Neuroprotective role of monocarboxylate transport during glucose deprivation in slice cultures of rat hippocampus
Neuroprotective role of monocarboxylate transport during glucose deprivation in slice cultures of rat hippocampus
The effects of energy substrate removal and metabolic pathway block have been examined on neuronal and glial survival in organotypic slice cultures of rat hippocampus. Slice cultures resisted 24 h of exogenous energy substrate deprivation. Application of 0.5 mM alpha-cyano-4-hydroxycinnamate (4-CIN) for 24 h resulted in specific damage to neuronal cell layers, which could be reversed by co-application of 5 mM lactate. Addition of 10 mM 2-deoxyglucose in the absence of exogenous energy supply produced widespread cell death throughout the slice. This was partly reversed by co-application of 5 mM lactate. These effects of metabolic blockade on cell survival were qualitatively similar to the effects on population spikes recorded in the CA1 cell layer following 60 min application of these agents. The data suggest that monocarboxylate trafficking from glia to neurons is an essential route for supply of energy substrates to neurons particularly when exogenous energy supply is restricted.
459-466
Cater, H.L.
5bc60807-1566-433e-a43f-d93bb3a6b872
Benham, C.D.
26e36295-dcbb-421e-9151-0c29878c1101
Sundstrom, L.E.
41cd4162-0bf0-452e-8f13-8a7cf8cfa5b1
2001
Cater, H.L.
5bc60807-1566-433e-a43f-d93bb3a6b872
Benham, C.D.
26e36295-dcbb-421e-9151-0c29878c1101
Sundstrom, L.E.
41cd4162-0bf0-452e-8f13-8a7cf8cfa5b1
Cater, H.L., Benham, C.D. and Sundstrom, L.E.
(2001)
Neuroprotective role of monocarboxylate transport during glucose deprivation in slice cultures of rat hippocampus.
Journal of Physiology, 531 (Pt 2), .
Abstract
The effects of energy substrate removal and metabolic pathway block have been examined on neuronal and glial survival in organotypic slice cultures of rat hippocampus. Slice cultures resisted 24 h of exogenous energy substrate deprivation. Application of 0.5 mM alpha-cyano-4-hydroxycinnamate (4-CIN) for 24 h resulted in specific damage to neuronal cell layers, which could be reversed by co-application of 5 mM lactate. Addition of 10 mM 2-deoxyglucose in the absence of exogenous energy supply produced widespread cell death throughout the slice. This was partly reversed by co-application of 5 mM lactate. These effects of metabolic blockade on cell survival were qualitatively similar to the effects on population spikes recorded in the CA1 cell layer following 60 min application of these agents. The data suggest that monocarboxylate trafficking from glia to neurons is an essential route for supply of energy substrates to neurons particularly when exogenous energy supply is restricted.
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Published date: 2001
Organisations:
Clinical Neurosciences
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Local EPrints ID: 27544
URI: http://eprints.soton.ac.uk/id/eprint/27544
ISSN: 0022-3751
PURE UUID: e2c34eb2-ac77-4494-8430-18b98ef73f66
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Date deposited: 28 Apr 2006
Last modified: 08 Jan 2022 15:52
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Author:
H.L. Cater
Author:
C.D. Benham
Author:
L.E. Sundstrom
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