pharmocological treatments such as SSRIs are selective serotonin reuptake inhibitors- they block the reuptake of serotonin from the presynaptic neuron and levels of serotonin in the synaptic cleft rise so there is more available to bind to post synaptic receptors, resulting in an increase in serotonin usually over a period of weeks.
SNRIs similarly block the reuptake of serotonin, but also block the reuptake of norepinephrine, leading to increased levels of norephinephrine.
Goldapple (2004) found that an SSRI called paroxetine increased metabolism in the brainstem, cerebellum, DLPFC, inferior temporal cortex and inferior parietal cortex, and decreased metabolism in the ventral subgenual cingulate, anterior insula, thalamus and hippocampus. this increase in DLPFC activity can be predicted my serotonin hypotheses of depression, as it is part of the frontal striatal pathway, in which serotonin is important for transporting information, and in MDD, the DLPFC is hypoactive, meaning it cannot regulate negative schema in depression, so increasing it and reducing negative schema may reduced depressive symptoms such as anhedonia
However McGrath et al (2013) had differential findings. They found that participants on escitalopram oxidase showed a decrease in metabolism in the insula, right motor cortex, left motor cortex, right inferior temporal cortex, and showed an increase in metabolism in the left prenuceus and amygdala. the increase in amygdala metabolism is interesting, because in depression, the amygdala is already hyperactive, and further research into both the accuracy and implications of this finding are important for understanding the cause and treatment of MDD.