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Cortical spreading depression (CSD) is a depolarization wave associated with neurological disorders such as migraine, cerebral ischemia and traumatic brain injury. The mechanism of action of this phenomenon still remains unclear. Although it is suggested that extracellular K(+) accumulation contributes to CSD, other ions may play a relevant role in the mechanism of propagation of the wave. In this context, we hypothesize that Ca(2+) may play an important function in the wave propagation. Our results demonstrate that enhancing Ca(2+) influx into the cells by topical cortical application of the ionophore A23187 (10 μM, 50 μM and 100 μM solutions) increases the velocity of CSD propagation in a dose-dependent manner, and a much higher dose of this compound (2 mM) triggers CSD. In conclusion, increased Ca(2+) influx can be a key element in the induction mechanism of the CSD, and should be assessed in further experimental strategies targeting brain disorders related to CSD.

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Cortical spreading depression (CSD) is a slowly propagating wave of spontaneous cortical electrical activity and it shares underlying mechanisms with neurological diseases such as migraine and epilepsy. It is well known that the neuronal tissue is susceptible to oxidative stress because of its high oxygen consumption and modest antioxidant defenses; alteration of the physiological pattern can enhance the oxidative stress (OS). Furthermore, ω‐3 polyunsaturated fatty acid of fish oil (FO) protects the brain by reducing OS and moderate treadmill also (MT) counteracts OS. We evaluated the effects of FO supplementation and MT on antioxidant enzymes in rat’s cortexes (right and left hemisphere). All rats were submitted to 2%KCl stimulus to elicit CSD in the right hemisphere. In order to study OS, we analyzed BW, MDA, SOD, CAT and GST. In the left hemisphere, FO supplementation increases MDA production. MT + FO also increases MDA; there is no difference in any antioxidant enzyme. In the right hemisphere, FO supplementation, MT and MT + FO supplementation groups showed decrease in MDA production, on the other hand, there was no influence on enzymatic activities. Briefly, data show that CSD, FO or MT don’t induce significant modulation in antioxidant enzymes, which suggest that CSD is a useful phenomenon that contributes to the study of FO and MT on neurological diseases without cumulative effects of oxidative stress. Grant Funding Source: Supported by FACEPE and CNPq

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