Date of Graduation

Spring 2008


Master of Science in Biology



Committee Chair

Paul Durham


neuron-glia interactions, gap junctions, connexins, tonabersat, trigeminal

Subject Categories



Activation of trigeminal nerves in response to an inflammatory stimulus causes increased communication between neurons and surrounding satellite glial cells via gap junctions in the trigeminal ganglion (TG). The goal of this study was to identify the gap junction proteins, or connexins (Cxs), in the ganglion in response to three different models of inflammation: acute, acute-sensitization, and chronic. Initially, quantitative PCR was used to demonstrate that mRNA for Cxs: 26, 29, 36, 37, 40, 43, 50, and 57 was expressed in TG under basal conditions. Next, protein expression of Cxs: 26, 32, 36, 40, 43, 46, and 50 was demonstrated in TG by immunohistochemistry. Expression of Cxs: 26, 36, and 40 were increased in response to acute and chronic inflammation of the jaw, or temporomandibular joint (TMJ). Importantly, the formation of gap junction plaques by Cx26 was observed between neurons and satellite glial cells. In other studies, a model of acute-sensitization was used to simulate the significant comorbitities between rhinosinusitus and migraine. In this model, increased gap junction signaling between neurons and satellite glial cells as well as increased Cx26 plaque formation was observed. Significantly, the anti-migraine drug tonabersat decreased neuron-glial cell communication and decreased the formation of Cx26 plaques. To my knowledge, this is the first study to look at connexin expression in trigeminal ganglion under basal and inflammatory conditions. Results from my study provide evidence that Cx26 plays an important role in facilitating neuron-satellite glial cell communication and hence, a role in peripheral sensitization. Furthermore, my data suggest that tonabersat may function as an anti-migraine drug by blocking gap junction communication in trigeminal ganglion.


© Filip G. Garrett

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