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Abstract

The endogenous depression represents a wide and complex panorama whose origin is partially unknown. In spite of this, there are several genesis that have led the scientific knowledge in the last years, being these, in the first place, the mono-aminergic dysfunctions. These consist mainly of the low levels of synaptic neurotransmission of amines at the neurological level, as it is exposed in the hypothesis of the monoamines. Secondly, there are the neuroendocrine alterations, which indicate a decrease in the levels of secretion of certain hormones in the hypothalamic-hypophyseal-suprarenal axis, especially cortisol. Finally, thirdly, there are the neuroanatomical alterations, which are related to dysfunctions in anatomical circuits such as the limbic-thalamic-cortical circuit, and in point structures such as the hippocampus and the amygdala.  In turn, this disorder has various traditional treatments at the physiological level, such as MAOI inhibitors, which are responsible for reducing the activity of the MAO enzyme, which degrades neurotransmitter vesicles. Other traditional antidepressants are serotonin reuptake inhibitors and tricyclic antidepressants, which are responsible for increasing the concentration of serotonin and noradrenaline with serotonin respectively in the synaptic space, by preventing these neurotransmitters from being reuptake by their pre-synaptic neuron. However, in recent years innovation has been made in creating new and more effective antidepressants such as ketamine, thus achieving the development of neuroplasticity as a useful finding for the treatment of depression. Finally, two of the existing scales to measure depression will be discussed, being these the Hamilton scale and the Beck inventory, the most used and recognized at a psychological level.