I am an MD/PhD with fellowship training in neuromuscular disease and over 25 years of experience in both clinical and basic science studies of electrophysiologic deficits in neuromuscular disease. I have published over 75 articles. My laboratory is currently focused on three main projects.
- We have found that neurologic and cardiac deficits in patients recovering from intensive care unit acquired weakness (ICUAW) are due to abnormal behavior of sodium channels. We are working to develop novel therapies for these patients.
- We study mechanisms underlying muscle dysfunction in the inherited muscle disease myotonia congenita. Muscle in this disorder is hyperexcitable due to a mutation in the muscle chloride channel gene. We are working to develop novel therapies for these patients.
- We study mechanisms underlying activity-induced changes in synaptic strength. We use the neuromuscular junction as a model synapse in which it is possible to determine both the signals triggering changes in synaptic strength as well as the types of changes underlying alterations in synaptic strength.
Selected, since 2009
Kong L, Wang X, Choe DW, Polley M, Burnett BG, Bosch-Marcé M, Griffin JW, Rich MM, Sumner CJ. (2009) Impaired synaptic vesicle release and immaturity of neuromuscular junctions in spinal muscular atrophy mice.Journal of Neuroscience 29(3):842-51.
Novak KR, Nardelli P, Cope TC, Filatov G, Glass JD, Khan J, Rich MM. (2009) Inactivation of sodium channels underlies reversible neuropathy during critical illness in rats. Journal of Clinical Investigation. 119(5):1150-8.
Wilhelm JC, Rich MM, Wenner P. (2009) Compensatory changes in cellular excitability, not synaptic scaling, contribute to homeostatic recovery of embryonic network activity. Proceedings of the National Academy of Sciences. 106(16):6760-5.
Filatov, GN, Pinter MJ, Rich MM. (2009) The role of Ca2+ in membrane injury-induced changes in sodium current in rat skeletal muscle. American Journal of Physiology. 297(2):C352-9.
Wright MC, Potluri S, Wang X, Dentcheva E, Gautam D, Tessler A, Wess J, Rich MM, Son YJ. (2009) Distinct muscarinic acetylcholine receptor subtypes contribute to stability and growth, but not compensatory plasticity, of neuromuscular synapses. Journal of Neuroscience. 25;29(47): 14942-55.
Wang X, Pinter MJ, Rich MM. (2010) Ca2+ dependence of the binomial parameters p and n at the mouse neuromuscular junction. Journal of Neurophysiology. 103:659-666.
Foust KD, Wang X, McGovern VL, Braun L, Bevan AK, Haidet AM, Le TT, Morales PR, Rich MM, Burghes AH, Kaspar BK. (2010) Rescue of a Spinal Muscular Atrophy Mouse Model by Early Postnatal scAAV9-SMN Delivery. Nature Biotechnology. 28(3):271-4.
Gladman JT, Bebee TW, Edwards C, Wang X, Sahenk Z, Rich MM, and Chandler DS (2010) A humanized Smngene containing the SMN2 nucleotide alteration in exon 7 mimics SMN2 splicing and the SMA disease phenotype. Human Molecular Genetics. 19(21):4239-52.
Wang X, Wang Q, Engisch KL, Rich MM (2010) Activity-dependent regulation of the binomial parameters p and n at the mouse neuromuscular junction in vivo. Journal of Neurophysiology. 104: 2352-2358.
Wang X, Wang Q, Yang S, Bucan M, Rich MM, Engisch KL, (2011) Impaired activity-dependent plasticity of quantal amplitude at the neuromuscular junction of Rab3A deletion and Rab3A Earlybird mutant mice. Journal of Neuroscience. 31(10):3580-8.
Kraner SD, Wang Q, Novak KR, Cheng D, Cool DR, Peng J, Rich MM. (2011) Upregulation of the CaV 1.1-ryanodine receptor complex in a rat model of critical illness myopathy. Am J Physiol Regul Integr Comp Physiol.300(6):R1384-91.
Bullinger KL, Nardelli P, Wang Q, Rich MM and Cope TC, (2011) Oxaliplatin Neurotoxicity of Sensory Transduction in Rat Proprioceptors. Journal of Neurophysiology. 106(2):704-9.
Le TT, McGovern VL, Alwine IE, Wang X, Massoni-Laporte A, Rich MM, Burghes AH. (2011) Temporal requirement for high SMN expression in SMA mice. Human and Molecular Genetics 20(18):3578-91.
Martinez TL, Kong L, Wang X, Osborne MA, Crowder ME, Van Meerbeke JP, Xu X, Davis C, Wooley J, Goldhamer DJ, Lutz CM, Rich MM, Sumner CJ (2012) Survival Motor Neuron Protein in Motor Neurons Determines Synaptic Integrity in Spinal Muscular Atrophy. Journal of Neuroscience 20;32(25):8703-8715.
Kraner SD, Novak KR, Wang Q, Peng J, Rich MM. (2012) Altered sodium channel-protein associations in critical illness myopathy. Skeletal Muscle. Aug 30;2(1):17.
Carrasco DI, Bichler EK, Rich MM, Wang X, Seburn KL, Pinter MJ. (2012) Motor terminal degeneration unaffected by activity changes in SOD1G93A mice; a possible role for glycolysis. Neurobiology of Disease 48(1):132-40.
Nardelli P, Khan J, Powers RK, Cope TC, Rich MM. (2013) Reduced motoneuron excitability in a rat model of sepsis. Journal of Neurophysiology 109(7):1775-81.
Koesters A, Engisch KL, Rich MM. (2014) Decreased cardiac excitability secondary to reduction of sodium current may be a significant contributor to reduced contractility in a rat model of sepsis. Critical Care. 26:18(2):R54.
Fan E, Cheek F, Chlan L, Gosselink R, Hart N, Herridge MS, Hopkins RO, Hough CL, Kress JP, Latronico N, Moss M, Needham DM, Rich MM, Stevens RD, Wilson KC, Winkelman C, Zochodne DW, Ali NA (2014) An Official American Thoracic Society Clinical Practice Guideline: The Diagnosis of Intensive Care Unit-acquired Weakness in Adults. American Journal of Respiratory and Critical Care Medicine 190(12):1437-46.
Novak KR, Norman J, Mitchell JR, Pinter MJ and Rich MM. (2015) Sodium channel slow inactivation as a therapeutic target for myotonia congenita. Annals of Neurology 77(2):320-32.
McGovern VL, Massoni-Laporte A, Wang X, Le TT, Le HT, Beattie CE, Rich MM, Burghess AHM (2015) Plastin 3 Expression Does Not Modify Spinal Muscular Atrophy Severity in the Δ7 SMA Mouse. PLOS 1 Jul 2;10(7):e0132364.
Friedrich O, Reid MB, Van den Berghe G, Vanhorebeek I, Hermans G, Rich MM, Larsson L (2015) The Sick and the Weak: Neuropathies/Myopathies in the critically ill - Cellular Mechanisms of complex Disease Entities in the ICU. Physiological Reviews Jul;95(3):1025-109.
Wang X, Pinter MJ, Rich MM. (2016). Reversible Recruitment of a Homeostatic Reserve Pool of Synaptic Vesicles Underlies Rapid Homeostatic Plasticity of Quantal Content. Journal of Neuroscience. 2016 Jan 20;36(3):828-36.
Nardelli P, Vincent JA, Powers R, Cope TC, Rich MM. (2016) Reduced motor neuron excitability is an important contributor to weakness in a rat model of sepsis. Experimental Neurology.