RT Journal Article
SR Electronic
T1 Protein Phosphatase-1 Regulation in the Induction of Long-Term Potentiation: Heterogeneous Molecular Mechanisms
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 3537
OP 3543
DO 10.1523/JNEUROSCI.20-10-03537.2000
VO 20
IS 10
A1 Patrick B. Allen
A1 Øivind Hvalby
A1 Vidar Jensen
A1 Michael L. Errington
A1 Mark Ramsay
A1 Farrukh A. Chaudhry
A1 Timothy V. P. Bliss
A1 Jon Storm-Mathisen
A1 Richard G. M. Morris
A1 Per Andersen
A1 Paul Greengard
YR 2000
UL http://www.jneurosci.org/content/20/10/3537.abstract
AB 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.