Research Research Projects

Brainstem circuits that control migraine

Migraine, a disabling and episodic brain disorder, is common and its origins are complex. Trigeminal nociceptors and the trigeminal nucleus caudalis (TNC) are key brain structures for the integration and processing of craniofacial pain. Animal models suggest that sensitization of this pathway plays a major role in the pathology of migraine, yet surprisingly little is known about long-term changes in trigeminal afferents or their synapses in the TNC. Given its importance in migraine and the small number of physiologic studies of the TNC, we have been investigating migraine-related plasticity at primary nociceptive afferent synapses in the TNC. To selectively stimulate primary nociceptive afferents we use a novel mouse strain that expresses a light-activated channel protein in nociceptive, or pain responsive, afferent neurons; simply shining a light on these neurons causes them to fire. We are using this model to study sensitization of nociceptive fibers both in mouse behavior and in brainstem slices.

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The trigeminal ganglion is a hub for peripheral nerve inputs critical for migraine. Shown here are nociceptor (pain) nerve terminals (from our TRPV1 mouse model; red) in the brainstem trigeminal nucleus, which receives major input from the trigeminal ganglion. Both non-peptidergic nociceptors (IB4, purple) and C-fiber low-threshold mechanoreceptors (TH, green) inputs are co-labeled. Credit: H. B. Shin and B. Pradier.