Perisynaptic astrocytes as a potential target for novel antidepressant drugs

Emerging evidence suggests that dysfunctions in glutamatergic signaling are associated with the pathophysiology of depression. Several molecules act on glutamate binding sites, so-called modulators, rapid-acting antidepressants stimulate synaptogenesis. Their antidepressant response involves elevation both extracellular and brain-derived neurotrophic factor (BDNF) levels, as well postsynaptic activation mammalian target rapamycin complex 1. The mechanisms involved outcomes including ketamine, suggest astrocytes must be considered a cellular for developing antidepressants. It is known levels intrasynaptic time-coursing maintained by perisynaptic astrocytes, where inwardly rectifying potassium channels 4.1 (Kir4.1 channels) regulate uptake. In addition, ketamine reduces membrane expression Kir4.1 channels, which raises increasing neural activities. Furthermore, inhibition stimulates BDNF may enhance synaptic connectivity. this review, we discuss modulators’ actions regulating reinforce importance development novel drugs.