Prolonged enhancement of synaptic transmission in area CA1 of rat hippocampal slices induced by NaF/AlCl3 does not require NMDA receptor activation but is suppressed by inhibitors of phosphoinositide-mediated signalling pathways.

The processes underlying the action of AlF4- (10 mM NaF/10 microM AlCl3) in inducing long-lasting enhancement of synaptic transmission in area CA1 of rat hippocampal slices have been investigated. Exposure of hippocampal slices to AlF4- for 10 min caused population EPSP slope to rise by approximately 50% within 60 min of washing off the NaF/AlCl3 saline. This effect was not inhibited either by APV (50 microM), or by temporary interruption of the delivery of test stimuli during and for up to 20 min after application of the AlF4- -containing medium. However, pretreatment of preparations with either thapsigargin (1 microM) or staurosporine (1 microM), 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 signalling pathway are necessary for potentiation to occur. Ca2+ influx is also a requirement, but does not occur through the NMDA receptor.