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The Journal of Neuroscience, May 15, 2000, 20(10):3537-3543

Protein Phosphatase-1 Regulation in the Induction of Long-Term Potentiation: Heterogeneous Molecular Mechanisms

Patrick B. Allen¹, Øivind Hvalby², Vidar Jensen², Michael L. Errington⁴, Mark Ramsay⁵, Farrukh A. Chaudhry³, Timothy V. P. Bliss⁴, Jon Storm-Mathisen³, Richard G. M. Morris⁵, Per Andersen², and Paul Greengard¹

¹ Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, NY 10021, ² Department of Physiology and ³ Anatomical Institute, Institute of Basic Medical Sciences, University of Oslo, Blindern, N-0317 Oslo, ⁴ Division of Neurophysiology, National Institute for Medical Research, London NW7 1AA, United Kingdom, ⁵ Center for Neuroscience, University of Edinburgh, Edinburgh EH8 9LE, United Kingdom

Protein phosphatase inhibitor-1 (I-1) has been proposed as a regulatory element in the signal transduction cascade that couples postsynaptic calcium influx to long-term changes in synaptic strength. We have evaluated this model using mice lacking I-1. Recordings made in slices prepared from mutant animals and also in anesthetized mutant animals indicated that long-term potentiation (LTP) is deficient at perforant path-dentate granule cell synapses. In vitro, this deficit was restricted to synapses of the lateral perforant path. LTP at Schaffer collateral-CA1 pyramidal cell synapses remained normal. Thus, protein phosphatase-1-mediated regulation of NMDA receptor-dependent synaptic plasticity involves heterogeneous molecular mechanisms, in both different dendritic subregions and different neuronal subtypes. Examination of the performance of I-1 mutants in spatial learning tests indicated that intact LTP at lateral perforant path-granule cell synapses is either redundant or is not involved in this form of learning.

Key words: synaptic plasticity; LTP; phosphoprotein phosphatase-1 (PP-1); inhibitor-1 (I-1); CA1 pyramidal cells; dentate granule cells; perforant path; spatial learning

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Copyright © 2000 Society for Neuroscience  0270-6474/00/20103537-07$05.00/0

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