John
Cameron John
Cameron
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Department: |
Biological Sciences, Professor |
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Office: |
Science Center 388 |
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Research Interests: |
Comparative Animal Physiology/Cardiac Electrophysiology |
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Fall Courses: |
My research is concerned with the cardiovascular physiology of ectothermic ('cold-blooded') animals; in particular, I am interested in the ionic mechanisms that promote tolerance of low-oxygen and low temperature conditions in vertebrates.
Over the past few years, my students and I have been using microelectrodes to investigate the cellular electrophysiology of isolated cardiac muscle tissue and individual heart cells. We are particularly interested in the cellular mechanisms underlying tolerance to hypoxia and hypothermia in ectothermic vertebrates. Many fish and amphibians, for example, can withstand prolonged exposure to environmental conditions of cold and low oxygen that would prove lethal to mammals, or even other fish. One difference between tolerant species and those sensitive to hypoxia and hypothermia may lie at the level of specific ion channels in the cell membrane of essential organs. Tolerant tissues might respond with a reduction in the density and/or rate of activation of such channels, thus reducing membrane permeability and compensating for decreased ATP-dependent ion pumping capacity in the face of low oxygen or cold environments.
Student Projects:
In the coming years, I expect that there will be numerous opportunities for a student to initiate projects in line with her own interests. We are currently using intracellular and single-channel, patch-clamp recording techniques to monitor the activity of individual ion channels (ie., K+, Ca++, etc.) on the surface of living heart muscle cells.
Following are some of the more recently published papers from this lab that have benefited from the contributions of student coauthors(*). Many of these papers were presented by students at national conferences:
Papers:
Chen, J*, Zhu, J*, Wilson, I* and Cameron, JS. Cardioprotective effects of KATP channel activation during hypoxia in goldfish, Carassius auratus. J. Exp. Biol. 208:2765-2772, 2005.
Cameron, JS, Hoffmann, KE*, Zia, C*, Hemmett, HM*, Kronsteiner, A* and Lee, CM*. A role for nitric oxide in hypoxia-induced activation of cardiac KATP channels in goldfish. J. Exp. Biol. 206:4057-4065, 2003.
Coyne, MD, Kim, CS, Cameron, JS and Gwathmey, JK. Effects of temperature and calcium availability on ventricular myocardium from rainbow trout. Am. J. Physiol. 278:R1535-1544, 2000.
Ganim RB*, Peckol EL*, Larkin J*, Ruchhoeft ML and Cameron JS. ATP-sensitive K+ channels in cardiac muscle from cold-acclimated goldfish: Characterization and altered response to ATP. Comp. Biochem. Physiol. 119A:395-401, 1998.
Sodder VH, Bowie LD* and Cameron JS. Trypsin alters ATP-sensitivity of KATP channels in control and hypertrophied myocytes. Eur. J. Pharmacol. 315:115-118, 1996.
Abstracts/Presentations:
Park, S.D.* and Cameron, J.S. Role of PKG in the hypoxia-induced activation of cardiac KATP channels in goldfish. FASEB Journal 21(5):A593, 2007.
Zhu, J.* Wilson, I.*, Gannon, J.M.* and Cameron, J.S. Cardioprotective activation of cardiac KATP channels during hypoxia in goldfish. FASEB Journal 18(4): A367, 2004.
Zia, C.*, Hemmett, H.M.*, Kronsteiner, A., Moglia, S.M.*, Tsurumi, N.* and Cameron, J.S. Role of nitric oxide in hypoxia-induced activation of cardiac KATP channels in goldfish. Am. Zool. 41(6):1636, 2001.
Cameron, J.S., Szucsik, A.M., Reinker, L.N., Vaurio, R.G. and Gwathmey, J.K. The effects of hypoxia on ATP-sensitive K+ channels in cardiac muscle of goldfish. Proceedings of the Society for Experimental Biology, 2000.
Holzman, JL* and Cameron JS. Lidocaine blocks the ATP-sensitive potassium channel in cardiac muscle from control and spontaneously hypertensive rats. FASEB Journal 12:, 1998.
Kim CS*, Coyne MD, Cameron JS. and Gwathmey JK. Characterization of calcium currents in ventricular myocytes of rainbow trout at different temperatures. Biophys. J., 1998.
Cameron JS, Kibler K.A*, Berry H*, Barron DN* and Sodder VH. Nitric oxide activates ATP-sensitive potassium channels in hypertrophied ventricular myocytes. FASEB Journal 10:A65, 1996.
