Gregory O. Dussor PhD

Assistant Professor, Pharmacology

Life Sciences - North 648
P.O. Box 245050
Tucson, AZ 85724-5050

Phone: 
(520) 626-6726
Email Address: 
dussorg@email.arizona.edu
Education: 
  • The University of Texas Health Science Center, San Antonio, 2002 (PhD)
Honors & Awards: 
  • Recipient of Future Leaders in Pain Research Award from the American Pain Society, 2008
  • Associate Editor, PAIN
  • Vernon and Virginia Furrow Award for Excellence in Graduate Student Education 2011
Major Areas of Research Interest: 
  • Neurology of pain
  • Ion channels contributing to nociceptive tansmission
  • Pathophysioloy  of headache disorders
Selected Publications: 

http://msrp.medicine.arizona.edu/sites/all/libraries/fckeditor/editor/sk...); background-position: 0px -544px;" alt="" />Edelmayer RM, Le LN, Yan J, Wei, X, Nassini R, Materazzi S, Preti D, Appendino G, Geppetti P, Dodick D, Vanderah TW, Porreca F, Dussor G.(2012) Activation of TRPA1 on Dural Afferents: A Potential Mechanism of Headache Pain. Pain. In press.

Patwardhan A, Edelmayer R, Annabi E, Price T, Malan P, Dussor G. (2012) Receptor Specificity Defines Algogenic Properties of Propofol and Fospropofol.Anesth Analg. In press.

Yan J, Melemedjian OK, Price TJ, Dussor G. (2012) Sensitization of dural afferents underlies migraine-related behavior following meningeal application of interleukin-6 (IL-6). Mol Pain. Jan 24;8:6.

Tillu DV, Melemedjian OK, Asiedu MN, Qu N, De Felice M, Dussor G, Price TJ (2012) Resveratrol engages AMPK to attenuate ERK and mTOR signaling in sensory neurons and inhibits incision-induced acute and chronic pain. Mol Pain. Jan 23;8:5.

Wei X, Edelmayer RM, Yan J, Dussor G (2011) Activation of TRPV4 on dural afferents produces headache-related behavior in a preclinical rat model. Cephalalgia. Dec;31(16):1595-600

Melemedjian OK, Asiedu MN, Tillu DV, Sanoja R, Yan, J, Lark A, Khoutorsky A, Johnson J, Peebles KA, Lepow T, Sonenberg N, Dussor G, Price TJ. (2011) Targeting adenosine monophosphate-activated protein kinase (AMPK) in preclinical models reveals a potential mechanism for the treatment of neuropathic pain. Molecular Pain. Sept 21; 7:70.

De Felice M, Sanoja R, Wang R, Vera-Portocarrero L, Oyarzo J, King T, Ossipov MH, Vanderah TW, Lai J, Dussor GO, Fields HL, Price TJ, Porreca F. (2011) Engagement of descending inhibition from the rostral ventromedial medulla protects against chronic neuropathic pain. Pain. Dec;152(12):2701-9.

Fioravanti B, Kasasbeh A, Edelmayer R, Skinner DP Jr, Hartings JA, Burklund RD, De Felice M, French ED, Dussor GO, Dodick DW, Porreca F, Vanderah TW. (2011) Evaluation of cutaneous allodynia following induction of cortical spreading depression in freely moving rats. Cephalalgia. Jul;31(10):1090-100.

Yan J, Edelmayer RM, Wei, X, De Felice M, Porreca F, Dussor G. (2011) Dural afferents express acid-sensing ion channels: A role for decreased meningeal pH in migraine headache. Pain. Jan;152(1):106-13.

Melemedjian OK, Asiedu MN, Tillu DV, Peebles KA, Yan J, Ertz N, Dussor GO, Price TJ. (2010) IL-6- and NGF-induced rapid control of protein synthesis and nociceptive plasticity via convergent signaling to the eIF4F complex. J Neurosci.2010 Nov 10;30(45):15113-23.

 

Research Activities: 

The senses of touch, taste, and hearing are thought to be signaled by sensory neurons that innervate specialized structures (e.g. Meissner’s complex, taste receptor cells, and hair cells of the inner ear). In contrast, pain is likely signaled through sensory neurons that innervate their respective tissues with free nerve endings. Questions that remain unanswered are whether nociceptors (pain-sensing neurons) are activated directly by noxious stimuli or whether the innervated tissue itself acts as the receptive structure. Current research in the laboratory is focused on determining the molecular mechanisms by which nociceptors are activated in the skin. Specifically, the laboratory is interested in a sub-population of primary sensory neurons that express the mas-related gene receptor D (MrgD) and project selectively to the stratum granulosum of the epidermis. By using mice genetically engineered to express green fluorescent protein (GFP) in all neurons containing the MrgD receptor, we can ask specific questions about these neurons that attempt to uncover the relevant stimuli for this sub-population of nociceptors.

In addition, the laboratory has recently begun to study migraine headache. While migraine headache was traditionally thought to be a disease of vascular origin, it has become increasingly apparent that it is also a disorder of the nervous system. Thus, it represents the most common neurological condition affecting up to 30% of women and 10% of men at some point in their lifetime. Despite the widespread prevalence of migraine, relatively little is known about the pathophysiological changes that lead to the development of migraine. Current research in the laboratory is focused on the nociceptors that innervate the cranial meninges and play an important role in the pathogenesis of migraine headache. By applying retrograde tracers to the meninges, we can identify trigeminal neurons in culture that innervate the dura and begin to learn more about what conditions activate these nociceptors leading to the sensation of headache. We can also examine how the properties of these neurons change in animal models of migraine headache and whether these changes can be reversed by novel anti-migraine treatments.

The principle methods utilized by the laboratory to answer these questions are patch-clamp electrophysiology and ratiometric calcium imaging on isolated sensory neurons in primary culture as well as whole animal behavioral models of cutaneous pain and migraine.

Sponsored Research Through MSRP: 
  • Nicholas Jacobson (MSRP 2012) "Location and plasticity of the AIS in pain-signaling neurons"
NIH Undergraduate Diversity Program: 

2012  Priscilla Valenzuela  Nogales High School

NIH High School Student Research Program: 

-Priscilla Valenzuela, Nogales High School, 2012

-Daline Do, 2013

-Kimberly Henderson, 2013

Last Updated: 
March 3, 2014