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Heat Acclimation, Heat Exposure and Thirst

Principal Investigator: Dr. Christopher C. Barney

Research in my laboratory is focused on regulatory physiology, in particular on the way the cardiovascular, water balance and thermoregulatory systems interact to maintain homeostasis in response to environmental conditions. Previously, undergraduate students in my lab have determined that repeated intermittent exposure to a hot environment alters water intake and kidney function in rats, leading to improvements in rehydration following thermal dehydration. These altered responses are indicative of the ability of homeotherms to adjust to different environmental conditions, such as may occur with global warming. During the summer of 2010, we will continue working on this project in order to determine what physiological mechanisms may be responsible for these changes. Undergraduate students will utilize rats in experiments in which water, NaCl, and sucrose intakes and urine output and electrolyte concentrations are determined using various exposure protocols. Additional experiments quantifying blood indicators of dehydration and overhydration will be carried out in order to determine how repeated exposure to a hot environment alters the osmotic and volemic controls of water intake and urine output. Other potential experiments include using immunohistochemistry to determine changes in water balance proteins in various brain regions during and following intermittent heat exposure. Students will analyze the primary literature in this field, develop hypotheses, design experiments, learn statistical analysis, and further develop their skills at scientific communication.

Investigating QUIS Neurotixicity in the Rat Hippocampus, Striatum and Substantia Nigra

Dr. Christopher C. Barney and Dr. Leah Chase, Departments of Biology and Chemistry

This project is focused on the in vivo function of a neurotransmitter transport system, System xc-, that 1) provides neurons and glia with the precursors required to synthesize glutathione, an endogenous antioxidant, and 2) regulates the extracellular level of glutamate in several areas of the brain. Previous in vitro studies performed in rat hippocampal slices have demonstrated that System xc- is also a transport system for a few select neurotoxins, including quisqualic acid (QUIS), that when ingested, lead to various motor and behavioral deficits. These studies provided evidence for a model for QUIS neurotoxicity in which the neurotoxin is initially sequestered into glial cells in the brain by System xc- and then is subsequently released from the cell by System xc- during exposure to endogenous cystine. This process results in the overactivation of receptors located on surrounding neurons and neuronal death. Recently, System xc- was also localized to the striatum, an integral part of the motor circuitry of the brain, suggesting that neurotoxins may exert their neurotoxic action in this region of the brain. It has been well established that loss of proper functioning of the basal ganglia/striatal circuitry leads to profound motor defects, most notably characterized by the pathogenesis associated with Parkinsonís Disease. The specific aims of this study are 1) to use microdialysis combined with high performance chromatography to test aspects of the aforementioned model of QUIS neurotoxicity in the hippocampus, striatum, and substantia nigra of the rat and 2) to correlate these neurochemical studies with parallel studies of animal behavior and postmortem neurotoxicity analysis following injection of QUIS into these brain regions. Students involved in the project must be comfortable working with rats and will learn how to perform brain surgery on rats, assay their behavior and motor function, and complete immunohistochemical analyses of brain tissue. In addition, students will learn how to measure neurotransmitter and neurotoxin levels in brain fluid samples using HPLC.

Representative Publications:

  • Babcock, L.*, C. Rodriquez*, C. C. Barney, and G. Fraley. 2006. ICV galanin-like peptide increases metabolic rate in male rats. FASEB J. 20: A830, 2006.
  • Gayheart, K.* and C. C. Barney. 2005. Endogenous angiotensin II does not regulate oxygen consumption and core temperature in rats. FASEB J., 19:A1194.
  • Burnatowska-Hledin, M. A., J. B. Kossoris*, C. J. Van Dort*, R. L. Shearer*, P. Zhao, D. A. Murrey*, J. L. Abbott*, C. E. Kan*, and C. C. Barney. 2004. T47 D breast cancer cell growth is inhibited by expression of VACM-1, a cul-5 gene. Biochem. Biophys. Res. Commun. 319:817-825.
  • Barney, C. C., D. M. Kurylo*, and J. L. Grobe*. 2003. Thermal dehydration-induced thirst in lithium-treated rats. Pharmacol. Biochem. Behav. 75:341-347.
  • Burnatowska-Hledin, M., A. Zeneberg*, A. Roulo*, J. Grobe*, P. Zhao, P. I. Lelkes, P. Clare, and C. Barney. 2001. Expression of VACM-1 protein in cultured rat endothelial cells is linked to the cell cycle. Endothelium. 8:49-63.
  • Barney, C. C., G. L. Smith*, and M. M. Folkerts*. 1999. Thermal dehydration-induced thirst in spontaneously hypertensive rats. Am. J. Physiol. 276 (Regulatory Integrative Comp. Physiol. 45): R1303-R1310.
  • Barney, C. C. 1997. Effects of preloads of water and saline on thermal dehydration-induced thirst. Physiol. Behav. 61:763-769.

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