Mark Rich

Summary

Affiliation: Wright State University
Country: USA

Publications

  1. pmc Resting potential-dependent regulation of the voltage sensitivity of sodium channel gating in rat skeletal muscle in vivo
    Gregory N Filatov
    Department of Neuroscience, Cell Biology, and Physiology, Wright State University, Dayton, OH 45435, USA
    J Gen Physiol 126:161-72. 2005
  2. pmc Reduced motoneuron excitability in a rat model of sepsis
    Paul Nardelli
    Department of Neuroscience, Cell Biology, and Physiology, Wright State University, Dayton, OH, USA
    J Neurophysiol 109:1775-81. 2013
  3. pmc Altered sodium channel-protein associations in critical illness myopathy
    Susan D Kraner
    Department of Neuroscience, Cell Biology, and Physiology, Wright State University School of Medicine, 3640 Colonel Glenn Hwy, Dayton, OH, 45435, USA
    Skelet Muscle 2:17. 2012
  4. ncbi request reprint Sensing and expressing homeostatic synaptic plasticity
    Mark M Rich
    Department of Neuroscience, Cell Biology and Physiology, Wright State University, Dayton, OH 45435, USA
    Trends Neurosci 30:119-25. 2007
  5. ncbi request reprint The control of neuromuscular transmission in health and disease
    Mark M Rich
    Department of Neuroscience, Cell Biology and Physiology, Wright State University, Dayton, OH 45435, USA
    Neuroscientist 12:134-42. 2006
  6. ncbi request reprint Prolongation of evoked and spontaneous synaptic currents at the neuromuscular junction after activity blockade is caused by the upregulation of fetal acetylcholine receptors
    Xueyong Wang
    Department of Neuroscience, Cell Biology, and Physiology, Wright State University, Dayton, Ohio 45435, USA
    J Neurosci 26:8983-7. 2006
  7. pmc Ca2+ dependence of the binomial parameters p and n at the mouse neuromuscular junction
    Xueyong Wang
    Department of Neuroscience, Cell Biology, and Physiology, Wright State University, Dayton, Ohio 45435, USA
    J Neurophysiol 103:659-66. 2010
  8. pmc Upregulation of the CaV 1.1-ryanodine receptor complex in a rat model of critical illness myopathy
    Susan D Kraner
    Department of Neuroscience, Cell Biology and Physiology, Wright State University, Dayton, Ohio, USA
    Am J Physiol Regul Integr Comp Physiol 300:R1384-91. 2011
  9. pmc Inactivation of sodium channels underlies reversible neuropathy during critical illness in rats
    Kevin R Novak
    Department of Neuroscience, Cell Biology and Physiology, Wright State University, Dayton, Ohio 45435, USA
    J Clin Invest 119:1150-8. 2009
  10. pmc Rat motoneuron properties recover following reinnervation in the absence of muscle activity and evoked acetylcholine release
    Edyta K Bichler
    Department of Physiology, Emory University School of Medicine, 615 Michael Street, Atlanta, GA 30322, USA
    J Physiol 585:47-56. 2007

Research Grants

Collaborators

  • RANDALL POWERS
  • Peter Wenner
  • Russell W Teichert
  • Z Yan
  • Amy L Thompson
  • Xueyong Wang
  • Martin J Pinter
  • Susan D Kraner
  • Timothy C Cope
  • Kevin R Novak
  • Kathrin L Engisch
  • Qingbo Wang
  • Edyta K Bichler
  • Paul Nardelli
  • Stan T Nakanishi
  • Dario I Carrasco
  • Ramachandran Thiagarajan
  • Junmin Peng
  • Yingjie Li
  • Tim C Cope
  • Jaffar Khan
  • Dusan M Jeftinija
  • Qing Bo Wang
  • Teclemichael Tewolde
  • Gregory N Filatov
  • Shawn J Bird
  • Dongmei Cheng
  • David R Cool
  • Gregory Filatov
  • Jonathan D Glass
  • Christopher M Norris
  • Sadie L Hebert
  • Baldomero M Olivera
  • Sara E Dodson
  • Gary W Miller
  • Peter L Becker

