Date of Degree

2-2014

Document Type

Dissertation

Degree Name

Ph.D.

Program

Psychology

Advisor(s)

Susan D. Croll

Subject Categories

Neuroscience and Neurobiology

Keywords

Dextran Sodium Sulfate (DSS), Gene Profile, Inflammatory Bowel Disease (IBD), Neuroimmune, Neuropeptide Y, Visceral Pain

Abstract

Neuropeptide Y (NPY) is a 36-amino acid peptide widely expressed in the central and peripheral nervous systems. In addition to other cells, NPY is also synthesized and co-released from sympathetic nerve fibers functioning as a potent sympathetic neuromodulator. NPY has been implicated in playing important roles in the regulation of energy balance, appetite, anxiety, vascular tone, and immune cell functioning. In addition, immune cells of both the innate and adaptive immune systems express functional NPY receptors. Some immune cells can produce and secrete NPY, and genetic alteration of these receptors results in altered immune cell functioning. Its direct association with the immune system, its presence in sympathetic neurons innervating primary and secondary immune organs and its close association with vasculature, make NPY a candidate for mediating, at least in part, the neuroimmune crosstalk. The gene expression results presented here suggest that DSS is a valid model of human IBD and that pain-related behavior in the open field is closely associated with DSS-induced gene changes. Furthermore, the data suggest that NPY signaling via its Y1 receptor plays some regulatory role in the immune process induced by DSS. Y2 receptor antagonism resulted in a mild attenuation of immune activity but also slightly attenuated pain-related behavior in the open field. In sum, it appears that NPY signaling via its Y1 and Y2 receptors plays a role in various features of DSS induced disease.

 
 

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