My lab is focused upon defining neurochemical, structural and functional impairments attributable to hypoxic insults arising from either intrinsic physiologic or extrinsic environmental conditions. We established that postnatally occurring hypoxic insults induce increased sequestering of dopamine within the vesicular monoamine transporter. We also found increased levels of Dopamine D1 receptors and apoptosis within the substantia nigra pars compacta and ventral tegmental areas. Concomitant behavioral traits of enhanced responsiveness to novelty, diminished working memory, and hyperactivity coupled with enhanced somnolence provided new insight into symptoms and other manifestations of perturbed dopaminergic function. Our ongoing studies are now characterizing neural structure and function in a cohort of children, aged 10-14 years, who were prematurely born and experienced hypoxic insults.

Concurrent and synergistic efforts focus upon characterizing changes in neural structure and function emerging following extremely high altitude, high speed flight, such as that experienced by tactical aviators and astronauts. Such aviation is accompanied by ever-present risks of environmental hypoxia, venous gas emboli and decompression sickness. Protection against those hazards is conferred by fractional inspired oxygen (FiO2) concentrations of 60-100%. Our ongoing studies reveal that 100% FiO2 leads to a rapid and sustained reduction in cerebral perfusion. Corresponding changes in cortical electroencephalographic alpha power across central, parietal and temporal cortical regions, as well as enhanced cognitive performance, emerge during 100% FiO2. This suggests that oxygen-induced reductions in brain perfusion trigger cortical arousal mechanisms, perhaps representing a fight-or-flight response.