BECOMING A NEW NEURON IN THE INJURED BRAIN: LESSONS FROM ADULT NEUROGENESIS

Traumatic brain injury (TBI) is one of the most prevalent neurological conditions, yet no effective treatment exists. Interestingly, neural stem cells (NSCs) in the adult brain respond to TBI by increasing their proliferation. The neuronal progeny is recruited to the injury site, but there, they fail to survive and integrate. Curiously, the impact of NSC activation on the neurogenic axis remains elusive. Using mice, we observed an increase in newborn neurons in the olfactory bulb (OB), the physiological target of adult subventricular zone (SVZ) neurogenesis in rodents, upon primary visual cortex (V1) damage. This increase in cell number is accompanied by an increase in neuronal activity in olfactory-related regions 2.5 months post-injury. Other visual impairments (dark rearing and eye enucleation) or injury in a non-sensory region do not lead to such an increase in newborn cells in the OB, pointing to the combined need of both injury signals and enhanced olfactory demand for effective neuronal maturation. In fact, mice subjected to TBI in V1 show increased sniffing behavior. This suggests an intermodal attention shift from vision to olfaction during exploration, and current work explores the activation state of the nasal epithelium. Altogether, our work provides new insights into the brain’s adaptive response to a focal injury, revealing a significant degree of plasticity in remote sensory circuits, and indicates a role of adult neurogenesis in sensory compensation after injury. Understanding more about the injury-induced neurogenesis may provide a foundation for the design of regenerative strategies to treat neurological conditions.