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Experimental findings from transgenic migraine mouse models that carry a human FHM1 gain-of-function mutation in CaV2.1 (P/Q-type) calcium channels underscore the role of neuronal hyperexcitability in migraine [1,2]. However, functional data that link the excitability changes to neuronal network activity and the enhanced propensity to cortical spreading depression (CSD), the likely mechanism underlying migraine aura, are largely lacking.

Monitoring cortical neuronal activity and spreading depression in freely behaving familial hemiplegic migraine Cacna1a R192Q knockin mice