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.