The following faculty members are faculty who may serve on dissertation and thesis committees. Please click on the name of each member to learn more about them.
Program Affiliations: Physiology, Sarver Heart Center, Physiological Sciences
Website and Publications: Sarver Heart Center Profile
Contact Information: (520) 621-5485, zcohen@email.arizona.edu
Research Interests: Platelets, Immunobiology
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Program Affiliations: Physiology, Bio5 Institute, Physiological Sciences
Website and Publications:
Contact Information: (520) 621-3104, crankin@u.arizona.edu
Research Interests: Physiology/Teaching Workshop
Program Affiliations: Neuroscience, Bio5 Institute, Physiological Sciences
Website and Publications:
Contact Information: (520) 626-2006, ssherman@u.arizona.edu
Research Interests: Neuroscience: Parkinsons, PD, Basal Ganglia, Potassium Channels, Cell-based Therapy
- Our basic research program explores cell-based and gene-based strategies for the treatment of movement disorders including Parkinson’s disease. We are exploring the possibility of using genetic alteration of voltage-gated potassium channels to modify specific pathways in the basal ganglia. Our current project utilizes primary neuronal culture coupled with patch-clamp electrophysiology to measure the electrical activity in isolated basal ganglia neurons. We have developed viral gene-transfer vectors utilizing cell type specific promoters to modify potassium channel expression in these neurons. We are presently studying the effect of these gene-transfer agents on the electrical activity in vitro.
A second project seeks to develop a cell-based therapy for Parkinson’s disease. We have found that retinal pigment epithelial cells, normally found in the retina, can provide a neuroprotective effect on degenerating neurons that are involved in Parkinson’s disease. These cells could provide an easily transplantable source for a cell-based therapy.
Program Affiliations: Physiology, Physiological Sciences
Website and Publications:
Contact Information: (520) 621-2795, stanescu@email.arizona.edu
Research Interests: Physiology/Director TA's
Program Affiliations: Pharmacology, Bio5 Institute, Physiological Sciences
Website and Publications:
Contact Information: (520) 626-7801, vanderah@email.arizona.edu
Research Interests: Neuroscience - Pharmacology of acute and chronic models of pain; endogenous opioid systems; sensory neural systems; opioid tolerance; antiociceptive synergy between cannabinoids and opioids
- Cholecystokinin and receptors as therapeutic targets
- Recently we have demonstrated both behaviorally and by using microdialysis that the neuropeptide, cholecystokinin (CCK), promotes neuropathic pain by activating descending projection neurons that originate in a region of the brainstem known as the rostral ventromedial medulla (RVM). An increase in the level of release of CCK in the RVM is evident after nerve injury as well as after repeated administration of morphine. This enhanced activity of CCK mediated activation of RVM neurons maintains neuropathic pain, and is also important in the development of analgesic tolerance to spinal morphine after chronic morphine treatment. Thus, CCK antagonism may potentiate morphine antinociception under conditions of neuropathy or chronic morphine. Our collaboration with Dr. Victor Hruby in the Department of Chemistry aims to identify novel molecules that have bifunctional opioid agonist and CCK antagonist actions as prototypes for analgesics for chronic, neuropathic pain.
- Sensory neuron function and GPCR
- Sensory nerves that propagate painful signals are highly specialized nerves called nociceptors. The activation of these nociceptors includes noxious stimuli like heat, cold, pressure and chemicals. The excitability of these nociceptors is modulated by a number of G-protein coupled receptors (GPCR) both at their central termini in the spinal cord and in their peripheral nerve endings, which contain one or more specialized cation channels that are activated by specific noxious input. We are interested in how GPCR modulate the activity of these specialized cation channels, in particular the vanilloid receptors that mediate noxious heat, to regulate sensory thresholds in acute and chronic pain conditions