University of Vermont

College of Medicine

Department of Neurological Sciences

Bio for Rodney Parsons, PhD
Rodney Parsons, PhD

Rodney Parsons, PhD

Department of Neurological Sciences

Contact Information
Office Location:
Neurological Sciences Dept, Given C425A, Burlington


Parsons Lab


1965: Ph.D., Physiology, Stanford University, Stanford, California
1962: AB, Biology, Middlebury College, Middlebury, Vermont

Academic Interests

My primary teaching responsibilities include lectures in the VIC Neural Science Course on basic neurophysiology and synaptic mechanisms, and on motor system structure and function.


Cardiovascular disease is a major cause of death in the USA and dysfunction of the neural regulation of the heart is an important factor in the etiology of cardiac disease. An emphasis of current research activities is the elucidation of mechanisms that regulate the excitability of parasympathetic cardiac and sympathetic neurons innervating cardiac tissues.

One question under investigation analyzes mechanisms that underlie synaptic integration and excitability of neurons within the intrinsic cardiac ganglia. Historically, the parasympathetic cardiac ganglia were considered relay stations: sites simply transmitting preganglionic information with minimal modification to the postganglionic cells innervating cardiac tissue. We now know that afferent fibers and sympathetic postganglionic axons, in addition to parasympathetic preganglionic fibers, innervate the cardiac ganglia. Each of these neural inputs utilizes different chemical neurotransmitters. Ongoing studies test the hypothesis that the collective cardiac ganglia form an Intrinisic Cardiac Nervous System (ICNS), which receives multiple neurochemical signals that are capable of modulating the inhibitory output of the cardiac neurons to the heart. Recent studies have shown that exogenous or neurally-released pituitary adenylate cyclase-activating polypeptide (PACAP) depolarizes and increases membrane excitability of the cardiac neurons. We are determining the underlying ionic mechanisms and intracellular signaling cascades responsible for PACAP’s actions. These experiments use whole cell patch clamp recording techniques on dissociated neurons and intracellular recordings from neurons in intact whole mount ganglia preparations to determine second messenger-induced modulation of ion channel function. In addition, high speed, confocal imaging techniques analyze transmitter-induced alterations in intracellular calcium.

A second area of interest is the response of the cardiac neurons to injury. Cardiac neurons can be axotomized during transplantation or injured during laser surgery to ablate ectopic pacemaker sites. However, the cardiac ganglia are not readily accessible for in vivo studies. Thus, we have developed an explant-cultured guinea pig ICNS preparation in which concentrations of parasympathetic preganglionic fiber-derived regulatory factors such as PACAP and cardiac tissue-derived regulatory factors such as neurturin are minimal. This preparation allows us to analyze, using electrophysiological, immunocytochemical and PCR techniques, the role of PACAP and neurturin in the regulation of the electrical and chemical phenotype of the cardiac neurons. The studies of the modulation of electrical properties and chemical phenotype of neurons within the ICNS should elucidate how alterations in the neural input or response following injury might contribute to the initiation of cardiac arrhythmias.

A third question concerns the mechanisms underlying somatic release of quantal ATP from dissociated guinea pig sympathetic stellate neurons. Somatic transmitter release may be a key mechanism by which neurons signal within peripheral ganglia, including the sensory dorsal root ganglia and autonomic ganglia. Our earlier studies showed that somatic vesicular ATP was released in a voltage- and calcium-dependent mechanism and that the released ATP activated P2X receptors expressed on the same neurons. The ongoing studies analyze the role of calcium-induced calcium release and calcium sequestration by mitochondria in the regulation of somatic ATP release. These studies use a combination of current clamp and voltage clamp recording from dissociated neurons.

Administrative Interests

I am the Director of the COBRE Center for Neuroscience Excellence grant that supports two multi-user research facilities, the Cell/Molecular Biology Core and the Imaging/ Physiology Core.

Academic Appointments

2013-Present: Professor, Department of Neurological Sciences, University of Vermont
2012-2013: Professor and Co-Chair, Department of Neurological Sciences, University of Vermont
1979-2012: Professor and Chairman, Department of Anatomy and Neurobiology, University of Vermont
1973-1979: Professor of Physiology and Biophysics, University of Vermont
1969-1973: Associate Professor of Physiology and Biophysics, University of Vermont
1967-1969: Assistant Professor of Physiology and Biophysics, University of Vermont
1965-1967: Postdoctoral Fellow in Physiology, Columbia University, National Institutes of Health

Research Grants

8P30GM103498 "Center for Neuroscience Excellence", Principal Investigator, 8/01/2011-6/30/2016 The overall goal of the Neuroscience COBRE has been to integrate and expand neuroscience research and training at UVM by building a collaborative intellectual infrastructure, developing cutting-edge shared core facilities, supporting recruitment of new junior faculty, and providing research project and pilot project funding for neuroscience faculty, especially junior faculty, in multiple colleges.

Awards and Honors

1989-1996: Jacob Javits Neuroscience Investigator Award
1990-1991: University Scholar
1965-1967: National Institutes of Health Postdoctoral Fellowship in Physiology, Columbia University


May V, Buttolph TR, Girard BM, Clason TA and Parsons RL.  PACAP-induced ERK activation in HEK cells expressing PAC1 receptors involves both receptor internalization and PKC signaling. Am J Physiol Cell Physiol, 306: C1068-C1079, 2014.

Merriam LA, Girard BM, Baran CN, Hardwick JA, May V and Parsons RL. PAC1 receptor internalization and endosomal signaling mediate the PACAP-induced increase in guinea pig cardiac neuron excitability. J Neuroscience, 33: 4614-4622, 2013.

Tompkins, JD, Vizzard MA and Parsons RL. Synaptic transmission at parasympathetic neurons of the major pelvic ganglion from normal and diabetic mice. J Neurophysiol.109: 988-995, 2013.

Hoover, DB, Girard, BM, Hoover, JL and Parsons, RL. PAC1 receptors mediate positive chronotrophic responses to PACAP-27 and VIP in isolated mouse atria.  European Journal of Pharmacology, 713: 25-30, 2013.

Herring N, J. Cranley, M.N. Lokalel,  D. Li, J. Shanks, E.N. Alston, B.M. Girard, E. Carter, R.L. Parsons, B.A. Habecke and D.J. Paterson. The cardiac sympathetic co-transmitter galanin reduces acetylcholine release and vagal bradycardia: implications for neural control of cardiac excitability. J Mol Cell Cardiol. 52:667-676, 2012.

Hamill, R.W., Tompkins, J.D., Girard, B.M., Kershen, R.T., Parsons, R.L. and M.A. Vizzard. Autonomic dysfunction and plasticity in micturition reflexes in human a-synuclein mice. Dev Neurobiol 72(6):918-36, 2012.

To view more of Dr. Parsons' publications, please visit PubMed.