Department of Physiology
ellis.cooper [at] mcgill.ca
Education: B.Eng (SGWU); MSc (Surrey); PhD (McMaster)
Research Area: Neurophysiology / Neuroscience
Currently the Cooper lab has a few openings for graduate students and postdoctoral trainees. Contact E. Cooper for more information.
Research in the Cooper lab focuses on activity-dependent mechanisms that govern the rearrangement and function of synapses as neural circuits become established during early postnatal life. Our projects address 2 main issues: One is to understand how activity influences the formation of connections between preganglionic terminals and postganglionic sympathetic neurons in the superior cervical ganglion (SCG) of wild type and mutant mice.
The second project addresses a new concept for diabetic autonomic neuropathies. We are investigating the idea that these diabetic-induced dysautonomias results, in part, from a synaptic defect and our work points to the ganglionic nAChRs as targets of hyperglycemia-induced downstream signals.
Our experiments use interdisciplinary approaches that combine different molecular and cellular techniques, such as: electrophysiology, cellular imaging, quantitative PCR, viral-mediated gene transfer techniques. In addition, we are developing a new mouse model to investigate the role of synaptic activity in the formation of functional neural circuits. The Cooper lab gratefully acknowledges funding from CIHR, JDRF and HSFC.
Graduates from the Cooper lab
S. McFarfane Professor, University of Calgary
P. De Koninck, Professor, LavalUniversity
A.P. Haghighi, Professor, McGillUniversity
V. Campanucci, Professor, University of Saskatchewan
A. Krishnaswamy, Postdoc, HarvardUniversity
I. Virard, Institut de Neurobiologie de la Méditerranée
A. Mandelzys, CEO, Thallion Pharmaceutical Inc
A. Sherman, President, Alembic Instruments
D. Wheeler, Research Scientist, Dart NeuroScience
Campanucci, VA., Krishnaswamy, A., Cooper, E. (2010) Diabetes depresses synaptic transmission in sympathetic ganglia by inactivating nAChRs through a conserved intracellular cysteine residue. Neuron (in press).
Krishnaswamy, A., Cooper, E. (2009) An Activity-Dependent Retrograde Signal Induces the Expression of the High-Affinity Choline Transporter in Cholinergic Neurons. Neuron 61, 272–286.
Caffery, P.M., Krishnaswamy, A., Sanders, T., Hartlaub, H., Liu, J, Klysik, J., Cooper, E., Hawrot, E. (2009) Engineered a-bungarotoxin-sensitivity enables visualization and pharmacological characterization of postsynaptic a3-containing nicotinic acetylcholine receptors in a novel knock-in mouse. Eur. J Neurosci. 30: 2064-2076.
Campanucci, VA., Krishnaswamy, A., Cooper, E. (2008) Mitochondrial reactive oxygen species inactivate neuronal nicotinic acetylcholine receptors and induce long-term depression of fast nicotinic synaptic transmission. J. Neuroscience 28: 1733 - 1744.
Rassadi, S., Krishnaswamy, A., Pié, B., McConnell, R., Michele H. Jacob, M.H., and Cooper, E. (2005). A null mutation for the a3 nicotinic acetylcholine (ACh) receptor gene abolishes fast synaptic activity in sympathetic ganglia and reveals that ACh output from developing preganglionic terminals is regulated in an activity-dependent retrograde manner. J. Neuroscience 25 (37): 8555-9566.
Gingras, J., Rassadi, S., Cooper, E., and Ferns, M. (2002) Agrin plays an organizing role in the formation of sympathetic synapses. Journal of Cell Biology 158: 1109-1118.
Wheeler, D. G. and Cooper, E. (2001) Depolarization Strongly Induces Human CMV Major Immediate-Early Promoter Activity in Neurons. J. Biological Chemistry. 276: 31978-31985.
Haghighi, A. and Cooper, E. (2000). A molecular link between inward rectification and calcium permeability of neuronal nicotinic acetylcholine a3b4 and a4b2 receptors. Journal of Neuroscience 20: 529-541.
Haghighi, A. and Cooper, E. (1998). Neuronal nicotinic acetylcholine receptors are blocked by intracellular spermine in a voltage-dependent manner. Journal of Neuroscience 18: 4050-4062.