Analysis of the protective effects of the α2/δ subunit of voltage-gated Ca2+ channels in brain injury

A cryogenic method was used to induce brain injury. The mice pretreated with 100 mg/kg Gabapentin exhibited a decrease in lesion size, while the 40 mg/kg Gabapentin injection was effective in rol/+ mice but not +/+ mice. The administration of 100 mg/kg Gabapentin also attenuated reactive astrocyte activity and neuronal degeneration; the pattern of results was similar to that for lesion size. An analysis of phosphorylated p38 (pp38) expression revealed that Gabapentin suppressed the p38 mitogen-activated protein kinase (MAPK) signaling cascade by interrupting glutamate-signaling induced by the inhibition of VGCCs. The present findings demonstrated that the administration of the α2/δ subunit inhibitor, Gabapentin, had neuroprotective effects following brain injury.