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|Anatoly E Martynyuk|
|Anatoly E. Martynyuk, PhD
Departments of Anesthesiology and Neuroscience
University of Florida
Dr. Anatoly Martynyuk was trained at the Bogomoletz Institute of Physiology in Kyiv, Ukraine where he received his Ph.D. and D.Sc. degrees under the mentorship of Dr. Platon Kostyuk, a pioneer of modern electrophysiology. After receiving his doctoral degrees, he continued to work at the institute collaborating with Dr. Kostyuk in the area of neuronal cell electrophysiology. In 1993-96, he decided to complement his prior research training in neuronal electrophysiology by doing a postdoctoral fellowship in cardiac research at the University of Glasgow, United kingdom. During his time in Scotland, he studied the ionic mechanisms underlying the effects of adenosine on single, isolated atrioventricular (AV) nodal myocytes. He continued these studies at the University of Florida. His collaborators and he had obtained important experimental results providing an explanation for the increase in efficacy of adenosine action in the heart during supraventricular tachycardia (rate-dependent effect of adenosine). The mechanisms of this clinically important action of adenosine difficult to explain based on known action of the nucleoside-activation of the time-independent inwardly-rectifying potassium current. He found that adenosine also augments a delayed rectifying K+ current and slows recovery from inactivation of a high threshold Ca2+ current in AV nodal cells. Because of specific kinetic properties, these ionic currents may mediate more efficient action of adenosine at fast heart rate. He also demonstrated that this effect of adenosine can further be potentiated by hyperkalemia and free oxygen radicals, which are released in increased amounts during ischemia/reperfusion. The sensitization of the AV node to the depressant effects of adenosine during ischemia provides means whereby adenosine causes AV nodal conduction block, even at concentrations of the nucleoside that are ordinarily subthreshold for its negative dromotropic effect under normal conditions.
His research interests is the mechanisms underlying the causes of epilepsy in phenylketonuria (PKU). Despite the fact that hyperphenylalaninemia is the most common biochemical cause of mental retardation in man, the cellular mechanisms that underlie impaired brain function remain unclear. His group obtained evidence that phenylalanine-caused depression of glutamatergic synaptic transmission in the brain may be a major player in etiology of PKU. The credibility and importance of this approach is evident from the publications in Molecular Psychiatry, Brain, Epilepsia. The antiglutamatergic action of phenylalanine is unique in that that it depresses functioning of glutamate synapse at multiple pre- and postsynaptic sites. Considering the polyvalent antiglutamatergic action of phenylalanine, he suggested that derivatives of phenylalanine with greater potency may be safe and efficacious neuroprotectors in conditions characterized by excessive activation of excitatory glutamatergic synaptic transmission. They tested this hypothesis using rat models of focal brain ischemia, several rodent models of epileptic seizures and sensorimotor gating deficit. The results of these studies were published in Stroke, Mol. Pharmacol., Br. J. Pharmacol and served as the experimental basis for several patents. His current research at U.F predominantly focuses on investigation of the cellular mechanisms contributing to immediate and delayed neurological, cognitive and metabolic defects caused by anesthesia with sevoflurane and isoflurane in neonatal.
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