Migraine is thought to be triggered by excessive neocortical neuronal excitability that leads to cortical spreading depression. In this issue of Neuron, Tottene et al. study a mouse model of familial hemiplegic migraine type 1, and provide evidence for the hyperactivity of P/Q-type calcium channel-mediated cortical glutamatergic synaptic transmission as an underlying mechanism for the susceptibility of cortical spreading depression initiation in migraine disorders.
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