This laboratory examines the physiology of mammalian skeletal muscle and the neuromuscular junction.  The emphasis is to use functional and molecular mechanisms to examine the physiology of mammalian skeletal muscle.  To achieve this goal, the laboratory employs a combination of electrophysiological, optical, pharmacological and biochemical techniques.  For example, this approach has been used to reveal that extracellular ATP, which is released by muscle during exercise, inhibits pathways for the movement of chloride across muscle membranes (chloride channels). Because chloride movement across the membrane acts to buffer the resting membrane potential, the inhibition of chloride channels causes the muscle to become hyperexcitable.  The inhibition of chloride channels by extracellular ATP has implications for muscle fatigue and inherited diseases that affect skeletal muscle function. 

The current goals of the laboratory are to determine each step of the molecular mechanism that links extracellular ATP to the inhibition of chloride channels and to determine exactly how this molecular mechanism influences skeletal muscle physiology.

Additionally, we have started examining skeletal muscle dysfunction in Huntington's disease.

Huntington's disease is a fatal degernative disorder characterized by severe cognitive and motor defects. Using the techniques described above, we are examining potential causes of the motor defects.

Current projects in the lab include:

  • Purinergic signaling in mammalian muscle
  • Skeletal muscle dysfunction in Huntington's disease

Lab location: Building 8 Room: 28 Phone: (909) 869-2463