Glutamate-dependent excitotoxicity during neuronal injuries. A, Traditional model of the mechanisms for glutamate-dependent excitotoxicity. B, Novel model of the mechanisms of glutamate-dependent excitotoxicity. b1, Existing neuronal gap junctions (GJ) contribute substantially to neuronal death caused by overactivation of NMDARs. b2, New neuronal gap junctions are induced by activation of group II mGluRs (IImGluRs) and also contribute to glutamate-dependent neuronal death. ⊕, This sign indicates the increase. See text for details.