Herron C E, Lester R A, Coan E J, Collingridge G L
Neurosci Lett. 1985 Sep 16;60(1):19-23. doi: 10.1016/0304-3940(85)90375-1.
Rat hippocampal CA1 pyramidal neurones were monosynaptically activated via stimulation of the Schaffer collateral-commissural pathway. On changing from a 1 mM Mg2+-containing to a Mg2+-free medium there was a pronounced prolongation of the intracellularly recorded excitatory postsynaptic potential. This effect was reversibly abolished by the selective N-methyl-D-aspartate (NMDA) antagonist, D-2-amino-5-phosphonovalerate (APV). We propose that Mg2+ normally prevents expression of NMDA receptor-mediated responses during low-frequency stimulation. During a period of tetanic stimulation, however, cells may depolarize sufficiently to allow a significant NMDA component of the response to be manifest. This could then initiate long-term potentiation.
通过刺激海马体的Schaffer侧支-连合通路，对大鼠海马CA1区锥体神经元进行单突触激活。当细胞外液从含1 mM镁离子的溶液换成无镁离子溶液时，细胞内记录到的兴奋性突触后电位显著延长。这种效应可被选择性N-甲基-D-天冬氨酸（NMDA）拮抗剂D-2-氨基-5-磷酸戊酸（APV）可逆性消除。我们认为，在低频刺激期间，镁离子通常会阻止NMDA受体介导的反应的表达。然而，在强直刺激期间，细胞可能会充分去极化，从而使反应中显著的NMDA成分得以显现。这可能继而引发长时程增强。
