Department of Physiology
McIntyre Medical Sciences Building,
3655 Promenade Sir William Osler
Montréal, Québec H3G 1Y6
several decades, electrophysiological and neuropharmacological techniques
have been used to identify synaptic transmitters (glutamate, GABA and
acetylcholine), their modes of action, and the role of cytoplasmic calcium
in the control of neuronal excitability. In recent years, main focus has
been on the effects of acute energy deprivation (hypoxia and hypoglycemia)
on brain function, in hippocampal slices from normal and diabetic rats,
as well as mice (both wild-type and some mutants). By means of extra-
and intracellular recording (including voltage clamp), we have studied
endogenous modulators and membrane channels involved in the rapid but
reversible suppression of synaptic transmission and neuronal excitability
triggered by hypoxia/hypoglycemia, with special emphasis on the long-term
potentiation of synaptic responses induced by a blocker of glycolysis,
Education: M.B.Ch.B., Edinburgh,
Calcium dependence of LTP induced by 2-deoxyglucose in CA1 neurons.
J Neurophysiol. 1996 Oct;76(4):2343-52.
G, Xu YZ, Krnjevič
Potassium conductance causing hyperpolarization of CA1 hippocampal neurons
J Neurophysiol. 1998 Nov;80(5):2378-90.
Persistent block of CA1 synaptic function by prolonged hypoxia.
Neuroscience. 1999 Mar;90(3):759-70.
Diabetes mellitus preserves synaptic plasticity in hippocampal slices
from middle-aged rats.
JM, Tekkök SB, Krnjevič
Hypoxia on hippocampal slices from mice deficient in dystrophin (mdx) and
J Cereb Blood Flow Metab. 2000 Jan;20(1):145-52.
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