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Richard D. Dey, PhD

Chairman, Professor (ret.)

 Richard D. Dey



Neurobiology & Anatomy (former); Blanchette Rockefeller Neurosciences Institute 

Graduate Training

Ph.D., Anatomy, Michigan State University


NIH Individual Postdoctoral Fellow, Departments of Internal Medicine and Pharmacology, University of Texas Health Science Center at Dallas

Research Interest

The research in my lab focuses on neuroanatomical organization and embryological development of airway innervation, examining interconnections between airway neurons and airway structures (smooth muscle, blood vessels, glands, epithelium), and on determining neuronal responses to inhaled irritants. Different types of nerves including sensory, sympathetic, parasympathetic, and nonadrenergic/noncholinergic supply the trachea and bronchi. Released neurotransmitters mediate bronchial and vascular smooth muscle tone, mucous secretion, coughing, and breathing patterns in normal conditions and produce defensive responses after inhalation of irritant substances. Airway nerves may also contribute to lung diseases like asthma, chronic cough, and chronic obstructive pulmonary disease (COPD). Although there is considerable information regarding the actions of neurotransmitters, such as acetylcholine, norepinephrine, vasoactive intestinal peptide, substance P and nitric oxide, the mechanisms through which airway nerves contribute to asthma and other airway diseases is not clear.  Regulatory molecules like neurotrophins may be critical in altering neurotransmitter expression and airway innervation leading to asthma and airway inflammation.  Combinations of immunocytochemical, molecular biological, neurophysiological and pharmacological approaches are used to investigate pulmonary neural responses to inhaled irritants such as ozone, a photochemical environmental pollutant, and toluene diisocyanate, a catalyst associated with occupational asthma used in manufacturing polymers. 

Lab Personnel










  • Wu ZX, Hunter DD, Kish VL, Benders KM, Batchelor TP, Dey RD. Prenatal and early, but not late, postnatal exposure of mice to sidestream tobacco smoke increases airway hyperresponsiveness later in life. Environ Health Perspect (2009), 117(9):1434-40.
  • Nadeem A, Ponnoth DS, Ansari HR, Batchelor TP, Dey RD, Ledent C, Mustafa SJ. A2A adenosine receptor deficiency leads to impaired tracheal relaxation via NADPH oxidase pathway in allergic miceJ Pharmacol Exp Ther. (2009), 330(1):99-108.


  • Wu ZX, BarkerJS, Batchelor TP, Dey RD. Interleukin (IL)-1 regulates ozone-enhanced tracheal smooth muscle responsiveness by increasing substance P (SP) production in intrinsic airway neurons of ferret. Respir Physiol Neurobiol (2008), 164(3):300-11.