• Cèlia Sintas, Noèlia Fernàndez-Castillo, Marta Vila-Pueyo, Patricia Pozo-Rosich, Alfons Macaya, and Bru Cormand.
• Departament de Genètica, Microbiologia i Estadística, Facultat de Biologia, Universitat de Barcelona, Barcelona, Catalonia, Spain; Institut de Biomedicina de la Universitat de Barcelona (IBUB), Barcelona, Catalonia, Spain; Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Spain.
• J Pain. 2017 Apr 1; 18 (4): 366-375.

AbstractMigraine with aura is a subtype of migraine characterized by transient neurological disturbances that usually precede headache. Cortical spreading depression (CSD) is the likely pathophysiological correlate of the aura phase of migraine, found in common and rare forms of migraine, such as familial hemiplegic migraine. CSD is a depolarization wave that propagates across the cerebral gray matter transiently suppressing neuronal activity. Prophylactic treatments for migraine, such as topiramate or valproate, reduce the number of CSD events. We evaluated changes in gene expression in rat cortex and brainstem after inducing CSD in the cortex, with and without a prophylactic treatment with topiramate or valproate. CSD induction showed similar transcriptomic profiles with and without treatment in cortex, involving genes related to hormone stimulus, apoptosis, synaptic transmission, and interleukin signaling. In brainstem, CSD with and without treatment, although to a lesser extent, also induced gene expression changes involving genes related to apoptosis. Half of the genes altered in brainstem after CSD were also differentially expressed in the same direction in cortex. No differences in gene expression were identified after CSD as a consequence of the treatments, neither in cortex nor in brainstem.Copyright © 2016 American Pain Society. Published by Elsevier Inc. All rights reserved.

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