Moreover, in our previous study, consistent with the presumed dysfunction of glutamatergic transmission and consequent neuroplasticity changes in depression [69], [72], the downregulation of different AMPA and metabotropic glutamate receptor subunits and the upregulation of the NR2B subunit of NMDA receptors was detected in the amygdala of P2rx7−/− mice [25]. This evidence concerns the gene GRIN2B and depressive symptom measurement.