Detail Information

Publications23

  1. pmc Resting potential-dependent regulation of the voltage sensitivity of sodium channel gating in rat skeletal muscle in vivo
    Gregory N Filatov
    Department of Neuroscience, Cell Biology, and Physiology, Wright State University, Dayton, OH 45435, USA
    J Gen Physiol 126:161-72. 2005
    ..We propose that resting potential-induced shifts in the voltage dependence of sodium channel gating are essential to properly regulate muscle excitability in vivo...
  2. pmc Reduced motoneuron excitability in a rat model of sepsis
    Paul Nardelli
    Department of Neuroscience, Cell Biology, and Physiology, Wright State University, Dayton, OH, USA
    J Neurophysiol 109:1775-81. 2013
    ..Our data are the first to suggest that reduced excitability of neurons within the central nervous system may contribute to ICUAW...
  3. pmc Altered sodium channel-protein associations in critical illness myopathy
    Susan D Kraner
    Department of Neuroscience, Cell Biology, and Physiology, Wright State University School of Medicine, 3640 Colonel Glenn Hwy, Dayton, OH, 45435, USA
    Skelet Muscle 2:17. 2012
    ..abstract:..
  4. ncbi request reprint Sensing and expressing homeostatic synaptic plasticity
    Mark M Rich
    Department of Neuroscience, Cell Biology and Physiology, Wright State University, Dayton, OH 45435, USA
    Trends Neurosci 30:119-25. 2007
    ....
  5. ncbi request reprint The control of neuromuscular transmission in health and disease
    Mark M Rich
    Department of Neuroscience, Cell Biology and Physiology, Wright State University, Dayton, OH 45435, USA
    Neuroscientist 12:134-42. 2006
    ..The review concludes with a discussion of mechanisms that may contribute to failure of neuromuscular transmission during repetitive stimulation...
  6. ncbi request reprint Prolongation of evoked and spontaneous synaptic currents at the neuromuscular junction after activity blockade is caused by the upregulation of fetal acetylcholine receptors
    Xueyong Wang
    Department of Neuroscience, Cell Biology, and Physiology, Wright State University, Dayton, Ohio 45435, USA
    J Neurosci 26:8983-7. 2006
    ..This might occur if acetylcholine escapes from endplates and binds to extrajunctional fetal-type AChRs only during large, evoked EPCs. Our study is the first to demonstrate a functional role for upregulation of extrajunctional AChRs...
  7. pmc Ca2+ dependence of the binomial parameters p and n at the mouse neuromuscular junction
    Xueyong Wang
    Department of Neuroscience, Cell Biology, and Physiology, Wright State University, Dayton, Ohio 45435, USA
    J Neurophysiol 103:659-66. 2010
    ..Our results suggest that the apparent Ca(2+) dependence of n at the NMJ can be explained by an underlying Ca(2+) dependence of a spatially variable p such that p increases abruptly at a subset of sites as Ca(2+) is increased...
  8. pmc Upregulation of the CaV 1.1-ryanodine receptor complex in a rat model of critical illness myopathy
    Susan D Kraner
    Department of Neuroscience, Cell Biology and Physiology, Wright State University, Dayton, Ohio, USA
    Am J Physiol Regul Integr Comp Physiol 300:R1384-91. 2011
    ..There was also selective degradation of myosin heavy chain relative to actin in CIM muscle. Taken together, our findings suggest that increased Ca(2+) release from the sarcoplasmic reticulum may contribute to pathology in CIM...
  9. pmc Inactivation of sodium channels underlies reversible neuropathy during critical illness in rats
    Kevin R Novak
    Department of Neuroscience, Cell Biology and Physiology, Wright State University, Dayton, Ohio 45435, USA
    J Clin Invest 119:1150-8. 2009
    ..Acquired sodium channelopathy may be the mechanism underlying acute neuropathy in critically ill patients...
  10. pmc Rat motoneuron properties recover following reinnervation in the absence of muscle activity and evoked acetylcholine release
    Edyta K Bichler
    Department of Physiology, Emory University School of Medicine, 615 Michael Street, Atlanta, GA 30322, USA
    J Physiol 585:47-56. 2007
    ..Our results indicate that spontaneous release of acetylcholine from regenerated motor terminals is sufficient to operate the system...
  11. pmc Crucial role of sodium channel fast inactivation in muscle fibre inexcitability in a rat model of critical illness myopathy
    Mark M Rich
    Department of Neurology, Emory University School of Medicine, Atlanta, GA 30322, USA
    J Physiol 547:555-66. 2003
    ..These results highlight the importance of the change in fast inactivation in causing inexcitability of SD fibres...
  12. ncbi request reprint A selective role for MRF4 in innervated adult skeletal muscle: Na(V) 1.4 Na+ channel expression is reduced in MRF4-null mice
    Amy L Thompson
    Department of Molecular and Biomedical Pharmacology, University of Kentucky Medical Center, Lexington, KY 40536, USA
    Gene Expr 12:289-303. 2005
    ..4 Na+ channel expression either in the extrajunctional membrane or at the synapse. Thus, MRF4 appears to play a novel and selective role in adult muscle...
  13. ncbi request reprint Regulation of motoneuron excitability via motor endplate acetylcholine receptor activation
