Ursula Pena ’25, Izabella Espinal San Miguel ’25, Ana Rodriguez ’25
PTEN deficiency in developmental Purkinje cells alters dendritic development leading to deficits in mouse neonatalmotor skills and behavior
Ursula Pena ’25, Neuroscience major
Izabella Espinal San Miguel ’25, Neuroscience major
Ana Rodriguez ’25, Biology major
Faculty mentor: Dr. Ileana Soto Reyes, Neuroscience
Conditional deletion of the Pten gene in cerebellar Purkinje cells (PCs) leads to cellular hypertrophy, neurodegeneration, and autistic-like behaviors in adult mice. This study explores the impact of Ptendeficiency on PCs and associated mouse behaviors during postnatal development. We investigated how Pten deficiency influences PC dendritic growth and early mouse motor and social behaviors. Our findings reveal that Pten deficiency disrupts postnatal dendritic development in PCs by increasing mTORC1 activation and reducing AMPK phosphorylation. This alteration results in motor deficits and gender-specific variations in social and non-social behaviors among Pten-deficient and control mice. Additionally, Ptendeficiency modifies the volume of mitochondria and lysosomes in developing dendrites, observable in vivo. Remarkably, ex-vivo treatments with AICAR (an AMPK activator) or Torin1 (an mTORC1 inhibitor) can restore normal dendritic organelle volume in mutant cells. These results suggest that Pten deficiency affects dendritic development by disrupting key signaling pathways that regulate metabolic balance during postnatal growth. Consequently, these pathological changes in Pten-deficient PCs lead to variable motor and behavioral alterations, influenced by postnatal age and sex.
Poster Presentation: Wednesday, April 23, 1:30 – 3 p.m.
