The image above is of the dorsal subventricular zone in a young mouse (postnatal day 18) showing expression of Endothelin-1 (green), Glial fibrillary acidic protein (GFAP, red) and cell nuclei (DAPI, blue). GFAP+ astrocytes express the Endothelin-1 protein.
Work in the Gallo Laboratory is focused on postnatal neural development and the impact of injury and disease on development and regeneration of neurons and glia. The lab uses a multidisciplinary approach to study postnatal development under normal physiological and pathological conditions. We are particularly interested in identifying cellular signals and molecular pathways that regulate development of neurons and glia in white matter, cortex and cerebellum, and in the possibility of translating our understanding of developmental mechanisms to cell repair and regeneration after injury of the brain. To reach these goals, the Gallo Laboratory is using integrated molecular, cellular, anatomical, electrophysiological and behavioral approaches applied to animal models of brain injury and disease, including perinatal brain injury (perinatal hypoxia and hyperoxia/oxidative stress), Down syndrome and multiple sclerosis.
We have been particularly interested in investigating the neural progenitor cell response to injury/disease, and in identifying novel molecular mechanisms that can enhance neural repair and functional recovery. More recently, we have also integrated studies in mouse models — which offer the advantage of direct genetic manipulation of specific signaling pathways — with investigation in large mammals (piglets), which display brain anatomy and cellular structure practically identical to humans. These studies are performed in collaboration with Nobuyuki Ishibashi, MD, at Children’s National Hospital. We have established animal models of perinatal brain injury that occurs in very low birth weight (VLBW) infants born prematurely. These models reproduce gray and white matter (WM) alterations observed in brains of premature infants. We are now focused on the identification of the cellular and physiological mechanisms that underlie cognitive, behavioral and motor abnormalities found in premature infants, with a particular focus on cerebellum and its functions. Ongoing studies integrate analysis in animal models and post-mortem human brains.