We have demonstrated that the trigeminal ganglion sends a projection to the auditory brain stem and to the cochlear vasculature. The terminations in the brainstem end in granular and magnocellular regions of the ventral cochlear nucleus (VCN) and at the locations of olivocochlear neurons in the superior olivary complex. The cochlear portion of the innervation modulates blood flow within the cochlea. However, the function of the brainstem projection is unknown. Preliminary findings suggest that the projection to the VCN is excitatory. The axons of granule' cells (parallel fibers) project to the dorsal cochlear nucleus (DCN). Therefore, excitation by the trigeminal innervation could affect most of the output neurons of the cochlear nucleus (CN). A series of studies is designed to elucidate the function of the CN portion of this new projection and define its neurotransmitters: The trigeminal ganglion will be electrically stimulated while observing the responses of single units in the CN. The candidate neurotransmitters, Substance P and Nitric Oxide, will be evaluated using immunocytochemistry and neuropharmacology. A role for the trigeminal ganglion in the generation and modulation of tinnitus will be explored: As many as two thirds of tinnitus patients are able modulate their tinnitus by clenching the jaw or touching the skin on the face, areas innervated by the trigeminal ganglion. Others can attribute the onset of tinnitus to a somatic insult in the head and neck region (""""""""somatic tinnitus""""""""). On the assumption that increased spontaneous rate is a manifestation of tinnitus, its modulation by somatosensory input to the CN could play a role in the generation and modulation of tinnitus. The hypothesis wifi be tested by electrically stimulating the trigeminal ganglion while recording spontaneous activity in single units of the CN. Identifying the neurotransmitter used in this pathway could then set the stage for later drug treatments.
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