RESEARCH INTERESTS - BAYLISS
Mechanisms of Neuromodulation in Central Neurons Signaling between cells in the brain relies on electrical and chemical transmission. Ion channels traverse brain cell membranes to serve as conduits for the flow of ionic current; this current creates the potential differences across the membrane that are ultimately responsible for triggering release of the chemical messengers that act on nearby neurons.
Our laboratory attempts to characterize neuronal signaling in terms of identifying the molecular basis for neuronal ion channels and understanding cellular mechanisms that modulate their activity. We are particularly interested in studying those ion channels that determine intrinsic excitability of brain cells, because they are often subject to regulation by endogenous neurochemicals and since they ultimately mediate effects of many drugs, therapeutic and otherwise.
A number of technical approaches are employed in our laboratory, including chemical neuroanatomy, cellular electrophysiology in brain tissue and transfected cells, molecular biology and in vivo gene transfer. Our hope is that information combined from these different approaches will illuminate mechanisms responsible for physiological and pharmacological modulation of neuronal excitability.
GRANT SUPPORT
2 R01 NS33583-07 (Bayliss) 4/1/2001-3/31/2006 30% NIH/NINDS Molecular Bases for Motoneuronal Modulation.
The major goals of this project are: [1] determine if TASK channels can form functional heterodimers; [2] determine G protein subunits and channel domains involved in receptor-mediated TASK inhibition; and [3] determine contributions of TASK channels to motoneuronal currents and mechanisms of their modulation.
1 R01 GM66181-01 (Bayliss) 7/1/2002 - 6/30/2006 25% NIH/NIGMS Anesthetic Action: Channels, Substrates & Mechanisms.
The major goals of this project are: [1] Elucidate molecular mechanisms underlying volatile anesthetic effects on 'leak' K+ (TASK) channels; [2] Elucidate molecular mechanisms underlying volatile anesthetic effects on hyperpolarization-activated cationic (HCN) channels.
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