CALCIUM-DEPENDENCE OF LTP INDUCED BY 2-DEOXYGLUCOSE IN CA1 NEURONS. TEKKoK, S. and K. KRNJEVI. Anaesthesia Research and Physiology Departments, McGill University, Montr[acute]eal, QC, H3G 1Y6, Canada.
APStracts 3:0151N, 1996.
SUMMARY AND CONCLUSIONS
1. As previously reported, in hippocampal slices from Sprague-Dawley rats, 13 min applications of 2-deoxy-D-glucose (2-DG) (substituting 10 mM 2-DG for glucose) --which sharply depress field EPSPs -- are followed by a sustained potentiation of the initial slopes of EPSPs (2-DG-LTP). 2. Such 2-DG-LTP is not prevented by exposing slices to Ca 2+ -free medium for 25 min before the 13 min 2-DG applications (in Ca 2+ -free medium). Therefore 2-DG-LTP is not dependent on influx of external Ca 2+ during the 2-DG applications. 3. When the Ca 2+ -free conditions begin 15 min before, and are maintained for 10 min after the 13 min 2-DG applications (in Ca 2+ -free medium), 2-DG-LTP is either totally suppressed or much reduced. A delayed Ca 2+ influx thus plays a crucial role in the induction of 2-DG-LTP. 4. Much longer Ca 2+ -free pretreatment (for 77 min) largely abolishes 2-DG-LTP. Therefore Ca 2+ release from a compartment (presumably intracellular) that is not readily depleted is also important for the induction of 2-DG-LTP. 5. This intracellular Ca 2+ store is sensitive to dantrolene Na (10 [mu]M) -- which prevents 2-DG-LTP - but not 10 [mu]M thapsigargin. 2-DG-LTP of isolated NMDA receptor-mediated EPSPs is only partly reduced by dantrolene. 6. Dantrolene (10 [mu]M) also reduces or abolishes post-tetanic potentiation, but not paired-pulse facilitation. 7. Depotentiation by 1 Hz stimulation is abolished by 20 [mu]M dantrolene. 8. In contrast to item 5, LTP elicited by tetanic stimulation is prevented by 10 [mu]M thapsigargin but not by dantrolene (
Received 21 March 1996; accepted in final form 24 June 1996.
APS Manuscript Number J232-6.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 25 July 1996