Roger Lee Papke, B.A., M.S., Ph.D.

Contact Information

Roger Lee Papke B.A., M.S., Ph.D.

Professor of Pharmacology and Therapeutics & Affiliate Professor of Neuroscience

Department of Pharmacology and Therapeutics

University of Florida College of Medicine
Academic Research Building

1200 Newell Drive

Box 100267, Gainesville, Florida 32610

Office location: Academic Research Building, R5-295
Office: (352) 392-4712, Lab: (352) 392-3257, Cell: (352) 494-9920


Professor of Pharmacology and Therapeutics & Affiliate Professor of Neuroscience

Research Area

We study brain nicotine receptors as therapeutic targets and as they relate to the management/treatment of addiction.



New York University

Washington Square College of Arts and Sciences, 1971 – 1975

Majors in Biology and Classical Civilization

Bachelor of Arts awarded May 1975

New York University

Graduate School of Arts and Sciences, 1975 – 1976

Thesis advisor:  Dr. Fleur L. Strand

Thesis title:  An Alpha Adrenergic Response of Cardiac Muscle at an Alkaline pH

Master of Science awarded May 1976

Cornell University, Graduate School of Arts and Science

Section of Neurobiology and Behavior

Thesis Advisor:  Dr. Robert Oswald

Primary research topic:  Pharmacology of nicotinic acetylcholine receptors

Thesis Title:     The Gating of Single Channel Currents Through the Nicotinic Acetylcholine Receptors of BC3H-1 Cells:  Effects of Agonists and Allosteric Ligands

Ph.D. conferred January 1987

Postdoctoral training

1987             Department of Pharmacology, Cornell University
Mentor, Professor Robert Oswald

1988-1993    Molecular Neurobiology Laboratory, Salk Institute
Mentor, Professor Stephen F. Heinemann

Current Research

Current Research Related to Addiction:

The characterization and development of partial agonists for smoking cessation therapies:

There is a great unmet need for drugs to aid smoking cessation attempts. The one most successful drug to date, varenicline, was, by Pfizer’s admission, inspired by my characterization of the related compound cytisine as a partial agonist of the brain nAChR subtypes that contain β2 subunits [1]. The nAChR in the brain that contain β2 show a high affinity for nicotine and are essential for mediating the dopamine-associated “reward” signal that promotes smoking. We have demonstrated that partial agonists for these receptors, such as varenicline and cytisine, will blunt the transient activation of β2-containing receptors and also produce low levels of steady-state activation, which may be important for decreasing symptoms of nicotine withdrawal [2]. Additionally, we have shown that cytisine-like compounds may decrease the depression that frequently occurs during smoking cessation attempts [3]. While cytisine-based therapies have some modest effects aiding smoking cessation in normal individuals, it is unlikely that they will be as useful in the large smoking population that suffer from mental illnesses such as schizophrenia. For these people, smoking may be a form of self-medication addressing deficiencies in the function of their a7 nAChR. To address the special needs of these smokers, we have proposed alternative therapies using alternative β2-receptor partial agonists with less off-target a7 activity [4], possibly in combination with an a7 drug such as GTS-21, which is in trials as an anti-schizophrenic.

Betel quid addiction and its connection to brain nicotine receptors:

Hundreds of millions of people worldwide are addicted to “betel nut” (areca), but unfortunately, to most people in Western nations, this addiction is perceived as little more than a curious Asian custom. Recent epidemiology has shown that betel use has concomitant health risks similar to tobacco use. Our recent research (5) suggests that there are links between nicotine and betel nut addictions.  More information on this topic is available at:


Recent Publications

  1. Papke, R.L. and S.F. Heinemann, The partial agonist properties of cytisine on neuronal nicotinic receptors containing the beta2 subunit. Mol. Pharm., 1994. 45:142-149. PMID: 8302273
  2. Papke, R.L., et al., Electrophysiological perspectives on the therapeutic use of nicotinic acetylcholine receptor partial agonists. J. Pharmacol. Exp. Ther., 2011. 337(2):367-379. PMC3083103
  3. Mineur, Y.S., et al., Cytisine-based nicotinic partial agonists as novel antidepressant compounds. J. Pharmacol. Exp. Ther., 2009. 329(1):377-86. PMC2670591
  4. Peng, C., et al., Differential modulation of brain nicotinic acetylcholine receptor function by cytisine, varenicline, and two novel bispidine compounds: emergent properties of a hybrid molecule. J. Pharmacol. Exp. Ther., 2013. 347(2):424-37. PMC3807070
  5. Roger L. Papke, Nicole A. Horenstein, and Clare Stokes. 2015. Nicotinic activity of arecoline, the psychoactive element of “betel nuts”, suggests a basis for habitual use and anti-inflammatory activity.  PLoS One Oct 21;10(10):e0140907. Press release and video:
  6. Nicole A. Horenstein†, Roger L. Papke†, Abhijit R. Kulkarni, Ganesh U. Chaturbhuj, Clare Stokes, Khan Manther and Ganesh A. Thakur. 2016. Critical Determinants of α7 Nicotinic Acetylcholine Receptor Allosteric Activation: Separation of Direct Allosteric Activation and Positive Allosteric Modulation.  J. Bio. Chem. 291(10):5049-67.  †These authors contributed equally.
  7. Can Peng, Matthew R. Kimbrell, Chengju Tian, Thomas F. Pack, Peter A. Crooks, E. Kim Fifer, and Roger L. Papke. 2013. Multiple modes of α7 nAChR non-competitive antagonism of control agonist-evoked and allosterically enhanced currents.  Mol. Pharm., 84(3):459-75.