Abstract
Extracellular application of tetraethylammonium (TEA) has been shown to elicit a prolonged synaptic potentiation in the CA1 region of the hippocampus that is unaffected by NMDA receptor antagonists, but is blocked by antagonists to voltage-dependent calcium channels (Aniksztejn and Ben-Ari, 1991; Huang and Malenka, 1993). In the present study the relation between TEA-induced potentiation and NMDA receptor- dependent long-term potentiation (LTP) was investigated in the CA1 region of the hippocampal slice using extracellular recordings and picrotoxin to block GABAA-mediated inhibition. Consistent with the finding of Huang and Malenka (1993), NMDA receptor-dependent LTP partially occluded the TEA-induced potentiation. However, this occlusion was abolished when the NMDA receptor antagonist D(-)-2-amino- 5-phosphonopentanoic acid (D-AP5) was present during the application of TEA, indicating one component of TEA-induced potentiation that is induced via NMDA receptor channels and another component that is distinct from NMDA receptor-dependent LTP. In the presence of antagonists to voltage-dependent calcium channels (nifedipine or nifedipine/flunarazine) application of TEA induced a potentiation that was largely occluded by NMDA receptor-dependent LTP. In common with NMDA receptor-dependent LTP, the TEA-induced potentiation, elicited in the presence of antagonists to voltage-dependent calcium channels, was associated with a symmetrical increase of the field EPSP. On the other hand, the TEA-induced potentiation elicited in the presence of D-AP5 produced an increase of the field EPSP that did not include the early part of the initial slope.(ABSTRACT TRUNCATED AT 250 WORDS)