Dayna L. Averitt, Ph.D.

Dayna Averitt portrait

Assistant Professor and Vivarium Director

Office: GRB 113
Office Phone: 940-898-2708
Lab Phone: 940-898-2529
Fax: 940-898-2382
Email: DAveritt@twu.edu 

Primary Teaching Areas: Mammalian Physiology, Pathophysiology, Biology of Aging, Biology Seminar

Research Interests: Sensory Neuroscience; Pain Mechanisms and Analgesia

Education

Position/Degree Date Institution Field
Principal Investigator   2011-2013   US Army Institute of Surgical Research   Pain Management
Postdoctoral 2008-2011 UTHSC San Antonio Physiology
M.S. 2009-2011 UTHSC San Antonio Clinical Investigation
Ph.D. 2003-2008 Georgia State University Biological Sciences
M.S. 2003-2005 Georgia State University Biology
B.A. 1999-2001 University of Texas, Austin Psychology

Major Academic/Research Interests

Research in the Averitt Lab focuses on the neurobiology of pain and analgesia. Ongoing research topics include (1) examining the mechanisms by which inflammatory mediators initiate and maintain pain sensitivity, (2) examining the neurophysiological substrate underlying sex differences in pain and analgesia, and (3) translational research to support optimizing pain associated with burn injury.

Projects

Sexually Dimorphic Effects of Serotonin on Pain: Many chronic pain conditions occur predominantly (migraine, fibromyalgia) or only (endometriosis, vulvodynia) in women. There is evidence that pain conditions are exacerbated by hormone fluctuations, yet the effect hormones have on pain mechanisms remains unclear. The peripheral serotonin (5HT) system represents one pain mechanism that may be modulated by hormones. Our previous research indicates that 5HT sensitizes sensory neurons expressing the transient receptor potential V1 (TRPV1) ion channel to send ‘pain’ signals to the brain. No studies have examined whether hormones modulate serotonergic potentiation of TRPV1-expressing sensory neurons. Current research in the Averitt lab indicates that 5HT evokes greater pain in female rodents, with the greatest sensitivity occurring when hormone levels are highest, although our most current research is indicating that this appears to be dependent on pain modality. The overall goal of this line of research in the Averitt lab is to identify whether hormones modulate the ‘pain-producing’ effects of 5HT on the TRPV1 population of sensory neurons and what interactions between hormones, 5HT receptors, and the TRPV1 ion channel occur. We postulate that this mechanism may underlie the increased prevalence some pain disorders in women. We are examining this mechanism utilizing pre-clinical behavioral studies, sensory neuron cultures, and translational methodologies. 

We also have ongoing collaborative projects (1) with the NIH and the Army examining the analgesic effects of the TRPV1 agonist resiniferatoxin on burn pain and preemptive anesthetics on neuropathic pain, (2) with Dr. Camelia Maier (TWU) discovering potential analgesic properties of novel plant extracts, and (3) with Dr. Michael Bergel (TWU) examining the epigenetics of chronic pain and morphine analgesia.

Select Publications

  1. Salas, M.M., Clifford, J.L., Hayden, J.R., Iadarola, M.J., Averitt, D.L. (2016) Local resiniferatoxin induces long-lasting analgesia in a rat model of full thickness thermal injury. Pain Medicine, doi: 10.1093/pm/pnw260.
  2. Clifford, J.L., Mares, A., Hansen, J., Averitt, D.L. (2015) Preemptive perineural bupivacaine attenuates the maintenance of mechanical and cold allodynia in a rat spinal nerve ligation model. BMC Anesthesiology, 15: 135. doi: 10.1186/s12871-015-0113-x.
  3. Nyland, J.E., McLean, S.A., Averitt, D.L. (2015) Prior stress exposure increases pain behaviors in a rat model of full thickness thermal injury. Burns, 41(8): 1796-1804.
  4. Clifford, J.L., Fowler, M., Hansen, J.J., Cheppudira, B.P., Nyland, J.E., Salas, M.M., McGhee, L.L., Petz, L.N., Loyd, D.R. (2014) State of the Science Review: Advances in pain management in wounded service members over a decade at war. Journal of Trauma and Acute Care Surgery, 77(3 Suppl 2): S228-236.
  5. Fowler, M., Clifford, J.L., Garza, T.H., Slater, T.M., Arizpe, H.M., Novak, J., Petz, L.M. and Loyd, D.R. (2014) A rat model of full thickness thermal injury characterized by thermal hyperalgesia, mechanical allodynia, pronociceptive peptide release and tramadol analgesia. Burns, 40(4): 759-771.
  6. Loyd, D.R. and Murphy, A.Z. (2014) The Neuroanatomy of Sexual Dimorphism in Opioid Analgesia. Invited Review in a Special Issue on The Importance of Sex in the Etiology, Presentation, and Treatment of Neurological Disorders. Experimental Neurology, 259C: 57-63.
  7. Cheppudira, B.P., Greer, A., Mares, A., Fowler, M., McGhee, L., Devore, D., Petz, L., Loyd, D.R., Clifford, J.L. (2013) Curcumin: A Novel Therapeutic for Burn Pain and Wound Healing. Expert Opinion on Investigational Drugs, 22(10): 1295-303.
  8. Loyd, D.R., Henry, M.A. and Hargreaves, K.M. (2013) Serotonergic Neuromodulation of Peripheral Nociceptors. Invited Review in a Special Issue on Signal Processing in Peripheral Sensory Organs. Seminars in Cell and Developmental Biology, 24: 51-57.
  9. Loyd, D.R., Sun, X.X., Locke, E., Salas, M.M., Henry, M.A. and Hargreaves, K.M. (2012) Sex differences in serotonin enhancement of capsaicin-evoked calcitonin gene-related peptide release from human dental pulp. PAIN, 153: 2061-2067.
  10. Loyd, D.R., Chen, P.B. and Hargreaves, K.M. (2012) Antihyperalgesic effects of anti-serotonergic compounds on serotonin- and capsaicin-evoked thermal hyperalgesia in the rat. Neuroscience, 203: 207-215.
  11. Loyd, D.R., Weiss, G., Henry, M.A., Hargreaves, K.M. (2011) Serotonin increases the functional activity of capsaicin-sensitive rat trigeminal nociceptors via peripheral serotonin receptors. PAIN, 152(10): 2267-2276.

Courses and Teaching Responsibilities

  • ZOOL 4243 Mammalian Physiology: Basic processes and functions of organs and organ systems in the mammalian body; consideration of human and other physiological functions.  
  • ZOOL 3313 Biology of Aging: Physiological, anatomical and neurological changes occurring with the aging process. 
  • BIOL 4344 Pathophysiology: Mechanisms responsible for improper functioning of the adult human body in disease states, building upon existing knowledge of normal functioning. Emphasis on the understanding of dysfunction at the cellular level and how dysfunction leads to pathological states. 
  • BIOL 4681 Biology Seminar: Student presentations based on summarizing and critiquing current peer-reviewed research literature on a topic of choice.
  • Dr. Averitt also mentors undergraduate and graduate students in research.