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.

174