Neural and behavioral correlates of motivation in sodium deplete animals

Abstract

Sodium is critical for survival and is maintained in strict homeostatic balance. Sodium depletion, by natural or experimental means, results in sodium appetite; a strong, specific drive characterized by the avid consumption of sodium-containing solutions at concentrations much higher than those accepted by sodium-replete animals. Research using experimental models of sodium appetite has demonstrated a role for brain regions including the subfornical organ and the supraoptic nucleus, and the hormones aldosterone and angiotensin, in the regulation of sodium balance. However, little research has focused on the role of the brain's motivation circuitry in the response to sodium appetite. Because sodium-deplete animals are highly motivated for sodium-containing solutions, and the effects of the drive state and reward experience can be studied separately, this model appears to be ideal for the study of reward motivation. The present work is aimed at characterizing sodium appetite as a model of natural reward. These studies use immunohistochemical and pharmacological measures to examine the role of the mesolimbic circuitry, specifically the nucleus accumbens, as well as dopamine and opiate receptors, in response to sodium depletion and expression of sodium appetite. Behavioral measures were also used to examine sodium appetite expression in a number of experimental conditions. The results of this work indicate that under normal conditions, sodium appetite is not a strong activator of the nucleus accumbens, nor does its expression require activation of dopamine receptors. However, under sham-drinking conditions, sodium appetite dramatically activates the nucleus accumbens and depends on dopamine receptor activation. This work also supports the hypothesis that sodium appetite is a highly specific motivation. Sodium depletion has no effect on the response for another reward. The present results also suggest that sodium appetite expression may be driven by the increased hedonic value of sodium solutions, as opiate receptor blockade reliably decreases NaCl intake. Overall, these findings contribute to the characterization of sodium appetite as a reward model. And while it differs from many other models, the unique properties of sham-drinking during sodium appetite expression revealed in this work suggest a valuable model to study natural reward motivation.