Date of Award

6-2026

Degree Type

Thesis

Degree Name

Master of Science in Biomedical Sciences

First Advisor

Arturo Bravo Nuevo PhD

Second Advisor

Mindy George-Weinstein PhD

Third Advisor

Julio González Martín-Moro MD, PhD

Abstract

The postnatal retina undergoes further development during the critical period, during which excess neurons are culled, and synapses are refined to shape the mature retinal circuitry. Brain-specific angiogenesis inhibitor-1 (BAI1) has been implicated in synaptic development, phagocytosis, the regulation of angiogenesis, and inflammatory signaling, suggesting it may play an important role in retinal maturation. The goal of this project was to determine how BAI1 deficiency affects retinal cell survival and layer morphology during the critical period. Mice were divided into three genotype groups: BAI1 +/+ Wild Type (WT), +/- (Het), and -/- (KO). Apoptotic cells were quantified using TUNEL staining at postnatal day 10 (P10) and P16 that correspond to peaks of cell death in the inner nuclear layer (INL) and outer nuclear layer (ONL), respectively. Retinal layer thickness measurements were also collected at both time points. Results indicate that BAI1 KO and Het mice exhibit significantly reduced TUNEL-positive cells in the INL at P10 compared to WT controls, suggesting reduced apoptosis during early neonatal retinal development. No significant differences in cell death were observed between groups at P16 in the ONL. Morphological analysis revealed increased INL thickness in WT mice compared to Het and KO mice at P10, while KO mice exhibited a significantly greater ganglion cell layer (GCL) thickness relative to WT and Het groups. Together, these findings suggest that BAI1 contributes to the regulation of neuronal survival and structural organization in the INL during the critical period, potentially influencing synaptic layer formation and neuronal connectivity within the developing retina.

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