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Journal of Neuroscience, Vol 13, 568-576, Copyright © 1993 by Society for Neuroscience
Examination of TEA-induced synaptic enhancement in area CA1 of the hippocampus: the role of voltage-dependent Ca2+ channels in the induction of LTP
YY Huang and RC Malenka
Department of Psychiatry, University of California, San Francisco 94143.
The role of voltage-dependent Ca2+ channels (VDCCs) in the induction of
long-term potentiation (LTP) in the CA1 region of rat hippocampus was
determined by examining the relationship between LTP and the long- lasting
synaptic enhancement induced by extracellular application of
tetraethylammonium (TEA). Consistent with previous findings (Aniksztejn and
Ben-Ari, 1991), the TEA-induced synaptic enhancement did not require NMDA
receptor activation. It was blocked by the L-type VDCC antagonist
nifedipine or by intracellular injection of the Ca2+ chelator
1,2-bis(2-amino-phenoxy)ethane N,N,N',N'-tetra-acetic acid (BAPTA) and
could be mimicked by direct activation of VDCCs with repetitive
depolarizing current pulses. In contrast to its effect on TEA-induced
synaptic enhancement, nifedipine had no effect on the magnitude or duration
of NMDA receptor-dependent LTP. Saturation of NMDA receptor-dependent LTP
reduced the magnitude of the TEA-induced synaptic enhancement. Similarly,
increasing synaptic strength by initial application of TEA reduced the
magnitude of the subsequent tetanus-induced LTP. Like LTP, the TEA-induced
synaptic enhancement did not significantly affect paired-pulse
facilitation. These results suggest that dihydropyridine-sensitive VDCCs do
not normally contribute to the induction of NMDA receptor-dependent LTP
even though their repetitive activation can generate an increase in
synaptic strength. The mutual occlusion of LTP and TEA-induced synaptic
enhancement suggests that they share a common expression mechanism and
perhaps are generated by activation of common Ca(2+)-dependent
intracellular processes.(ABSTRACT TRUNCATED AT 250 WORDS)
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