Document Type


Date of Degree

Spring 2015

Degree Name

PhD (Doctor of Philosophy)

Degree In


First Advisor

Johnson, Alan Kim

First Committee Member

Radley, Jason J.

Second Committee Member

Freeman, John H.

Third Committee Member

Blumberg, Mark S.

Fourth Committee Member

LaLumiere, Ryan T.


When most omnivores and herbivores become sodium depleted they engage in the motivated behavior of sodium appetite (AKA salt appetite), or the seeking out and ingestion of salty substances. Sodium appetite is associated with psychological processes that serve to enhance the incentive and rewarding value of salty substances in order to attract animals to salty substances and reinforce the ingestion of them. The experience of sodium depletion also produces long-lasting changes in behavior; one of the most apparent changes being a seemingly life-long increase in hypertonic salt intake which indicates sodium appetite is sensitized. Two neural circuits have been implicated in the sensitization of sodium appetite: 1) a forebrain neural circuit that regulates body fluid homeostasis, and 2) the mesolimbic dopamine system which mediates motivated behaviors. This dissertation has three aims that serve the overall purpose of providing a better understanding of the neurobiological mechanisms that mediate the sensitization of sodium appetite. The first aim is to develop a model of sodium depletion that is amenable to pharmacological manipulation in order to determine whether the -blockade of N-methyl-d-aspartate receptors, which are critical for neural plasticity, will prevent the sensitization of sodium appetite. The second aim is to determine whether sensitization is associated with relatively long-term molecular changes in forebrain areas that regulate body fluid homeostasis. The third aim is to identify how forebrain areas involved in body fluid homeostasis may connect to and influence activity in the mesolimbic dopamine system.

Public Abstract

People in Westernized societies tend to eat too much salt (also known as sodium). This “salt gluttony” has been implicated in many diseases including cardiovascular disease and autoimmune disease. When many mammals become sodium depleted (through excess vomiting, diarrhea, or hemorrhage) they enter a state of sodium deficiency that causes them to seek out and ingest foods and drinks that contain salt. Interestingly, when animals are repeatedly depleted of sodium they progressively increase their salt intake and essentially become salt gluttons. This dissertation investigates how sodium depletion changes the brain in order to elicit salt gluttony. The goal of this work is to provide a foundation for potential behavioral or pharmacological treatments that may one day help prevent excess salt intake.


publicabstract, Motivation and reward, Neural Plasticity, Orexin, Salt appetite, Thirst


viii, 92 pages


Includes bibliographical references (pages 84-92).


Copyright 2015 Seth Hurley

Included in

Psychology Commons