Date on Master's Thesis/Doctoral Dissertation

12-2014

Document Type

Doctoral Dissertation

Degree Name

Ph. D.

Department

Anatomical Sciences and Neurobiology

Committee Chair

Hubscher, Charles H.

Committee Co-Chair (if applicable)

Bickford, Martha E.

Committee Member

Magnuson, David S.

Committee Member

Petruska, Jeffrey C.

Committee Member

Stirling, David P.

Subject

Spinal cord--Wounds and injuries; Urinary incontinence

Abstract

Spinal cord injury (SCI) is a significant public health concern that leaves patients with a multitude of life-long disabilities. Major complications of SCI apart from paralysis, include deficits in bladder and bowel function. Lower urinary tract dysfunction continues to remain a top priority issue affecting quality of life for this population. The majority of visceral organs receive a dual sensory innervation from both spinal nerves as well as the vagus nerve. Following SCI, the vagus nerve is a potential pathway through which information from regions below the level of a spinal injury can travel directly to the brainstem, bypassing the spinal cord. The effect of SCI on the vagus nerve and the tissue it supplies has not been thoroughly examined. In order to advance bladder management after SCI, a thorough understanding of its neural control following chronic injury is needed to ultimately improve existing therapeutic options, as well as develop novel interventions that take advantage of this extraspinal route. The objective of this project was to describe the anatomical, neurochemical, and electrophysiological profiles of vagal innervation of the rat urinary bladder. Initially, the first study identified both single and double-labeled vagal afferents supplying the rat bladder and distal colon in the nodose ganglion (NG). The degree of neural innervation to the colon also was assessed, as a single axon that dichotomizes and innervates both organs can serve an important role for mediating both normal physiological and pathological reflexes. Following chronic SCI, we evaluated potential plasticity in subsets of NG neurons which contain projections that bypass the spinal cord from visceral organs, including those projections that specifically supply the bladder. Vagal sensory cell bodies displayed an increase in P2X3 expression and a decrease in IB4 binding, which also held true for many neurons innervating the bladder. Bladder-innervating neurons also displayed altered membrane electrophysiological properties, suggesting they are responsive to a chronic spinal injury. Even though SCI does not directly sever the vagus nerve, our results indicate vagal afferents, including those innervating the bladder, exhibit neurochemical plasticity post-injury that may have implications for visceral homeostatic mechanisms and nociceptive signaling.

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