We investigated calcium influx in the long lasting potentiation induced in area CA1 of rat hippocampus by brief bath application of the G-protein activator AlF4−(NaF/AlCl3). Brief (10 min) bath application of AlF4− in standard saline (with 2mM Ca2+) consistently induced a long lasting potentiation which was not observed if AlF4− was bath-applied in nominally calcium free saline. Increasing the potential calcium influx, either by raising extracellular calcium concentration to 3.5 mM or by addition of the voltage operated calcium channel (VOCC) agonist BayK8644. failed to increase the number of slices exhibiting potentiation or the mean level of potentiation. Bath application of AlF4− in the presence of the VOCC antagonist failed to block the potentiation and AlF4− readily induced a long lasting potentiation under voltage clamp conditions, strongly suggesting that the calcium influx required for AlF4-induced potentiation is not through NMDA receptors or VOCC channels. It is suggested that the calcium required may be provided by an ongoing recharging and emptying of IP3 sensitive intracellular Ca2+ stores.
Long-term potentiation of GABAergic synaptic transmission in neonatal rat hippocampus