Neuroprotective role of monocarboxylate transport during glucose deprivation in slice cultures of rat hippocampus
Article first published online: 5 AUG 2004
The Journal of Physiology
Volume 531, Issue 2, pages 459–466, March 2001
How to Cite
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. The Journal of Physiology, 531: 459–466. doi: 10.1111/j.1469-7793.2001.0459i.x
- Issue published online: 5 AUG 2004
- Article first published online: 5 AUG 2004
- (Received 16 May 2000; accepted after revision 31 October 2000)
- 1The effects of energy substrate removal and metabolic pathway block have been examined on neuronal and glial survival in organotypic slice cultures of rat hippocampus.
- 2Slice 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.
- 3Addition 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.
- 4These 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.
- 5The 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.