NMDA receptor-mediated synapses between CA1 neurones: activation by ischaemia

Neuroreport
T TsintsadzeO Krishtal

Abstract

Using an in situ patch clamp in hippocampal CA1 mini-slices, we measured excitatory postsynaptic currents (EPSC) by varying the strength of the stimulus applied to the axons of CA3 neurones. The kinetics of the EPSC was initially independent of the stimulus strength. Post-ischaemic potentiation of the EPSC was observed 60-80 min after brief periods (10 min) of anoxia/aglycaemia. The decay of the EPSC slowed significantly in most of the examined neurones. In 11 of 17 cells the EPSC kinetics became dependent on stimulus strength: a slower decay corresponded to a stronger stimulus. This effect was not abolished by N-methyl-D-aspartate (NMDA) or a non-NMDA receptor blocker (D-2-amino-5-phosphonovaleric acid or 6-cyano-7-nitroquinoxaline-2,3-dione respectively) indicating the polysynaptic nature of the modified EPSC: transient ischaemia led to the long-term recruitment of previously inactive, possibly latent NMDA synapses between CA1 neurones.

Citations

Mar 4, 2000·Clinical and Experimental Pharmacology & Physiology·M V KopanitsaI V Komissarov
Oct 5, 2007·The Neuroscientist : a Review Journal Bringing Neurobiology, Neurology and Psychiatry·Jérôme EpszteinValérie Crépel
Jun 10, 2003·Chembiochem : a European Journal of Chemical Biology·Natalya Lozovaya, Andrew D Miller

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