PROLONGED ENHANCEMENT OF SYNAPTIC TRANSMISSION IN AREA CA1 OF RAT HIPPOCAMPAL SLICES INDUCED BY NAF ALCL(3) DOES NOT REQUIRE NMDA RECEPTOR ACTIVATION BUT IS SUPPRESSED BY INHIBITORS OF PHOSPHOINOSITIDE-MEDIATED SIGNALING PATHWAYS/

Citation
Na. Breakwell et Sj. Publicover, PROLONGED ENHANCEMENT OF SYNAPTIC TRANSMISSION IN AREA CA1 OF RAT HIPPOCAMPAL SLICES INDUCED BY NAF ALCL(3) DOES NOT REQUIRE NMDA RECEPTOR ACTIVATION BUT IS SUPPRESSED BY INHIBITORS OF PHOSPHOINOSITIDE-MEDIATED SIGNALING PATHWAYS/, Brain research, 633(1-2), 1994, pp. 72-76
Citations number
22
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00068993
Volume
633
Issue
1-2
Year of publication
1994
Pages
72 - 76
Database
ISI
SICI code
0006-8993(1994)633:1-2<72:PEOSTI>2.0.ZU;2-J
Abstract
The processes underlying the action of AlF4- (10 mM NaF/10 mu M AlCl3) in inducing long-lasting enhancement of synaptic transmission in area CA1 of rat hippocampal slices have been investigated. Exposure of hip pocampal slices to AlF4- for 10 min caused population EPSP slope to ri se by approximately 50% within 60 min of washing off the NaF/AlCl3 sal ine. This effect was not inhibited either by APV (50 mu M), or by temp orary interruption of the delivery of test stimuli during and for up t o 20 min after application of the AlF4--containing medium. However, pr etreatment of preparations with either thapsigargin (1 mu M) or stauro sporine (1 mu M), or omission of Ca2+ from the AlF4--containing saline (no addition of EGTA) prevented the potentiating action of NaF/AlCl3. We conclude that the potentiating effect of AlF4- is via a G-protein linked to phosphoinositide turnover, and that both arms of this signal ling pathway are necessary for potentiation to occur. Ca2+ influx is a lso a requirement, but does not occur through the NMDA receptor.