Stephen D. Meriney, Ph.D.

  • Professor
  • Department of Neuroscience

Education & Training

  • BS, Zoology, University of Hampshire 1982
  • PhD, Physiology/Neuroscience, University of Connecticut 1986

Research Interest Summary

Our laboratory focuses on synaptic function and plasticity, especially as it relates to the regulation and modulation of presynaptic ion channels and transmitter release in both healthy and disease-model animals.

Research Categories

Research Interests

Our research program focuses on studying mechanisms that control synaptic plasticity in the nervous system. We use several model systems that provide the opportunity to study these mechanisms directly. In particular, we are interested in those events that occur in nerve terminals to regulate or modulate synaptic transmission in both normal and disease conditions.

Some projects explore the basic science of synaptic plasticity using neuromuscular synapses as model preparations.  We are exploring presynaptic homeostatic plasticity short-term synaptic plasticity in both healthy and diseased synapses to gain a better understanding of the presynaptic mechanisms that control transmitter release. 

Other projects in the lab focus on developing new treatments for diseases that lead to synaptic weakness.  These include neuromuscular diseases like Lambert-Eaton myasthenic syndrome and other rare synaptic diseases, but also the application of our novel drugs to the treatment of normal aging-induced synaptic weakness. 

Representative Publications

Luo F. Dittrich M. Stiles JR. Meriney SD. (2011) Single pixel optical fluctuation analysis of calcium channel function in active zones of motor nerve terminals. Journal of Neuroscience  31: 11268-11281.

Liang M. Tarr TB. Bravo-Altamirano K. Valdomir G. Rensch G. Swanson L. DeStefino NR. Mazzarisi CM. Olszewski RA. Wilson GM. Meriney SD. and Wipf P. (2012) Synthesis and Biological Evaluation of a Selective N- and P/Q-Type Calcium Channel Agonist.  ACS Medicinal Chemistry Letters 3: 985-990.

Tarr TB. Dittrich M. Meriney SD. (2013) Are Unreliable Release Mechanisms Conserved from NMJ to CNS?  Trends in Neuroscience 36: 14-22.

Tarr TB. Malick W. Liang M. Valdomir G. Frasso M. Lacomis D. Reddel SW. Garcia-Ocano A. Wipf P. Meriney SD. (2013) Evaluation of a novel calcium channel agonist for therapeutic potential in Lambert-Eaton Myasthenic Syndrome. Journal of Neuroscience 33: 10559-10567.

Dittrich M. Pattillo JM. King JD. Cho S. Stiles JR. Meriney SD. (2013) An excess calcium binding site model predicts neurotransmitter release at the NMJ.  Biophysical Journal 104: 2751-2763.

Meriney SD. Dittrich M. (2013) Organization and function of transmitter release sites at the neuromuscular junction.  Journal of Physiology 591: 3159-3165. 

Tarr TB. Lacomis D. Reddel SW. Liang M. Valdomir G. Frasso M. Wipf P. Meriney SD. (2014) Complete reversal of neuromuscular disease-induced synapse impairment by a combination of 3,4-DAP and a novel calcium channel agonist. Journal of Physiology 592: 3687-3696.

Ma J. Kelly L. Ingram J. Price TJ. Meriney SD. Dittrich M. (2015) New insights into short-term synaptic facilitation at the frog neuromuscular junction. Journal of Neurophysiology 113: 71-87.

Luo F. Dittrich M. Cho S. Stiles JR. Meriney SD. (2015) Transmitter release is evoked with low probability predominately by calcium flux through single channel openings at the frog neuromuscular junction. Journal of Neurophysiology 113: 2480-2489.

Tarr TB. Wipf P. Meriney SD. (2015) Synaptic pathophysiology and treatment of Lambert-Eaton myasthenic syndrome. Molecular Neurobiology 52:456-463.   

Full List of Publications