Project: Research project

Project Details


In many respects, sodium appetite differs little from other biological
motivations. As with sex, hunger, and thirst, it is the behavioral
expression of a larger physiological system that deals with a fundamental
problem of life, in this case electrolyte balance. As with other
motivations, salt appetite is hormonally driven and the hormones produce
much of their influence on behavior (and physiology) by acting on neurons
in the ventral forebrain. One advantage of salt appetite as a model for
studying biological motivation is that its adequate stimulus is simple,
the sodium ion, and in the external environment this stimulus is
transduced by a single sensory system, taste. Because the neuroanatomy
of the gustatory system has been documented, it should be possible to
follow gustatory afferent information into the brain and to determine
where and by what mechanisms it interacts with the neural areas that are
sensitive to the relevant hormone fluxes. The experiments outlined in
this proposal investigate such interaction. Neurons in anteroventral
third-ventricular forebrain areas will be tested iontophoretically for
their sensitivity to two of the principal hormones implicated in
eliciting sodium appetite, aldosterone and angiotensin II. The same
neurons also will be tested for responsiveness to electrical stimulation
in the parabrachial nuclei, which contains a gustatory relay that
projects directly to the ventral forebrain. Neurons that respond to
parabrachial stimulation, in turn, will be examined for responses to
sapid stimuli, The results will determine whether neurons that respond
to local changes in the concentration of either aldosterone or
angiotensin II also receive direct afferent neural influence from the
gustatory apparatus.
Effective start/end date9/3/959/2/96


  • Fogarty International Center
  • Fogarty International Center


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