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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)

Examination of TEA-induced synaptic enhancement in area CA1 of the hippocampus: the role of voltage-dependent Ca2+ channels in the induction of LTP