| Description |
Migraine neuroscience is a field in its infancy, with migraine being a remarkably common yet poorly understood sensory circuit disorder. It is characterized by attacks of unilateral, throbbing craniofacial pain, with sensitivity to movement, visual, auditory, and other afferent inputs. Migraines can increase in frequency and intensity over time, transitioning from episodic to chronic migraines that resemble a never-ending migraine attack. The long-lasting, debilitating pain of migraine attacks is thought to follow a circuit of neuronal networks connecting the peripheral nervous system to the central nervous system as it ascends to the cerebral cortex for processing of painful stimuli. Using in vivo two-photon microscopy calcium fluorescence imaging with a novel surgical preparation to image fluorescence from genetically encoded calcium indicators in the C2 dorsal root ganglion (DRG), we establish an imaging paradigm of sensory neurons from the C2 DRG in response to greater occipital nerve and associated dermatome stimulation. We observe that in a nitroglycerin-induced chronic migraine state, a greater number of sensory neurons in the DRG respond when the greater occipital nerve dermatome is electrically stimulated. Additionally, this responder expansion is noted in sodium-nitroprusside-induced acute migraine models. Importantly, the understanding of nociceptive network activation in migraine will allow us to look at changes in the pain circuit that serve as markers for a migraine attack, observe how they occur, and see if they can be reversed at a neuron or circuit level to prevent the pain associated with migraine. |
