Research Focus

The main theme of my research is defining the cellular and molecular signaling mechanisms involved in the central regulation of thermoregulation, fever and energy expenditure. In mammals, the hypothalamus has long been thought to represent the site of a neural integration that controls the characteristic physiologic changes seen during normal thermoregulation or during fever. However, the precise identity of the hypothalamic neurons involved has been unknown. Studies will characterize the neurons involved in these networks and explore the modes of neural signaling responsible for the generation of the physiological changes seen in normal thermoregulation and during fever. We use electrophysiological and optical techniques to measure ion currents and to record changes in intracellular calcium within single neurons, as well as immunocytochemistry and single cell RT/PCR. Current research efforts focus on histamine signaling in the preoptic area/ anterior hypothalamus and its role in thermoregulation and energy expenditure. Histamine exerts an important modulating action on these functions. Lowered hypothalamic histamine concentrations result in lower core body temperature and obesity. Conversely, pharmacological agents that increase hypothalamic histamine concentrations  are beneficial in animal models of diabetes, obesity and an increase body temperature. Other goals of my research are to identify the mechanisms underlying thermosensitive firing activity in anterior hypothalamic neurons and to study cryogen (substances that lower core body temperature) signaling in the hypothalamus.

 

Professional Experience

2002- 2006 Research Associate, The Scripps Research Institute, La Jolla, CA

1998-2002 Postdoctoral research fellow, Ottawa Health Research Institute, Ottawa (Canada)

1997-1998 Postdoctoral research fellow, Northwestern University Medical School, Chicago IL

Selected References

Gregorsson Lundius E, Sanchez-Alavez M, Klaus J, Szabo G, Tabarean IV (2010). Histamine influences body temperature by acting at H1 and H3 receptors on distinct populations of preoptic neurons. J Neurosci. 30:4369-81

Scott D, Tabarean IV, Tang Y, Cartier A, Masliah A, and Roy S (2010). A pathologic cascade leading to synaptic dysfunction in α-synuclein-induced neurodegeneration. J. Neurosci  30:8083-95.

Sanchez-Alavez M, Tabarean IV, Osborn O, Mitsukawa K, Schaefer J, Dubins J, Holmberg KH, Klein I, Klaus J, Gomez L, Kolb H, Jochems J, Myashiro K,  Buckley P, Hadcock J,  Eberwine J, Conti B and Bartfai T (2010). Insulin causes hyperthermia by direct inhibition of warm sensitive neurons. Diabetes 59:43-50

Tabarean I.V., Korn H., and Bartfai T. (2006). Interleukin-1β induces hyperpolarization and modulates synaptic inhibition in preoptic and anterior hypothalamic neurons. Neuroscience 141:1685-95

Davis C.N., Tabarean I.V , Gaidarova S, Behrens M.M. and Bartfai T. (2006). IL-1β induces a MyD88-dependent and ceramide-mediated activation of Src in anterior hypothalamic neurons. Journal of Neurochemistry 98:1379-89.

Tabarean I.V., Conti B., Behrens M., Gaidarova S. and Bartfai T. 2004. Electrophysiological characterization of preoptic area/anterior hypothalamus neurons in culture. Neuroscience. 135:433-49

Tabarean I.V., Behrens M., Bartfai T. and Korn H. 2004. Prostaglandin E₂-increased thermosensitivity of anterior hypothalamic neurons is associated with depressed inhibition. PNAS. 101:2590-5