Prenatal stress affects viability, activation, and chemokine signaling in astroglial cultures

•Astrocytes showed increased cell death and GFAP expression after prenatal stress.•Prenatal stress increased NO production, which was caused by enhanced iNOS levels.•CX3CL1 levels were upregulated in astrocytes derived from prenatally-stressed pups.•Prenatal stress altered the CXCL12/CXCR4-7 axis in astroglia.

CXCL12/SDF-1α and CX3CL1/fractalkine are constitutively expressed in the brain, which indicates their significant functions. Emerging evidence highlights the role of astrocytes and the immune system in the pathophysiology of stress-related disorders. The aim of this study was to assess whether prenatal stress affects chemokine signaling, cell viability/activation, and the iNOS pathway in astroglial cultures. Our results showed that prenatal stress lowered astrocyte viability and simultaneously increased GFAP expression. Furthermore, CX3CL1 production and the CXCL12/CXCR4-7 axis were also altered by prenatal stress. Taken together, malfunctions caused by prenatal stress may adversely influence brain development, leading to long-term effects on adult brain function and behavior.

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