Western University of Health Sciences Graduate College of Biomedical Sciences Western University of Health Sciences
Graduate College of Biomedical Sciences

Baudry Lab

1. Mechanisms
implicated in long-term synaptic potentiation and depression in hippocampus and
other brain regions.
My laboratory has been investigating for several years
the molecular and cellular mechanisms underlying LTP and LTD phenomena in
neonatal and adult rodents. In 1984, in collaboration with Gary Lynch, we
proposed a new and specific hypothesis for learning and memory, and several of
the components we proposed are now widely acknowledged to be involved in
synaptic plasticity and learning and memory. In particular, we proposed that
the calcium-dependent protease, calpain, played a critical role in synaptic plasticity
and in learning and memory. We are using a combination of electrophysiological,
neurochemical, and neuroanatomical techniques to study the roles of various
biochemical processes in regulating short-term as well as long-term changes in
synaptic efficacy. In collaboration with the laboratory of Dr. Xiaoning Bi at
WesternU, we are investigating the possibility that dysregulation of these
processes is involved in neurodevelopmental disorders, such as in the Angelma
Syndroms.

2. Regulation of
glutamate receptors.
My laboratory has been studying post-translational
mechanisms regulating the properties of AMPA and NMDA and metabotropic
glutamate receptors. In particular, we are investigating the mechanisms
involved in the maturation, processing, insertion and internalization of the
receptors. We are also evaluating the role of calpain-mediated truncation of
the C-terminal domains of certain subunits of the receptors in receptor
function and regulation.

3. Role of oxygen free radicals in central
nervous system.
As a result of my association with a small start-up
pharmaceutical company in Bedford, MA, my laboratory has been investigating the
roles of oxygen free radicals in neurodegenerative phenomena. In particular, we
have tested the protective effects of a new class of synthetic catalytic
scavengers of reactive oxygen intermediates on neuronal damage elicited by
excitotoxins, neurotoxins, and beta-amyloid peptides.

4. Mechanisms
underlying selective neuronal degeneration.
My laboratory is interested in
studying the role of calcium-dependent proteases, calpains, in neuronal
degeneration resulting from neuronal insults or injury. Using a combination of
pharmacology and mutant mice expressing deletion of calpain genes or mutation
of the gene for the endogenous calpain inhibitor, calpastatin, we are
evaluating their contribution to neuronal death in various models of
neurodegeneration, including models of ischemia and Parkinson’s disease.

View Dr. Baudry’s biographical information here