Theodore Cummins, Ph.D.

Department Chair and Professor, Biology

SL 306B
(317) 278-9342
Research Areas:
Biochemistry | Cell Biology | Neurophysiology


Ion channel biology and role of ion channels in neuronal and muscle disorders: Our main interest is the biology of ion channels and how they control the activity of muscle and nerve cells.  Ion channel mutations have been linked to several neurological and muscle disorders including epilepsy, pain and cardiac arrhythmias.

My lab uses electrophysiological, molecular biological, biochemical, imaging and computer modeling techniques to study how specific ion channels contribute to excitability and pathophysiological conditions.

We also try to develop strategies for the treatment of disorders that involve ion channels.  Therefore we explore the pharmacology of ion channels, working to identify small molecules, biological toxins and cannabinoids that can modulate ion channels and potential serve as candidate molecules for the development of new drugs.


  • 1983 B.A., Chemistry, Swarthmore College
  • 1985 M.S., Biomedical Engineering, Hartford Graduate Center
  • 1996 PhD, Neuroscience, Yale University
  • 1998 Postdoctoral Fellow, Department of Neurological Surgery, Yale University

Publications & Professional Activity

Pei Z, Xiao Y, Hudmon A, Cummins TR. Cardiac sodium channel palmitoylation regulates channel availability and myocyte excitability; implications for arrhythmia generation. Nature Communications, in press 2016.

Patel RR, Barbosa C, Cummins TR. Enhanced Resurgent Sodium Current Generated by Epilepsy-Associated Mutant Voltage-Gated Sodium Channels can be targeted with Cannabidiol.  Brain, in press 2016.

Ohlemacher SK, Sridhar A, Xiao Y, Hochstetler AE, Sarfarazi M, Cummins TR, Meyer JS. Stepwise Differentiation of Retinal Ganglion Cells from Human Pluripotent Stem Cells Enables Analysis of Glaucomatous Neurodegeneration. Stem Cells, in press 2016.;jsessionid=A101137D48970C14EA077FA4F8D3070E.f03t01

Xie W, Tan Z, Barbosa C, Strong JA, Cummins TR, Zhang JM. Knockdown of the sodium channel NaVβ4 regulatory subunit reduces pain behaviors, repetitive firing, and resurgent sodium currents induced by local inflammation of the rat sensory ganglia. Pain. In press, 2016.

Tan ZY, Piekarz AD, Priest B, Knopp K, Krajewski J, McDermott J, Nisenbaum E, Cummins TR. Tetrodotoxin-resistant sodium channels in sensory neurons generate slow resurgent currents that are enhanced by inflammatory mediators.  J Neuroscience. 34(21):7190-7, 2014.

*Rowe AH, *Xiao Y, Rowe MP, Cummins TR, Zakon HH. A voltage-gated sodium channel in predatory grasshopper mice blocks pain signals with the venom of their bark scorpion prey.  Science 342:441-446, 2013. *These authors are co-first authors.

Jarecki* BW, Piekarz* AD, Jackson JO, Cummins TR.  (*: co-first) Human voltage-gated sodium channel mutations that cause inherited neuronal and muscle channelopathies increase resurgent sodium currents.  Journal Clinical Investigation 120:369-378, 2010.