CHARACTERIZATION OF THE ROLE OF CALCIUM IN ALF4-INDUCED LONG-TERM POTENTIATION IN AREA CA1 OF RAT HIPPOCAMPUS

We investigated calcium influx in the long lasting potentiation induce d in area CAI of rat hippocampus by brief bath application of the G-pr otein activator AlF4-(NaF/AlCl3). Brief (10 min) bath application of A lF4- in standard saline (with 2 mM Ca2+) consistently induced a long l asting potentiation which was not observed if AlF4- was bath-applied i n nominally calcium free saline. Increasing the potential calcium infl ux, either by raising extracellular calcium concentration to 3.5 mM or by addition of the voltage operated calcium channel (VOCC) agonist Ba yK8644, failed to increase the number of slices exhibiting potentiatio n or the mean level of potentiation. Bath application of AlF4- in the presence of the VOCC antagonist failed to block the potentiation and A lF4- readily induced a long lasting potentiation under voltage clamp c onditions, strongly suggesting that the calcium influx required for Al F4--induced potentiation is not through NMDA receptors or VOCC channel s. It is suggested that the calcium required may be provided by an ong oing recharging and emptying of IP3 sensitive intracellular Ca2+ store s.