Opioid mechanisms that mediate the palatability of and appetite for salt in sodium replete and deficient states.

Sodium deficiency reliably produces a robust intake of saline in rats, which is associated with an increased preference for sodium solutions at hypertonic concentrations that would normally be avoided. The mechanisms underlying the shift to an increased preference for sodium in the deficient state are not well understood. The current experiments examined the role of opioids on changes of behavioral responses that are modified as a function of body sodium status by studying the intake of 0.3 M saline in a free access drinking test and by characterizing the changes in orofacial-related behaviors in response to intra-orally delivered 0.3 M NaCl. In intake tests, systemic treatment with morphine and naltrexone respectively, enhanced and attenuated intake of 0.3 M saline in sodium depleted rats. In taste reactivity tests systemic treatment with morphine significantly decreased negative responses to 0.3 M saline infusions in both sodium replete and sodium depleted rats. Systemically administered naltrexone significantly decreased positive hedonic responses to 0.3 M saline infusions only in sodium depleted rats. These results indicate that peripheral administration of opioid agonists and antagonists alter both hypertonic saline ingestion in a free access situation and taste reactivity responses to hypertonic saline under sodium replete and deplete conditions. The results indicate that endogenous opioids alter the processing of central information to affect hedonic mechanisms that influence behaviors related to sodium consumption and palatability.