Theodore R. Cummins, PhD

Professor of Pharmacology and Toxicology

Research Interest 

I research the biophysics of ion channels and the role of ion channels in neurological diseases.



B.A. Chemistry | Swarthmore College
Swarthmore, PA


M.S. Biomedical Engineering  
Hartford Graduate Center  
Hartford, CT


M.A. Neuroscience | Yale University  
New Haven, CT


PhD Neuroscience | Yale University
New Haven, CT
Advisor: FJ Sigworth


Postdoctoral Fellow | Department of Neurology  
Yale University School of Medicine
Mentor: SG Waxman



Reviewing Editor, Journal of Biological Chemistry


Interim Chair, Department of Pharmacology & Toxicology


Co-Director, Medical Neuroscience Graduate Program

2010, 2013

Recipient of the IUSM Trustee Teaching Award


Member, NIH Study Section SCS 


Recipient of the IUSM Trustee Teaching Award


Associate Editor, Neuroscience Letters

Our main interest is the biophysics of ion channels and the role of ion channels in neurological diseases. Sodium channel mutations have been linked to several neurological disorders including skeletal muscle non-dystrophic myotonias, episodic ataxia and epilepsy. We have shown that mutations in the human skeletal muscle sodium channel, for example,

play a crucial role in the development of hyperkalemic periodic paralysis. Changes in the expression and properties of voltage-gated sodium channels are also thought to play important roles in chronic pain.

My lab uses electrophysiological, molecular biological and computer modeling techniques to study how specific voltage-gated sodium channels contribute to excitability and to neurological diseases. 

The long-term goals of my research are to develop a better understanding of the roles that ion channels in play in pathophysiological conditions and to develop strategies for the treatment of neurological disorders that involve ion channels.

Current work in my laboratory is focused on:

  1. Understanding the role of peripheral neuronal sodium channels in nociception and neuropathic pain. Specific sodium channels are predominantly expressed in nociceptive sensory neurons. My lab is examining how the activity of these sodium channels are affected by inflammatory mediators and neurotrophins.
  2. Investigating the role of sodium channels in genetic diseases. Sodium channel mutations have been identified in patients with epilepsy and skeletal muscle diseases. My lab characterizes the functional consequences of the different disease mutations in heterologous expression systems using patch-clamp techniques. We are also examining the effects of these mutant sodium channels on excitability in neurons and muscle cells.
  3. Molecular pharmacology of voltage-gated sodium channels. Several projects focus on understanding the sensitivity of sodium channels to specific pharmacologic agents. Identify local anesthetics and anticonvulsants that preferentially target sodium channels involved in pain sensations. Identify the molecular determinants of sodium channel sensitivity to pore blockers. Identify biological toxins from marine cone snail and tarantula venoms that specifically target voltage-gated sodium channels. These studies will provide information on the pharmacology of specific voltage-gated sodium channels that are thought to play important roles in epilepsy and pain and hopefully will contribute to the development of better treatments for these neurological disorders.

Selected Publications

  • Patel RR, Barbosa C, Xiao Y, Cummins TR. Human Nav1.6 Channels Generate Larger Resurgent Currents than Human Nav1.1 Channels, but the Navß4 Peptide Does Not Protect Either Isoform from Use-Dependent Reduction. PLoS One. 2015 Jul 16;10(7):e0133485. PubMed PMID: 26182346; PubMed Central PMCID: PMC4504674.
  • Tan ZY, Priest BT, Krajewski JL, Knopp KL, Nisenbaum ES, Cummins TR. Protein kinase C enhances human sodium channel hNav1.7 resurgent currents via a serine residue in the domain III-IV linker. FEBS Lett. 2014 Nov 3;588(21):3964-9. doi: 10.1016/j.febslet.2014.09.011. Epub 2014 Sep 19. PubMed PMID: 25240195; PubMed Central PMCID: PMC4451938.
  • Xiao Y, Blumenthal K, Cummins TR. Gating-pore currents demonstrate selective and specific modulation of individual sodium channel voltage-sensors by biological toxins. Mol Pharmacol. 2014 Aug;86(2):159-67. PubMed PMID: 24898004.
  • Tan ZY, Piekarz AD, Priest BT, Knopp KL, Krajewski JL, McDermott JS, Nisenbaum ES, Cummins TR. Tetrodotoxin-resistant sodium channels in sensory neurons generate slow resurgent currents that are enhanced by inflammatory mediators. J Neurosci. 2014 May 21;34(21):7190-7. PubMed PMID: 24849353; PubMed Central PMCID: PMC4028496.
  • Rowe AH, Xiao Y, Rowe MP, Cummins TR, Zakon HH. Voltage-gated sodium channel in grasshopper mice defends against bark scorpion toxin. Science. 2013 Oct 25;342(6157):441-6. PubMed PMID: 24159039.
  • Song W, Xiao Y, Chen H, Ashpole NM, Piekarz AD, Ma P, Hudmon A, Cummins TR, Shou W. The human Nav1.5 F1486 deletion associated with long QT syndrome leads to impaired sodium channel inactivation and reduced lidocaine sensitivity. J Physiol. 2012 Oct 15;590(Pt 20):5123-39. PMID: 22826127; PMCID: PMC3497567.
  • Ashpole NM, Herren AW, Ginsburg KS, Brogan JD, Johnson DE, Cummins TR, Bers DM, Hudmon A. Ca2+/calmodulin-dependent protein kinase II (CaMKII) regulates cardiac sodium channel NaV1.5 gating by multiple phosphorylation sites. J Biol Chem. 2012 Jun 8;287(24):19856-69. PMID: 22514276; PMCID: PMC3370170.
  • Theile JW, Cummins TR. Recent developments regarding voltage-gated sodium channel blockers for the treatment of inherited and acquired neuropathic pain syndromes. Front Pharmacol. 2011;2:54. PMID: 22007172; PMCID: PMC3185237.
  • Xiao Y, Jackson JO 2nd, Liang S, Cummins TR. Common molecular determinants of tarantula huwentoxin-IV inhibition of Na+ channel voltage sensors in domains II and IV. J Biol Chem. 2011 Aug 5;286(31):27301-10 PMID: 21659528; PMCID: PMC3149324.
  • Xiao Y, Blumenthal K, Jackson JO 2nd, Liang S, Cummins TR. The tarantula toxins ProTx-II and huwentoxin-IV differentially interact with human Nav1.7 voltage sensors to inhibit channel activation and inactivation. Mol Pharmacol. 2010 Dec;78(6):1124-34. PMID: 20855463; PMCID: PMC2993464.
  • Jarecki BW, Piekarz AD, Jackson JO 2nd, Cummins TR. Human voltage-gated sodium channel mutations that cause inherited neuronal and muscle channelopathies increase resurgent sodium currents. J Clin Invest. 2010 Jan;120(1):369-78. PMID: 20038812; PMCID: PMC2799199.

Row 1: Yucheng Xiao,  Zifan Pei, Cindy Nunez-Barbosa; Row 2: Andrew Piekarz, Ted Cummins, Tumare Iqbal, Jonathan Theile, James Jackson

Department of Pharmacology and Toxicology | 635 Barnhill Drive, MS A401 | Indianapolis, IN 46202