Date of Graduation

Spring 2008


Master of Science in Biology



Committee Chair

Paul Durham


neuron-glia interactions, gap junctions, MAP kinase, ipsi-lateral, contra-lateral, trigeminal

Subject Categories



The goal of this study was to investigate neuronal-glial cell signaling in trigeminal ganglia under basal and inflammatory conditions using an in vivo model of acute temporomandibular joint (TMJ) inflammation. Inflammation of the TMJ and release of inflammatory mediators that cause activation of trigeminal nerves is implicated in TMJ pathologies. While neuron-glia interactions are known to be involved in all stages of inflammation and pain associated with several CNS diseases, the role of neuron-glia interactions within the trigeminal ganglion under normal and inflammatory conditions is not known. In control animals, only minimal gap junction communication was observed between neuronal cell bodies and satellite glial cells. However, gap junction communication between these cell types was greatly increased in response to capsaicin stimulation of trigeminal nerves that provide sensory innervation of the TMJ. In addition, capsaicin stimulation of trigeminal nerves increased the expression of the inflammatory proteins MAPKs and MKPs in both neurons and glia in all regions of the ganglion. Interestingly, increased levels of these proteins were also observed in the contra-lateral ganglion. This is the first evidence, to my knowledge, of neuron-glia signaling via gap junctions within the trigeminal ganglion. Based on my findings, it is likely that neuronal-glial communication via gap junctions and paracrine signaling are involved in the development of peripheral sensitization within the trigeminal ganglion and, thus, are likely to play an important role in TMJ pathologies. Furthermore, propose that propagation of inflammatory signals within the ganglion may help to explain commonly reported symptoms of co-morbid conditions associated with TMJ disorders.


© Srikanth Thalakoti

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