As a mean to advance mechanistic understanding of migraine, the research activity focuses on the investigation of the cellular and circuit mechanisms of the primary brain dysfunctions that cause familial hemiplegic migraine (FHM), a rare monogenic form of migraine with aura, using genetic FHM mouse models.
These animal models include knockin mice carrying FHM type 1 and type 2 mutations in the genes encoding the neuronal voltage-gated calcium channel CaV2.1 and the astrocytic alpha2 Na/K ATPase, respectively.

5 recent publications

  • Tottene A, Conti R, Fabbro A, Vecchia D, Shapovalova M, Santello M, van den Maagdenberg AMJM, Ferrari M and Pietrobon D.  Enhanced excitatory transmission at cortical synapses as the basis for facilitated spreading depression in CaV2.1 knockin migraine mice. Neuron (2009) 61: 762-773
  • Fioretti B, Catacuzzeno L, Sforna L, Gerke-Duncan MB, van den Maagdenberg AMJM, Franciolini F, Connor M and Pietrobon D. Trigeminal ganglion neuron subtype-specific alterations of Ca(V)2.1 calcium current and excitability in a Cacna1a mouse model of migraine. J Physiol (2011) 589: 5879-5895
  • Pietrobon D and Moskowitz M.  Pathophysiology of migraine. Ann Rev Physiol (2013) 75:365-91
  • Pietrobon D and Moskowitz M. Propagation of chaos and commotion in the wake of cortical spreading depression and spreading depolarizations. Nature Rev. Neurosci. (2014) 15:379-93
  • Capuani C, Melone M, Tottene A, Bragina L, Crivellaro G, Santello M, Casari G, Conti F and Pietrobon D. Defective glutamate and K+ clearance by cortical astrocytes in familial hemiplegic migraine type 2. EMBO Mol Med. (2016) 8:967-86



  • MIUR (Italian Ministry of University and Research) PRIN "The excitation-inhibition balance in the central nervous system: synaptic transmission, plasticity and synaptopathies" (2013-2016)
  • Telethon grant “ Familial hemiplegic migraine mechanisms” (2014-2017)