
Professor of Physiology
Dr. Nattie received his B.A. from Dartmouth College in 1966, his B.M.S. from Dartmouth Medical School in 1968, and his M.D. from Harvard Medical School in 1971. After a year as a medical intern at the Peter Bent Brigham Hospital in Boston, he returned to Dartmouth Medical School as a postdoctoral fellow in 1972. In 1975 he was appointed to the faculty as Assistant Professor and since 1985 he has been a Professor of Physiology.
His research focuses on the role of the brainstem in the regulation of breathing and blood pressure. Specifically, he is interested in central chemoreception, in how, where, and why the brain can sense changes in CO2 and/or pH and, as a result, effect changes in breathing and sympathetic nervous system outflow. These CO2 sensing functions appear to be located at many sites within in the brainstem. The mechanism of sensing CO2 may involve a specific pH or CO2 sensitive membrane receptor or it may involve effects on some membrane or synaptic function in an indirect manner. Dr. Nattie's lab is also pursuing the role of monoamine neurons (serotonergic, catcholaminergic) in the control of breathing, blood pressure and sleep.
Related to respiratory control is an observation that destruction of a small number of neurons in one specific region of the brainstem has very dramatic effects on breathing. Destruction of the region labeled the retrotrapezoid nucleus in the ventrolateral medulla results in cessation of breathing (apnea) and loss of CO2 responsiveness without effects on blood pressure. Destruction of nearby neurons in the subretrofacial region of the ventrolateral medulla results in decreased blood pressure with but minor effects on breathing. These adjacent regions of the ventrolateral medulla appear to be quite important in the control of breathing and blood pressure. In addition to study of central chemoreception, Dr. Nattie's lab is evaluating the role of these newly discovered and important ventrolateral medullary control regions with emphasis on effects in unanesthetised animals. These studies have evolved into an examination in a newborn piglet model of the role in the control of breathing of ventral medullary neuron groups that may be homologous with brainstem regions described as abnormal in SIDS victims.
Taylor NC, Li A, Nattie EE. Ventilatory effects of muscimol microdialysis into the rostral medullary raphe region of conscious rats. Respir Physiol Neurobiol. 2005 Dec 7; [Epub ahead of print]Li A, Nattie EE. Catecholamine neurons in rats modulate sleep, breathing, central chemoreception, and breathing variability. J Physiol. 2005 Oct 27; [Epub ahead of print]
Nattie, E. E., and Li, A. SP-SAP lesion of neurons with NK1 receptors in one chemoreceptor site in rat decrease ventilation and chemosensitivity. J. Physiol. (London) 544.2: 603-616, 2002.
Nattie, E. E., and Li, A. CO2 dialysis in nucleus tractus solitarius region of rat increases ventilation in sleep and wakefulness. J. Appl. Physiol. 92: 2119-2130, 2002.