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Michel Baudry

Publications and source records attributed to Michel Baudry.

21 records · Page 2Linked to original sources

Chronic multichannel recordings from organotypic hippocampal slice cultures: protection from excitotoxic effects of NMDA by non-competitive NMDA antagonists.

In vitro neuronal damage has traditionally been evaluated by biochemical or anatomical but not by electrophysiological techniques. In the present study, we combined two newly developed technologies, an 8 x 8 multi-electrode array (MED-64) and cultured hippocampal slices, to demonstrate the potential use of electrophysiological measures as index of neuronal damage. We first demonstrated the stability of electrophysiological recordings over prolonged periods of time (up to 14 days) in field CA1 of cultured hippocampal slices following electrical stimulation of the Schaffer collateral pathway. We then assessed the neurotoxic properties of NMDA and AMPA and determined that the time-course, potency, and efficacy of these two neurotoxins were similar to those assessed by other experimental approaches. We also compared the efficacy and potency of two non-competitive NMDA receptor antagonists to protect against NMDA-mediated neurotoxicity. Again, the results matched well with the results obtained from traditional techniques. Thus, this new technology might provide a new and powerful method to study the chronic effects of drugs or other experimental manipulations in an in vitro preparation.

Animals↗

Attenuation of zinc-induced intracellular dysfunction and neurotoxicity by a synthetic superoxide dismutase/catalase mimetic, in cultured cortical neurons.

Excessive extracellular zinc may contribute to neuronal cell death following ischemia and seizures, although the mechanisms mediating zinc-induced cell death remain largely unknown. In this study, we examined potential cellular and molecular mechanisms associated with zinc neurotoxicity and determined the neuroprotective effects of the superoxide dismutase (SOD)/catalase mimetic, EUK-134. Cortical neuron cultures exposed to zinc for 24 h exhibited concentration-dependent increases in lactate dehydrogenase (LDH) release and number of apoptotic cell bodies. Both effects were prevented by treatment with EUK-134. Zinc exposure resulted in increased release of cytochrome c from the mitochondria into the cytosol. Treatment with EUK-134 blocked this parameter of mitochondrial dysfunction. Exposure of cultures to zinc for 4 h produced an elevation of reactive oxygen species (ROS) as determined by increased 2,7-dichlorofluorescein (DCF) fluorescence, which was followed by an increase in lipid peroxidation. EUK-134 completely attenuated ROS production and subsequent oxidative damage. Finally, zinc exposure activated NF-kappaB, an effect also prevented by EUK-134. These data indicate that multiple cellular and molecular mechanisms are involved in zinc neurotoxicity. As all these mechanisms appear to be sensitive to treatment with EUK-134, our data suggest that oxidative stress occurs early in the cascade of events triggered by zinc.

Animals↗

Long-term recording of LTP in cultured hippocampal slices.

Long-term potentiation (LTP) was elicited by high frequency stimulation in hippocampal slices cultured on multi-electrode arrays. LTP lasting more than 1 h was recorded in 75% of slices, and a significant number of slices exhibited a non-decaying LTP that lasted more than 48 h. LTP induction was completely and reversibly blocked by an antagonist of the NMDA receptor, APV. Our results suggest the possibility of using chronic recording in hippocampal slices cultured on multi-electrode arrays to study the mechanisms underlying LTP maintenance and stabilization.

2-Amino-5-phosphonovalerate↗