Our results show that H2S treatment selectively enhanced GluN2B-mediated synaptic responses in the thalamo-LA pathway of aged rats and specific GluN2B antagonist abolished the benefits of H2S donor in amygdalar NMDAR-dependent cued fear memory and LTP, not only indicate that upregulation of GluN2B function is responsible for the effects of H2S in aged rats but also suggest that hypofunction of GluN2B-containing NMDARs contribute to aging-associated amygdalar synaptic plasticity and cognitive defects. This evidence concerns the gene GRIN2B and Cognitive impairment.