Gustatory Control of Sodium Appetite

Project: Research project

Project Details

Description

DESCRIPTION (provided by applicant): Motivation remains a central puzzle of
neuroscience. Understanding its neural bases is key in developing rational
therapies for a broad spectrum of maladies such as drug addiction, obesity,
anorexia nervosa, and depression. Salt appetite is a biological drive triggered
by a negative body sodium balance that offers a unique model for investigating
the central mechanisms of motivated behavior. Sodium appetite fulfills all of
the criteria for motivation, as do hunger and thirst, but has some distinct
advantages. Its adequate stimulus is simple, the sodium ion, and in the
external environment, this stimulus is transduced by a single sensory system,
taste. Unlike other sensory systems, except smell, taste has direct neural
connections with the limbic system, which is critical to the elaboration of
motivation. In most mammals, including humans, recognition of sodium is innate.
Thus, when a Na-appetite arises, the significance of the sensory neural
activity elicited by sapid sodium changes dramatically. The objective of this
project is to understand how the neural systems that control salt appetite
effect the change in avidity for salt. The premise is that at least part of the
change results from alterations in the gustatory neural code. We already know
that, during Na-appetite, changes do occur in the gustatory responses to NaCl
on the periphery and in the first central relay, the nucleus of the solitary
tract (NST). We also know that lesions of the second central relay, the
parabrachial nucleus (PBN), prevent the expression of Na-appetite, but that
damage to the third central relay, the thalamic gustatory area (TTA), does not.
Finally, chronically decerebrate rats, which have both the NST and PBN intact,
but no connections to or from the forebrain, also fail to exhibit a
Na-appetite. These facts constrain the hypotheses to interactions between the
PBN and the limbic system. Using these constraints, this proposal examines
three related hypotheses. During Na-appetite, (1) the sensory neural code for
taste in the PBN is altered to make sapid sodium more discriminable from other
chemicals, (2) parabrachial gustatory neural activity distributed to the
ventral forebrain is necessary and sufficient to change the hedonic value of
the salt signal, and (3) the mechanism for the increased discriminability and
the changed avidity involves reciprocal interaction between the limbic system
and the parabrachial nuclei.
StatusFinished
Effective start/end date7/1/025/31/14

Funding

  • National Institute on Deafness and Other Communication Disorders: $316,125.00
  • National Institute on Deafness and Other Communication Disorders: $284,513.00
  • National Institute on Deafness and Other Communication Disorders: $329,410.00
  • National Institute on Deafness and Other Communication Disorders: $315,850.00
  • National Institute on Deafness and Other Communication Disorders: $308,697.00
  • National Institute on Deafness and Other Communication Disorders: $315,850.00
  • National Institute on Deafness and Other Communication Disorders: $316,125.00
  • National Institute on Deafness and Other Communication Disorders: $12,600.00
  • National Institute on Deafness and Other Communication Disorders: $327,108.00
  • National Institute on Deafness and Other Communication Disorders: $316,125.00
  • National Institute on Deafness and Other Communication Disorders: $326,292.00

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