Other studies have reported that EA at GV20 reversed behavioral deficit and LTP impairment, possibly through the N-methyl-D-aspartate receptor 1 (NMDA-R1) and TRPV1 pathway, thus reversing NR1- (one of the NMDA receptor subunits) and TRPV1-mediated neurotoxicity in vascular dementia [208,209]. The gene discussed is GRIN1; the disease is vascular dementia.