• Name: James R. Groome, Ph.D.
  • Institution: Idaho State University
  • Department: Biological Sciences
  • Phone: 208-282-2791
  • Email: groojame@isu.edu

Summary: Our laboratory investigates the molecular basis of ion channel function. These proteins include the voltage-gated channels of nerve and muscle and the neurotransmitter receptors in the brain and periphery. We use a diversity of approaches to study these channels and the defects caused by mutations associated with disease states. Molecular biology techniques include site directed mutagenesis to reiterate the mutations in channels found in patients with channelopathy diseases such as myotonia and periodic paralysis, and microbiology techniques to work with the recombinant DNA with the goal of expressing these proteins in the oocytes of Xenopus frogs.  These oocytes serve as the expression system for our electrophysiological approach to study ion channels. Two electrode voltage clamp experiments are employed to study the response to acetylcholine for nicotinic acetylcholine receptors that are an important determinant of dopamine release and thus a target in Parkinson’s Disease therapy. Our third approach is computational.  We use sequence alignments and homology algorithms to create three dimensional models of the membrane proteins mentioned above and study their function in silico. We also use mathematical models of excitable cell membranes such as skeletal muscle fibers to investigate the functional impact of the channel defects determined with electrophysiology on action potential signaling to study the basis of paramyotonia congenita and other channelopathies of muscle fibers.

Minimum Classes: N/A

1. Two electrode voltage clamp electrophysiolgical investigation of nicotinic acetylcholine receptors.  Project will involve the construction of mutations in the alpha and beta subunit of these receptors and the determination of the effects of mutations on the response to the neurotransmitter acetylcholine
2. Computational modeling of action potentials in silico for a model of the human skeletal muscle fiber.  Project will involve the use of differential equations in the MatLab environment, to refine the cell model with parameters for sodium channel functions of activation and inactivation and determine the impact of mutations in paramyotonia congenita, a temperature sensitive disorder causing muscle weakness.
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