KET is known to have effects in synaptic plasticity: the fast-acting antidepressant action of KET is known to be dependent on rapid protein synthesis (namely of BDNF, PSD-95, GLuR1 and synapsin 1) and activation of intracellular pathways such as mTOR, all of them physiologically relevant for synaptic plasticity mechanisms, neuronal growth, differentiation and synaptogenesis.38, 39, 40, 41 Although the specific role of mTOR in NAc is not fully understood in depression, the effect of mTOR modulation is well studied in addiction. The gene discussed is BDNF; the disease is depressive disorder.