Stephen D. Meriney, PhD

Professor, Neuroscience, Psychiatry


461 Crawford Hall
F: 412-624-9198
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PhD, University of Connecticut (1986)


Regulation and modulation of presynaptic ion channels and transmitter release in healthy and diseased synapses.

Research Summary

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.

Electrical measurements of transmitter release and calcium imaging in nerve terminals:We use microelectrode recordings of transmitter release, in combination with high-resolution calcium imaging in adult motor nerve terminals to examine the characteristics and modulation of the calcium entry that control transmitter release at the synapse. We have developed a method for imaging the spatial distribution of calcium entry following a single action potential stimulus. Using this approach, we have provided evidence that a very small subset of the available calcium channels opens in the nerve terminal with each stimulus. We hypothesize that transmitter release is triggered by the opening of single calcium channels in these nerve terminals and have begun to study the modulation of this process. We are interested in the mechanisms that control calcium entry and how this entry triggers transmitter release. Calcium imaging experiments are combined with microelectrode recordings of the magnitude of transmitter release, and MCell computer models of ion diffusion and binding reactions within the nerve terminal, to aid in the interpretation of data collected.

Transmitter release in control and disease model mouse motor nerve terminals: We have been using mouse neuromuscular preparations to study the regulation of transmitter release in both normal mice, and those that have been passively-transferred the disease Lambert-Eaton Myasthenic syndrome. In addition, we also use con-focal imaging of neuromuscular junctions stained with various antibodies directed against presynaptic proteins to characterize the presence and distribution of relevant molecules. This work furthers our understanding of calcium-dependent mechanisms, and is part of our effort to evaluate the effects of novel calcium channel agonists that might be of therapeutic benefit in diseases that result in neuromuscular weakness.

Modulation of N- and P/Q-type calcium channels expressed in cell lines: We use cell lines expressing various calcium channel subtypes as a model system to examine directly the gating and modulation of these channels, and the effects of various novel drugs that we are developing. This allows us to study various forms of modulation in a model system where there are no other calcium channels expressed, and we can focus on studying in isolation the types of calcium channels that control transmitter release at many synapses.


Dittrich M. Meriney SD. (2016) Single calcium channels stand out in the crowd.  Channels 10:1-2.

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.   

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.

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.