Specifically, using a rodent model of depression, Li et al. (2010) demonstrated that administration of the dissociative anesthetic ketamine, a glutamate N-methyl-D-aspartic acid receptor (NMDAR) antagonist, rapidly activated the mTOR pathway, leading to increased synaptic signaling and new spine synapses in the prefrontal cortex (PFC). This evidence concerns the gene MTOR and major depressive disorder.