Journal of Neuroscience, Vol 14, 5028-5034, Copyright © 1994 by Society for Neuroscience
TEA elicits two distinct potentiations of synaptic transmission in the CA1 region of the hippocampal slice
E Hanse and B Gustafsson
Department of Physiology, University of Goteborg, Sweden.
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)
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