As Pur increased synaptic structural plasticity in BCCAO rats in this study, we hypothesized that the alleviated cognitive impairment and neuropathological alterations might be related to non-glutamatergic, Ca2+-dependent processes of ischemia-induced neuronal damage; meanwhile, TRPM2 was shown to mediate toxic Ca2+ influx (Hara et al., 2002; Aarts et al., 2003). Here, TRPM2 is linked to Cognitive impairment.