Effect of Maternal ±Citalopram Exposure on P11 Expression and Neurogenesis in the Mouse Fetal Brain

Area of Science:

• Neuroscience
• Developmental Biology
• Pharmacology

Background:

• Selective serotonin reuptake inhibitors (SSRIs) are linked to adverse neurodevelopmental outcomes in fetuses.
• In adults, SSRIs modulate p11 protein expression, which influences serotonin signaling and neurogenesis.
• Serotonin signaling via 5-HT1B/D receptors is crucial for fetal axonal circuit formation.

Purpose of the Study:

• To investigate p11 protein expression in the developing fetal mouse brain.
• To determine the impact of maternal SSRI exposure on fetal p11 expression.
• To assess whether maternal SSRI exposure affects fetal neurogenesis.

Main Methods:

• Pregnant mice were administered SSRI ± citalopram from gestational day 8 to 17.
• p11 expression in fetal brain tissue was analyzed.
• Neurogenesis was quantified in specific fetal brain regions.

Main Results:

• p11 protein is expressed in fetal thalamic neurons and thalamocortical axons.
• In utero citalopram exposure significantly decreased p11 protein levels in the fetal thalamus.
• Significant reductions in neurogenesis were observed in specific fetal brain regions following maternal SSRI exposure.

Conclusions:

• Maternal SSRI exposure alters p11 protein expression in the fetal brain.
• In utero SSRI exposure leads to decreased neurogenesis in the developing fetal brain.
• These findings suggest a mechanism by which SSRIs may impact fetal neurodevelopment.