Thesis Title

Regulation of S100B Expression in Trigeminal Ganglion Neurons and Glia

Date of Graduation

Spring 2007

Degree

Master of Natural and Applied Science in Biology

Department

Biology

Committee Chair

Paul Durham

Keywords

calcium, ganglion, glia, migraine, RAGE, S100B, TMJD, trigeminal

Subject Categories

Biology

Abstract

Trigeminal ganglia nerve activation is implicated in the underlying pathology of migraine and temporomandibular joint disorders (TMJD). The serum and dysfunctional disc levels of S100B, a low molecular weight calcium-binding protein, is elevated in patients suffering from migraine of TMJD. S100B localized in the cytoplasm of cells can directly modulate the function and expression of other intracellular proteins. In addition, S100B can be secreted from cells and function as a paracrine factor to stimulate other cells via activation of its receptor, receptor for advanced glycation endproducts (RAGE). While S100B is reported to play an important role in inflammatory diseases and is expressed by both neurons and glia, its function in trigeminal ganglion neurons and glia under basal and inflammatory conditions is not known. In initial experiments to determine whether S100B and RAGE are expressed in neuronal and glial cells of the trigeminal ganglion, primary cultures, an in vivo model, and cell lines were analyzed using immunohistochemistry. S100B and RAGE were shown to be expressed in neurons and glia in primary culture and in vivo sections, as well as in the three cell lines tested. Stimulation of primary cultures with KC1, capsaicin, CGRP, LPS,TNF-, SNAP, acidic HBS, and glutamate resulted in increased S100B expression in an inflammatory mediator dependent manner. Injection of capsaicin into the TMJ resulted in increased S100B expression in neurons and glia in as little as 15 minutes and levels remained high 120 minutes later. This increase was observed not only in V3 region of the ganglion but throughout the V2 and V1 as well. Results from my studies provide evidence to support a role of S100B in mediating neuronal and glial cell activation in trigeminal ganglia that is likely to contribute to migraine and TMJD pathology.

Copyright

© Lauren E. Langford

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