This understanding is relevant not only to better link the action of E-I homeostasis to current knowledge on post-stroke changes in excitability [36,38,39] but also to elucidate the etiology of stroke symptomatology, such as post-stroke seizures [3], depression [10] and chronic pain [7], which have been tied to changes in excitability. This evidence concerns the gene SERPINB1 and depressive disorder.