Characterisation of the role of calcium in AlF4-induced long-term potentiation in area CA1 of rat hippocampus

• Published in: Bioscience reports Vol. 17; no. 2; p. 209
• Main Authors: Breakwell, N A, Publicover, S J
• Format: Journal Article
• Language: English
• Published: England 01-04-1997
• Subjects: 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester - pharmacology; Aluminum Compounds - pharmacology; Animals; Calcium - physiology; Calcium Channel Blockers - pharmacology; Fluorides - pharmacology; Hippocampus - drug effects; Hippocampus - physiology; Ion Channel Gating; Ligands; Long-Term Potentiation - drug effects; Male; Nifedipine - pharmacology; Patch-Clamp Techniques; Rats; Rats, Wistar
• ISSN: 0144-8463
• DOI: 10.1023/A:1027337630321

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 A1F4-(NaF/AlCl3). Brief (10 min) bath application of A1F4 in standard saline (with 2 mM Ca2+) consistently induced a long lasting potentiation which was not observed if A1F4 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 A1F4- readily induced a long lasting potentiation under voltage clamp conditions, strongly suggesting that the calcium influx required for A1F4-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.