2-Deoxyglucose-Induced Long-Term Potentiation In Ca1 Is Not Prevented By Intraneuronal Chelator. Yong-Tao Zhao and Krešimir Krnjevi. Anaesthesia Research Department, McGill University, Montréal, QC, H3G 1Y6 Canada.
APStracts 6:0483N, 1999.
In hippocampal slices, temporary (10-20 min) replacement of glucose with 10 mM 2-deoxyglucose is followed by marked and very sustained potentiation of EPSPs (2-DG LTP). To investigate its mechanism, we examined 2-DG's effect in CA1 neurons recorded with sharp 3 M KCl electrodes containing a strong chelator, 50 or 100 mM ethylene glycol-bis(ß-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA). In most cases, field EPSPs were simultaneoulsy recorded; and conventional LTP was also elicited in some cells by tetanic stimulation of stratum radiatum. 2-DG potentiated intracellular EPSP slopes by 48 ? 5.1% (SEM) in nine cells recorded with plain KCl electrodes and by 52 ? 6.2% in seven cells recorded with EGTA-containing electrodes. In four of the latter, tetanic stimulation (twice 100 Hz for 1 s) failed to evoke LTP (2 ? 1.1%), though field EPSPs were clearly potentiated (by 28 ? 6.9%). Thus, unlike tetanic LTP, 2-DG LTP is not readily prevented by post-synaptic intraneuronal injection of EGTA. These findings are in keeping with other evidence that the rise in post-synaptic (somatic) [Ca2+]i caused by 2-DG is not the principal trigger for the subsequent 2-DG LTP and that it may be a purely presynaptic phenomenon.
Received 24 May 1999; accepted in final form 2 September 1999.
APS Manuscript Number J423-9.
Article publication pending Journal of Neurophysiology.
ISSN 1080-4757 Copyright 1999 The American Physiological Society.
Published in APStracts on 21 December 1999