MiR-186-5p inhibition restores synaptic transmission and neuronal network activity in a model of chronic stress.
Ontology highlight
ABSTRACT: Chronic stress exerts profound negative effects on cognitive and emotional behaviours and is a major risk factor for the development of neuropsychiatric disorders. However, the molecular links between chronic stress and its deleterious effects on neuronal and synaptic function remain elusive. Here, using a combination of in vitro and in vivo approaches, we demonstrate that the upregulation of miR-186-5p triggered by chronic stress may be a key mediator of such changes, leading to synaptic dysfunction. Our results show that the expression levels of miR-186-5p are increased both in the prefrontal cortex (PFC) of mice exposed to chronic stress and in cortical neurons chronically exposed to dexamethasone. Additionally, viral overexpression of miR-186-5p in the PFC of naïve mice induces anxiety
SUBMITTER: Rodrigues B
PROVIDER: S-EPMC11835755 | biostudies-literature | 2025 Mar
REPOSITORIES: biostudies-literature
ACCESS DATA