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Significance GSK3β is a serine/threonine kinase highly expressed in the brain that regulates several ion channels and receptors. Our study uncovers increased levels of active GSK3β in the nucleus accumbens (NAc) of mice with a depressive-like phenotype induced by chronic stress. We clarify that the increased levels of active GSK3β within the NAc of these mice lead to altered synaptic plasticity through phosphorylation of the Kv4.2 subunit, a molecular determinant of A-type K+ currents. Moreover, selective GSK3β silencing in the NAc prevents maladaptive synaptic plasticity and depression-related behavior, paving the way to consider the GSK3β–Kv4.2 axis as a strategy to manage the negative impact of chronic stress.

Chronic mild stress alters synaptic plasticity in the nucleus accumbens through GSK3β-dependent modulation of Kv4.2 channels