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Name, Field, Position, Department, and Keyword |
 
Faculty Keywords: Cell and Molecular Neuroscience (23), Ligand-activated ion channels (2), Mathematical Modeling (14), Neurotransmitter receptors and transporters (9), Patch clamp (2) Members of my laboratory are studying excitatory amino acid (EAA) or "glutamate" activated receptor-channels in the vertebrate central nervous system. The principal approach to these investigations involves recordings of EAA activated receptor-channels in mammalian brain neurons in primary culture and recombinant receptor-channels expressed in mammalian cell lines and in Xenopus oocytes. Single channel recordings are employed to determine basic biophysical parameters of receptor channel function. Hidden Markov models are develpoed to model channel opening and closing rates. Chimeric cross-family subunit proteins are designed to study channel ion selectivity, gating, and receptor trafficking. Whole cell voltage-clamp recordings are also combined with single cell molecular biology methods in an effort to ascertain the likely subunit compositions of pharmacologically and biophysically distinct receptor-channel subtypes observed in cerebellar granule neurons and cerebral cortical neurons. |
Faculty Keywords: Cell and Molecular Neuroscience (23), Ion channel (6), Neuromodulation (12), Neurotransmitter receptors and transporters (9), Proteins (3) My general research interest is in the modulation of receptor properties by neurotransmitters and drugs. Currently we are studying the mechanisms of modulation of the nicotinic cholinergic receptor by its neurotransmitter acetylcholine and by the neuropeptide substance P. Nicotinic receptor responsiveness is regulated by acetylcholine and other cholinergic agonists via desensitization. In fact there are several desensitization processes each of which occurs on a different time scale, ranging from milliseconds to several minutes. Nicotinic receptor responsiveness also appears to be regulated physiologically by substance P, an eleven amino acid peptide that inhibits nicotinic receptor activation. One reason we have focused on both of these modulatory mechanisms is that they appear to be interrelated since at least part of the inhibition by substance P seems to be mediated by an increase in the rate and extent of desensitization. For more information, follow the web link above. |
Please report corrections, questions, comments, and problems to: Lori Miller (lmm8 AT cornell.edu)