James R. Groome, Ph.D.
Associate Professor of Biology
- (208) 282-2791
- Gale Life Sciences Bldg, Rm 321
- Groome Laboratory of Molecular Neuroscience
- Neuroscience, ion channel disorders, pathology
- BA 1981 Wake Forest University, Winston Salem, NC
- PhD 1988 University of New Hampshire, Durham, NH
- Postdoc 1996 Utah State University, Logan, UT
Dr. Groome is interested in the cellular and molecular mechanisms of neuronal and muscle excitability in the brain and periphery. He began his training by studying invertebrate nervous systems and their modulation. He has worked on the neural regulation of muscle excitability horseshoe crabs, spiders, nudibranch mollusks and leeches. More recently the focus of the Groome laboratory has turned to ion channels as a focal point of studies of neuronal and muscular excitability and their dysfunction in human disease. At Idaho State University both graduate and undergraduate students in the Groome laboratory use site directed mutagenesis combined with patch clamp electrophysiology to study the molecular underpinnings of human, genetic channelopathies such as epilepsy, autism, and myotonia.
- BIOL 463/563 Human Pathophysiology
- BIOL 415/515 Human Neurobiology
- BIOL 460/50 Neuroscience
- PT/OT 402/502 Clinical Neuroscience
Groome JR, Watson WH III, 1989. Second messenger systems underlying amine and peptide modulation of cardiac muscle in the horseshoe crab, Limulus polyphemus. Journal of Experimental Biology 145, 419-437.
Groome JR, Tillinghast EKT, Townley MA, Vetrovs A, Watson WH III, Hunt DF, Griffin PR, Alexander JE, Shabonowitz J, 1990. Identification of proctolin in the central nervous system of the horseshoe crab, Limulus polyphemus. Peptides 11, 205-211.
Groome JR, Townley MA, deTschaschell M, Tillinghast EKT, 1991. Detection and isolation of proctolin-like immunoreactivity in arachnids: possible cardioregulatory role for proctolin in the orb-weaving spiders Argiope and Araneus. Journal of Insect Physiology 37 (1), 9-19.
Groome JR, Clark M, Lent CM, 1993. The behavioral state of satiation in the medicinal leech, Hirudo medicinalis, is regulated by distension and mimicked by serotonin depletion. Journal of Experimental Biology 182, 265-270.
Groome JR, Vaughn DKV, Lent CM, 1995. Ingestive sensory inputs excite serotonin effector neurones and mediate depletion from the leech CNS and periphery. Journal of Experimental Biology 198, 1233-1242.
Groome JR, Lehman H, 1995. Crustacean cardioactive peptide (CCAP) in the horseshoe crab Limulus polyphemus: distribution and characterization. Journal of Comparative Neurology 357 (1), 36-51.
Groome JR, Vaughan DKV, 1996. Glutamate as a transmitter in the sensory pathway from prostomial lip to serotonergic Retzius neurons in the medicinal leech Hirudo. Invertebrate Neuroscience 2, 121-128.
Groome JR, Fujimoto E, George AL Jr and Ruben PC, 1999. Differential effects of homologous S4 mutations in human skeletal muscle sodium channels on deactivation gating from open and inactivated states. Journal of Physiology 516 (3), 687-698.
Groome JR, Fujimoto E and Ruben, PC. 2000. The delay in recovery from fast inactivation in skeletal muscle sodium channels is deactivation. Cellular and Molecular Neurobiology 20 (4), 521-527.
Groome JR, Pryma D and Donahue RM, 2001. CREB-like immunoreactivity in the medicinal leech Hirudo. Invertebrate Neuroscience 4, 95-103.
Groome JR, Fujimoto E, Walter L and Ruben, PC. 2002. Outer and central charged residues in DIVS4 of skeletal muscle sodium channels have differing roles in deactivation. Biophysical Journal 82, 1293-1307.
Groome JR, Fujimoto E, and Ruben, PC. 2003. Negative charges in the DIII-DIV linker of skeletal muscle Na+ channels regulate deactivation gating. Journal of Physiology 548(1), 2003.
Groome JR, Fujimoto E, and PC Ruben. K-aggravated mutations at residue G1306 differentially alter deactivation gating of human skeletal muscle sodium channels. Cell Mol. Neurobiol. 25(7): 1075-1092