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Neuroprotective role of monocarboxylate transport during glucose deprivation in slice cultures of rat hippocampus
Author(s) -
Cater H. L.,
Benham C. D.,
Sundstrom L. E.
Publication year - 2001
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.2001.0459i.x
Subject(s) - hippocampus , neuroprotection , slice preparation , population , microbiology and biotechnology , cell , chemistry , substrate (aquarium) , programmed cell death , biology , neuroscience , biophysics , biochemistry , electrophysiology , apoptosis , medicine , ecology , environmental health
1 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. 2 Slice cultures resisted 24 h of exogenous energy substrate deprivation. Application of 0.5 mM α‐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. 3 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. 4 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. 5 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.