In this case, our data shows that ketamine's rapid antidepressant actions are probably mediated through the NMDAR/CaMKII pathway and result in a significant increase in synaptic plasticity in the DG region of depressive-like models of stroke (Figure 6), making it a viable option for the treatment of depression in stroke patients, and linking its lasting antidepressant properties with the resulting synaptic plasticity in key brain regions. This evidence concerns the gene CAMK2G and depressive symptom measurement.