Author ORCID Identifier


Defense Date


Document Type


Degree Name

Master of Science


Physiology and Biophysics

First Advisor

Dr. Liya Qiao

Second Advisor

Dr. John Grider

Third Advisor

Dr. Zhao Lin


A major portion of pain experienced by patients with an Irritable Bowel Disease (IBD) or Irritable Bowel Syndrome (IBS) can be attributed to visceral hypersensitivity. Visceral stimuli transmitted through primary afferent neurons in the dorsal root ganglia (DRG) induce a nociceptive response. Notably, a subset of patients has also experienced the development of somatic pain, such as leg pain, after diagnosis of a bowel disorder. The aim of this investigation is to ascertain which biochemical mediators are involved in the development of such viscerosomatic cross-sensitization. Initially, the Von Frey Test was used to find behavioral evidence of somatic referred pain; TNBS-induced mice exhibited a greater withdrawal response to hindpaw stimulation than control mice. Then, fast blue retrograde tracing was conducted and hindpaw innervation was identified to occur via primary afferent neurons located in the DRG at L4 spinal level. Immunohistochemical studies were conducted on L4 DRG tissue to evaluate levels of cellular mediators known to be involved in pain signaling, such as phosphor(p)-Akt. L4 DRG from TNBS-treated mice exhibited significantly higher levels of phospho-Akt than control animals. The increased p-Akt was located in Piezo2-expressing L4 DRG neurons and was suppressed in mice lacking TrkB.T1. These findings suggest that the PI3K/Akt pathway regulated by TrkB.T1-mediated cellular events participates in viscerosomatic cross-organ sensitization.


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