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FHM1 mutant mice carrying the R192Q gain-of-function mutation in CaV2.1 (P/Q-type) calcium channels display enhanced glutamatergic transmission and increased propensity for cortical spreading depression (CSD;1,2). Corticosteroids released after stress also enhance glutamatergic transmission but the relationship between stress and migraine is not well understood.

Corticosterone enhances CSD susceptibility via glucocorticoid receptor activation in familial hemiplegic migraine 1 Cacna1a knock-in mice