Abstract
Because LTP and LTD may contribute to experience-dependent plasticity, a prominent hypothesis is that developmental changes in the biophysical and molecular properties of NMDA receptors (NMDARs) may regulate the duration of critical periods1,2,3,4,5,6,7. Here we report that susceptibility to LTP at thalamocortical synapses in early postnatal mouse slices is lost at a time point when the duration of NMDAR-mediated excitatory post-synaptic currents (NMDAR EPSCs) is not significantly altered. However, changes in the subunit composition of NMDARs, as defined pharmacologically, correlate strongly with the loss of the ability to generate LTP.
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Acknowledgements
This work was supported by a Hitchings-Elion Fellowship from the Burroughs Wellcome Fund and Epilepsy Training Grant NS07280 (to A.L.B.) and grants from N.I.H. (R.C.M.). We thank S. Hestrin and the Malenka lab for suggestions and comments on the manuscript.
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Barth, A., Malenka, R. NMDAR EPSC kinetics do not regulate the critical period for LTP at thalamocortical synapses. Nat Neurosci 4, 235–236 (2001). https://doi.org/10.1038/85070
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DOI: https://doi.org/10.1038/85070
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