Pyk2 in the amygdala modulates chronic stress sequelae via PSD-95-related micro-structural changes

• DOI: 10.1038/s41398-018-0352-y
• Publication Date: 2019-01-21T11:02:40Z
• Authors: Enrica Montalban; Omar Al-Massadi; Anna Sancho-Balsells; Verónica Brito; Benoit de Pins; Jordi Alberch; Silvia Ginés; Jean-Antoine Girault; Albert Giralt
• Keywords: Anhedonia; Chronic Stress; Knockout mouse

Major depressive disorder (MDD) is a common with variety of symptoms including mood alterations, anhedonia, sleep and appetite disorders, cognitive disturbances. Stressful life events are among the strongest risk factors for developing MDD. At cellular level, chronic stress results in modification dendritic spine morphology density. Here, we study role Pyk2 development depressive-like induced by model unpredictable mild (CUMS). non-receptor calcium-dependent protein-tyrosine kinase highly expressed forebrain principal neurons involved structure density regulation. We show that knockout mice less affected to anxiety-like anhedonia-like phenotypes CUMS paradigm. Using region-specific knockout, demonstrate this phenotype fully recapitulated selective inactivation amygdala. also absence PSD-95 clustering, NMDA receptors changes paradigm prevented. Our reveal possible response synaptic markers expression regulation suggest contributes stress-induced responses through micro-structural its deficit may contribute resilience stress.