Mark M. Rich, M.D., Ph.D. Associate Professor Address: 251 Biological Sciences II Phone: (937) 775-2234 E-mail: mark.rich@wright.edu

Research Interests

My research focuses on two areas.

1. We study the cause of paralysis in patients with Critical Illness Myopathy. We have found that paralysis in this syndrome is due to abnormal behavior of skeletal muscle sodium channels. Our goal is to determine the cause of altered sodium channel behavior.
2. We study the 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.

See also: Synaptic Plasticity

Selected Publications

Critical Illness Myopathy:

Filatov GN, Pinter MJ, Rich MM (2005) Resting potential dependent regulation of the voltage sensitivity of sodium channel gating in rat skeletal muscle in vivo. Journal of Genderal Physiology 126:161-72.

Filatov GN, Rich MM (2004) Hyperpolarized shifts in the voltage dependence of fast inactivation of Na _v 1.4 and Na _v 1.5 in a rat model of critical illness myopathy. Journal of Physiology 559:813-820.

Rich MM and Pinter MJ (2003) Crucial role of sodium channel fast inactivation in muscle fibre inexcitability in a rat model of critical illness myopathy. Journal of Physiology 547:555-566.

Bird SJ, Rich MM (2002) Critical illness myopathy and polyneuropathy. Current Neurology and Neurosciences Reports 2:527-533.

Rich MM and Pinter MJ (2001) Sodium channel inactivation in an animal model of acute quadriplegic myopathy. Annals of Neurology 50:26-33.

Regulation of Synaptic Strength:

Wang X, Li Y, Engisch KL, Nakanishi ST, Dodson SE, Miller GW, Cope TC, Pinter MJ, Rich MM (2005) Activity dependent presynaptic regulation of quantal size at the mammalian neuromuscular junction in vivo. Journal of Neuroscience 25:343-351.

Wang X, Engisch KL, Pinter MJ, Cope TC, Rich MM (2004) Decreased synaptic activity shifts the calcium depdence of release at the mammalian neuromuscular junction in vivo. Journal of Neuroscience 24:10687-10692.