Treating the symptoms of depression has the purpose of reduce and control the dysfunction that patients could have in any areas of their life. The choice of treatment is based on the needs of the patient and can include drugs, therapy and other similar treatments. Regardless of the chosen treatment, it is necessary to consider possible side effects . In the case of depression associated with<unk>  and other associated structures, reducing the increased connectivity might play a critical role reducing depression symptomatology and thus represent a potential therapy target for affective disorders Since glutamate is the most abundant and major excitatory neurotransmitter in the brain, pathophysiological changes in glutamatergic signaling are likely to affect neurobehavioral plasticity, information processing and large-scales changes in functional brain connectivity. Ketamine, a fast-acting general anesthetic derived from phencyclidine and use as a pediatric inductor, plays a non-well known role in the neural network dynamics at the healthy brain . The administration of ketamine in abnormal brain has the potential of reduce the increased function of the networks that are seen in depression. The therapeutic potential of ketamine may be explained by reversing disturbances in the glutamatergic system and restoring parts of a disrupted neurobehavioral homeostasis where several structural, metabolic, and functional abnormalities have taken place. Long term ketamine treatments lead to cognitive impairment including problems of short-term memory, visual and verbal memory. On the other hand, short term treatments are generally well tolerated and any damage may be reversible. Electroconvulsive therapy (ECT) significantly reduces functional connectivity between the<unk> ateral prefrontal cortex<unk>  and the anterior cingulate cortex, the medial prefrontal cortex, and other areas implicated in major depression. Although electroconvulsive therapy has been used as a treatment for depression since 1930, it has several side effects as loss of memory, confusion and difficulties in forming new memories. Because of this reasons, this kind of treatment is limited to severely damaged patients.
Dorsal nexus
Pocock boundary
Cortical homunculus
Axon hillock
Neural clique
Collateral eminence
Ossification center
Epiphyseal plate