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Leszek
K. Kubin, Ph.D.
Research Professor of Physiology Department of Animal Biology 209E/VET
School of Veterinary Medicine
3800 Spruce Street
Philadelphia, PA 19104-6046
Tel: (215) 898-1893 Fax: (215) 573-5186
E-mail: lkubin@vet.upenn.edu
URL: http://phl.vet.upenn.edu/~lkubin/
Click here for selected publications since Dr. Kubin's arrival at Penn
RESEARCH INTERESTS
Respiratory, sleep and metabolic disorders associated with the obstructive sleep apnea syndrome; homeostatic regulation of sleep RESEARCH TECHNIQUES
Immunohistochemistry and tract-tracing; gene expression analysis; single-cell RT-PCR; intra- and extracellular recording in vivo ; iontophoresis and microinjections; behavioral analysis of sleep/movement in rodents
RESEARCH SUMMARY
Hypoventilations and apneas characteristic of the Obstructive Sleep Apnea Syndrome (OSAS) occur most frequently and are most severe during the desynchronized, rapid eye movement (REM) stage of sleep. The resulting loss of sleep further exacerbates the disorder. The goals of our research are to understand the pharmacological mechanisms of REM sleep and the accompanying suppression of motoneuronal activity, and to identify the cellular basis of the response to sleep deprivation. Due to the complex nature of sleep, we use complementary electrophysiological in vivo and in vitro techniques, neuroanatomy and molecular biology. In electrophysiological studies, we use of a novel pharmacological model of REM sleep. To characterize the role of different neurotransmitter receptors in sleep-related disorders of breathing, we use in vivo pharmacology and also study changes in receptor mRNA expression in brain regions and single cells involved in the regulation of sleep and breathing. Since OSAS frequently coexists with the metabolic syndrome (hypertension, obesity and diabetes), we also investigate whether oscillation in blood oxygen level (chronic intermittent hypoxia) cause changes in the central and peripheral control of glucose metabolism, such as in type 2 diabetes. In separate studies, we pursue our hypothesis that prolonged wakefulness leads to increased expression of GABA A receptors in the posterior hypothalamus, as region in which increased GABAergic inhibition acts to promote sleep.
KEY WORDS:
brainstem; breathing; chronic-intermittent hypoxia; diabetes; gene expression; hypothalamus; motoneurons; sleep; serotonin; single-cell RT-PCR
