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Department of Physiology
McGill University
McIntyre Medical Sciences Building,
Room 1127
3655 Promenade Sir William Osler
Montréal, Québec H3G 1Y6
(514) 398-4334
ellis.cooper@mcgill.ca |
Education:
B.Eng (SGWU); MSc
(Surrey); PhD (McMaster)
Research
Area: Neurophysiology / Neuroscience
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,
Laval
University
A.P. Haghighi, Professor,
McGill
University
V. Campanucci, Professor,
University
of Saskatchewan
A. Krishnaswamy, Postdoc,
Harvard
University
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
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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.
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