| First Author | Allen PB | Year | 2000 |
| Journal | J Neurosci | Volume | 20 |
| Issue | 10 | Pages | 3537-43 |
| PubMed ID | 10804194 | Mgi Jnum | J:76892 |
| Mgi Id | MGI:2180539 | Doi | 10.1523/JNEUROSCI.20-10-03537.2000 |
| Citation | Allen PB, et al. (2000) Protein phosphatase-1 regulation in the induction of long-term potentiation: heterogeneous molecular mechanisms. J Neurosci 20(10):3537-43 |
| abstractText | 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. |
