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It has been found that a form of long-term potentiation (LTP), the NMDA-receptor dependent LTP, occurs in the Schaffer collateral pathway connecting CA1 cells with CA3 cells (2122). Disrupting this type of LTP disrupts the formation of spatial memory. Kentros et al investigated this idea using ([+ or -])-3--(2-carboxypiperazin-4-yl)propyl-1-phorphoric acid (CPP) as a receptor antagonist to test three things: if blockade of the NMDA sites degrades the position firing patterns of the place cells; if it inhibits the formation of new spatial memories; and if it affects the stability of newly formed place fields, either short-term or long-term.
Result of this study showed that blocking of the NMDA sites had no effect on previously formed maps, or creating maps of new environments for the short-term, but it abolished the long-term stability of maps of new environments made after blockage (2123). This must mean that the place cells still receive spatial information from some other source when the NMDA-receptors are blocked. These facts also suggests that there are two forms of plasticity: one for short-term mapping and another one for long-term stability of mapping. These results are consistent with other studies, and add more information on the process of mapping by place cells.
The experiments of Kentros et al (1998) suggested that place cells can form spatial maps even when NMDA receptor activation is blocked, but Brun et al (2002) looked to see if these cells could receive input from a source other than the intrahippocampal associative network in the CA3 area. They questioned how distinct hippocampal circuits take part in this information transfer system, and what role each plays in the system (2243). Place fields still exist after selective dentate gyrus lesions, and they are not affected by moderately reducing area CA3 neuronal function, suggesting positional information may come to the place cells from the entorhin...