title: TEA elicits two distinct potentiations of synaptic transmission in the CA1 region of the hippocampal slice.
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)
authors.affiliation: Department of Physiology, University of Göteborg, Sweden.
authors.forename: E
authors.initials: E
authors.lastname: Hanse
authors.forename: B
authors.initials: B
authors.lastname: Gustafsson
mesh_terms: D015763:2-Amino-5-phosphonovalerate / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000502:physiology; D015220:Calcium Channels / Q000502:physiology; D005731:Ganglionic Stimulants / Q000494:pharmacology*; D006168:Guinea Pigs; D006624:Hippocampus / Q000502:physiology*; D017774:Long-Term Potentiation / Q000187:drug effects*; D010852:Picrotoxin / Q000494:pharmacology; D000644:Quaternary Ammonium Compounds / Q000494:pharmacology*; D016194:Receptors, N-Methyl-D-Aspartate / Q000502:physiology; D009435:Synaptic Transmission / Q000502:physiology*
chemical_list: D015763:2-Amino-5-phosphonovalerate; D002118:Calcium; D015220:Calcium Channels; D005731:Ganglionic Stimulants; D010852:Picrotoxin; D000644:Quaternary Ammonium Compounds; D016194:Receptors, N-Methyl-D-Aspartate; C027917:tetramethylammonium