    Stan T Nakanishi
    Department of Physiology, Emory University School of Medicine, Atlanta, Georgia 30322, USA
    J Neurosci 25:2226-32. 2005
    ..The results suggest the existence of a retrograde signaling mechanism located at the motor endplate that enables expression of adult motoneuron excitability and depends on acetylcholine receptor activation for its normal operation...
  14. ncbi request reprint Activity-dependent presynaptic regulation of quantal size at the mammalian neuromuscular junction in vivo
    Xueyong Wang
    Center for Neurodegenerative Disease, Emory University School of Medicine, Atlanta, Georgia 30322, USA
    J Neurosci 25:343-51. 2005
    ..We propose that presynaptic activity modulates quantal size at the neuromuscular junction by modulating the amount of acetylcholine released from vesicles...
  15. ncbi request reprint Decreased synaptic activity shifts the calcium dependence of release at the mammalian neuromuscular junction in vivo
    Xueyong Wang
    Center for Neurodegenerative Disease, Emory University School of Medicine, Atlanta, Georgia 30322, USA
    J Neurosci 24:10687-92. 2004
    ..Block of presynaptic P/Q channels eliminated the increase in probability of release. We propose that activity-dependent regulation of presynaptic calcium entry may contribute to homeostatic regulation of quantal content...
  16. ncbi request reprint Activity-driven synaptic and axonal degeneration in canine motor neuron disease
    Dario I Carrasco
    Department of Physiology, Emory University School of Medicine, 615 Michael Street, Atlanta, GA 30322, USA
    J Neurophysiol 92:1175-81. 2004
    ..The results indicate that motor neuron action potential activity is a major contributing factor to the loss of motor-unit function and degeneration in inherited canine motor neuron disease...
  17. ncbi request reprint Reduced endplate currents underlie motor unit dysfunction in canine motor neuron disease
    Mark M Rich
    Department of Physiology, Emory University School of Medicine, Atlanta, Georgia 30322, USA
    J Neurophysiol 88:3293-304. 2002
    ....
  18. pmc Regulation of quantal shape by Rab3A: evidence for a fusion pore-dependent mechanism
    Xueyong Wang
    Department of Physiology, Emory University School of Medicine, Atlanta, GA 30322, USA
    J Physiol 586:3949-62. 2008
    ..These data could be explained by a direct action of Rab3A on the fusion pore, or by Rab3A-dependent control of vesicles with unusual fusion pore characteristics...
  19. ncbi request reprint Enhanced transmission at a spinal synapse triggered in vivo by an injury signal independent of altered synaptic activity
    Edyta K Bichler
    Department of Physiology, Emory University, Atlanta, Georgia 30345, USA
    J Neurosci 27:12851-9. 2007
    ....
  20. pmc The Ca(V) 1.2 Ca(2+) channel is expressed in sarcolemma of type I and IIa myofibers of adult skeletal muscle
    Dusan M Jeftinija
    Department of Molecular and Biomedical Pharmacology, University of Kentucky Medical Center, Lexington, KY 40536, USA
    Muscle Nerve 36:482-90. 2007
    ..2 and type IIa-positive fibers. Taken together, these data suggest that the Ca(V) 1.2 Ca(2+) channel is expressed in adult skeletal muscle in a fiber type-specific manner, which may help to maintain oxidative muscle phenotype...
  21. ncbi request reprint Reduced neuromuscular quantal content with normal synaptic release time course and depression in canine motor neuron disease
    Mark M Rich
    Department of Physiology, Emory University School of Medicine, Atlanta, Georgia 30322, USA
    J Neurophysiol 88:3305-14. 2002
    ....
  22. pmc Rab3A negatively regulates activity-dependent modulation of exocytosis in bovine adrenal chromaffin cells
    Ramachandran Thiagarajan
    Department of Physiology, Emory University School of Medicine, 605 J Whitehead Research Building, 615 Michael Street, Atlanta, GA 30322, USA
    J Physiol 555:439-57. 2004
    ..Instead, the activity-dependent increase in exocytotic efficacy observed in control cells did not occur in Rab3AQ81L-expressing cells. Our results suggest that Rab3A in the GTP bound conformation prevents activity-dependent facilitation...
  23. ncbi request reprint Critical illness myopathy and polyneuropathy
    Shawn J Bird
    Department of Neurology, University of Pennsylvania School of Medicine, 3400 Spruce Street, Philadelphia, PA 19104, USA
    Curr Neurol Neurosci Rep 2:527-33. 2002
    ..In the case of CIM, an animal model has provided evidence that weakness in this disorder is caused by muscle membrane inexcitability due to altered membrane sodium currents and loss of myosin thick filaments...

Research Grants8

  1. Loss of muscle excitability in acute quadriplegic myopathy
    Mark Rich; Fiscal Year: 2009
    ..abstract_text> ..
  2. ACUTE QUADRIPLEGIC MYOPATHY
    Mark Rich; Fiscal Year: 2004
    ..Finally, we will use knowledge gained from our studies of the animal model and determine why they are paralyzed. Our long-term goal is to determine why muscle becomes paralyzed in this syndrome so that we can develop a therapy. ..
  3. Loss of muscle excitability in acute quadriplegic myopathy
    Mark Rich; Fiscal Year: 2007
    ....