several successive (on 2 to 4 occasions) depletion. The present experiment explored the nature of this plasticity by quantifying Fos-immunoreactivity (Fos-ir) in structures implicated in the mediation of sodium appetite and in the signaling of reward. Rats were depleted of sodium with the diuretic furosemide three times (3F), one time (2V1F) or sham depleted (i.e., vehicle treated; 3V). Rats were given sodium appetite tests for the first two treatments. The sodium appetite test was omitted after the third depletion. Fos-ir activity was quantified in the paraventricular nucleus (PVN), subfornical organ (SFO), supraoptic nucleus (SON), nucleus accumbens (NAc) shell and core, basolateral (BLA) and central amygdala (CeA), and medial prefrontal cortex (mPFC). Animals receiving repeated sodium depletions increased sodium ingestion across initial depletions. Fos-ir activity was markedly enhanced in the SFO, BLA, and shell of the NAc of 3F rats relative to 2V1F and 3V animals. These results indicate that repeated experience with sodium depletion and ingestion affect both behavioral and neural responses to sodium. Experience with sodium depletion enhances its ingestion and may have a direct impact on central structures implicated in sodium appetite and reward signaling.

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Section: Discussionmentioning

confidence: 99%

The neural substrates of enhanced salt appetite after repeated sodium depletions

Morris

Johnson

et al. 2007

Brain Research

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“…Indeed, the very behavior touted as the poster child of innate homeostatic regulation, increased salt appetite when plasma sodium is decreased, is superimposed upon an already high basal intake (i.e., a high operant level) of mild sodium solutions relative to pure water, as Richter himself noted (Richter 1939). Further, learning has been found to interact with the initial bout of salt intake in response to an experimentally induced lowering of plasma sodium (Krieckhaus & Wolf 1968;Weisinger et al 1970). The point is that Richter perhaps overzealously viewed behaviors that participate in the control of homeostatic variables as being solely examples of innate regulation.…”

Section: Regulation Vs Control: Body Adiposity Vs Food Intakementioning

confidence: 99%

Homeostasis: Beyond Curt Richter

Woods

Ramsay

2007

Appetite

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Curt Richter introduced behavioral control into the concept of homeostasis, thereby opening entire fields of research. The prevailing dogma, and the techniques he used, conspired to lead Richter and others to interpret regulation in strict negative feedback terms. Although this point of view continues to be embraced by many contemporary biologists, we believe that prevailing sentiment favors a broader view in which organisms integrate anticipatory pre-emptive control over regulated variables whenever possible.

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“…Consequently, we tested whether reducing the contribution of the AI pathway (or pathways) with a large anion affected sodium recognition. Other researchers have shown that rats will ingest a variety of sodium salts when depleted of sodium (Fregly, 1958;Handal, 1965;Krieckhaus & Wolf, 1968;Morrison & Young, 1971;Nachman, 1962;Richter & Eckert, 1938;Schulkin, 1982); however, no one to our knowledge has made a direct comparison among sodium salts using different concentrations in a brief-access test. A brief-access test was used so that preference for several salts could be analyzed simultaneously without potentially confounding postingestive effects.…”

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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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Acquisition of sodium by rats: Interaction of innate mechanisms and latent learning.

Cited by 140 publications

References 6 publications

The neural substrates of enhanced salt appetite after repeated sodium depletions

The neural substrates of enhanced salt appetite after repeated sodium depletions

Homeostasis: Beyond Curt Richter

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

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