Intracellular demonstration of an N-methyl-D-aspartate receptor mediated component of synaptic transmission in the rat hippocampus.
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.
D000818:Animals; D004558:Electric Stimulation; D005260:Female; D006624:Hippocampus / Q000502:physiology*; D008274:Magnesium / Q000502:physiology; D008564:Membrane Potentials; D009434:Neural Pathways / Q000502:physiology; D051381:Rats; D016194:Receptors, N-Methyl-D-Aspartate; D017981:Receptors, Neurotransmitter / Q000502:physiology*; D013569:Synapses / Q000502:physiology; D009435:Synaptic Transmission
D016194:Receptors, N-Methyl-D-Aspartate; D017981:Receptors, Neurotransmitter; D008274:Magnesium