The University of Arizona


Jill Roberts

jmr1@email.arizona.edu

B.S. in Molecular and Cellular Biology, University of Arizona


Lab
Frank Porreca

Lab Website
www.pharmacology.arizona.edu/profiles/porreca-f_profile.html

Rotation Labs
Frank Porreca, Naomi Rance, Josephine Lai

Minor
Pharmacology

Research Summary
Pathological pain is characterized by an amplified response to acute pain or to normally innocuous stimuli and has long been thought to be the result of dysfunctional neuronal activity.  While neuronal function is indeed altered, there is significant evidence that non-neuronal cells play a critical role in the initiation and maintenance of chronic pain.  These cells are glia; specifically, microglia and astrocytes.  The activation of glial cells in the spinal cord has been shown to cause exaggerated pain states.  Our knowledge of the mechanisms that drive enhanced pain states has grown considerably over the past few decades.  We now understand that chronic pain states depend on sensitization of the spinal cord, activation of nociceptive pathways projecting to brainstem sites, and on activation of descending pain-facilitatory systems from the brainstem.  My studies investigate the possibility that inflammation results in the activation of glial cells within the brainstem which in turn activates descending facilitation.

 

 
Graduate Program in Neuroscience
1548 E. Drachman St.
P.O. Box 210476
Tucson, AZ 85721
(520) 621-8380