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Michael J. Decker, PhD
Associate Professor
PhD, Anatomy/Neuroscience, Case Western Reserve University School of Medicine
View Curriculum Vitae (pdf)

Mailing Address:
Robbins E510
Cleveland , OH 44106
Phone: 216-368-2467
Fax: 216-368-5586
ORCiD:0000-0003-4792-4692
michael.decker@case.edu

Research Interests

Defining mechanisms affecting neural structure & function during exposure to extremely high altitude. 

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.

Featured Publications
  • Decker M.J., Jones K.A., Solomon I.G., Keating G.L., Rye D.B.  Postnatal Hypoxia evokes persistent changes within the male rat’s dopaminergic system. Sleep Breath. 2017 Aug 22. doi: 10.1007/s11325-017-1558-6.
     
    Decker, M.J., Jones, K.A., Solomon, I.G., Keating, G.L., Rye, D.B. Reduced extracellular dopamine and increased responsiveness to novelty: neurochemical and behavioral sequelae of intermittent hypoxia. SLEEP 2005;28(2): 169-176.  Accompanying Editorial SLEEP 28;2:165-167
     
    Decker, M.J., Hue, G.E., Caudle, W.M., Miller, G.W., Keating, G.L., Rye, D.B. Episodic neonatal hypoxia evokes executive dysfunction and regionally specific alterations in markers of dopamine signaling. Neuroscience 2003;117(2):417-425.
     
    Beall, C.M., Decker, M.J., Brittenham, G.M., Kushner, I., Gebremedhin, A., Strohl, K.P. An Ethiopian pattern of human adaptation to high-altitude hypoxia. Proceedings of the National Academy of Sciences of the United States of America 2002  Dec 24;99(26): 17215-17218.
     
    Beall, C.M., Almasy, L.A., Blangero, J., Williams-Blangero, S., Brittenham, G.M., Strohl, K.P., Decker, M.J., Vargas, E., Villena, M., Soria, R., Alarcon, A.M., Gonzales, C. Percent of oxygen saturation of arterial hemoglobin among Bolivian Aymara at 3900-4000m.  American Journal of Physical Anthropology 1999;108(1): 41-51.
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