Spontaneous activity is a hallmark feature of the developing brain, and it is known to play a fundamental role in the establishment of brain circuits by creating patterns of neuronal coactivation. Highly synchronized and stereotyped, this form of activity responds rapidly to brain insults, serving as a sensitive indicator of underlying circuit reorganization.

By monitoring real-time calcium transients in vivo, we aim to understand how this highly stereotyped and rhythmic activity influences the formation of neuro-glial networks and OPC function during development and in the context of brain tumors (a disease of dysregulated development).

Oligodendrocyte precursor cells (OPCs) play a key role in circuit development by generating myelinating oligodendrocytes. Although myelination is known to be modulated by experience-dependent activity in the adult, the influence of developmental spontaneous activity in OPC proliferation and differentiation remains unknown. Furthermore, beyond their canonical role in myelination, OPCs have been getting increasing attention for performing myelin-independent functions during development. 

Our goal is to disentangle the role of spontaneous activity in OPC development and function.

In brain cancer, malignant cells often co-opt mechanisms of neural development to achieve brain invasion and alter neural function. However, whether developmental spontaneous activity is disrupted by cancer cells remains unexplored, partly due to the scarcity of available syngeneic models of pediatric brain cancer. 

In the lab, we set up a model of early brain cancer by injecting neurotropic malignant cells into the cortex of newborn mice expressing a genetically encoded calcium indicator in glutamatergic neurons. In vivo calcium imaging is used to assess neuronal activity throughout the course of the disease.