ReviewFrontiers in behavioral neuroscience2025
Translational implications of circadian activity alterations in an experimental model of late-onset depression induced by prenatal excess of glucocorticoids.
Review in Frontiers in behavioral neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Most neuropsychiatric conditions, including neurodevelopmental disorders, can have different etiology depending on genetic influences, environmental factors, and gene-environment interactions. Consistent evidence points to low birth weight, commonly associated with prenatal exposure to excess glucocorticoids (GC), as risk factor for neuropsychiatric disorders including depression, ADHD and schizophrenia. In this review we give an overview of our behavioral and mechanistic studies linking prenatal exposure to GC to depression. The behavioral analyses in our mouse model revealed that prenatal exposure to synthetic GC dexamethasone (DEX) alters hippocampal neurogenesis and induces depression-like behavior that responds differently to antidepressive therapies. Using neural progenitor cells as an
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