“…Interestingly, the control animals subchronically treated with FP also showed a reduction in hippocampal CA3 neurones. In different kindling models an antiepileptic and protective effect was observed with MK-801, a non-competitive glutamate receptors (N-methyl-d-aspartic acid receptor, NMDA) antagonist (Minabe et al, 1992;Gilbert 1994;Gilbert and Burdette, 1996;Applegate et al, 1997;Yoshida et al, 1997;Krug et al, 1998) and there are abundant evidence that MK-801 could also induce neuronal damage in a dose-dependent manner (Peng et al, 2013). Interferences with the Akt1/GSK3 signaling pathway (Peng et al, 2013), adenosine A1 mediated neurotransmission (Okamura et al, 2004), oxidative stress and apoptotic changes (Ozyurt et al, 2007;Willis and Ray 2007) and other mechanisms contribute to MK-801 neurotoxicity.…”