Abstract

Schizophrenia, one of the most serious and widespread mental disorders in the world, makes its debut often in late adolescence and early adulthood, which allows us to focus our attention on those brain areas that still retain plasticity during this period. Parvalbumin interneurons, GABAergic and inhibitory, in both cortical and hippocampal areas, maintain their plasticity and are particularly vulnerable to oxidative stress due to their high energy requirements. Evidence has shown that their damage favors the triggering of schizophrenia by altering the neurobehavioral development of individuals. These neurons have melatonin receptors of MT1 and MT2, and the cytoprotective role of melatonin has been reported on these neurons. However, the role of this indolamine played in adolescence in protecting parvalbumin interneurons, reducing their oxidative stress and/or preventing their disappearance, which could prevent the onset of schizophrenia, is not yet known. The importance of this activity and its implications on patient therapy require the urgent studies

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