Impaired learning in mice with abnormal short-lived plasticity

Silva, A. J., Rosahl, T. W., Chapman, P. F., Marowitz, Z., Friedman, E., Frankland, P. W., Cestari, V., Cioffi, D., Sudhof, T. C., Bourtchuladze, R. (1996) Impaired learning in mice with abnormal short-lived plasticity. Current Biology, 6 (11). pp. 1509-18. ISSN 0960-9822

URL: http://www.ncbi.nlm.nih.gov/pubmed/8939606
DOI: 10.1016/S0960-9822(96)00756-7

Abstract

BACKGROUND: Many studies suggest that long term potentiation (LTP) has a role in learning and memory. In contrast, little is known about the function of short-lived plasticity (SLP). Modeling results suggested that SLP could be responsible for temporary memory storage, as in working memory, or that it may be involved in processing information regarding the timing of events. These models predict that abnormalities in SLP should lead to learning deficits. We tested this prediction in four lines of mutant mice with abnormal SLP, but apparently normal LTP-mice heterozygous for a alpha-calcium calmodulin kinase II mutation (alpha CaMKII +/-) have lower paired-pulse facilitation (PPF) and increased post-tetanic potentiation (PTP); mice lacking synapsin II (SyII-/-), and mice defective in both synapsin I and synapsin II (SyI/II-/-), show normal PPF but lower PTP; in contrast, mice just lacking synapsin I (SyI-/-) have increased PPF, but normal PTP. RESULTS: Our behavioral results demonstrate that alpha CaMKII +/-, SyII-/- and SyI/II-/- mutant mice, which have decreased PPF or PTP, have profound impairments in learning tasks. In contrast, behavioral analysis did not reveal learning deficits in SyI-/- mice, which have increased PPF. CONCLUSIONS: Our results are consistent with models that propose a role for SLP in learning, as mice with decreased PPF or PTP, in the absence of known LTP deficits, also show profound learning impairments. Importantly, analysis of the SyI-/- mutants demonstrated that an increase in PPF does not disrupt learning.

Item Type: Paper
Uncontrolled Keywords: Animals Ca(2+)-Calmodulin Dependent Protein Kinase/genetics/ metabolism Gene Deletion Learning/ physiology Mice Mice, Inbred C57BL Neuronal Plasticity/ physiology Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. Research Support, U.S. Gov't, P.H.S. Synapsins/genetics/ metabolism Synaptic Transmission
Subjects: bioinformatics > genomics and proteomics > genetics & nucleic acid processing > Long term potentiation
bioinformatics > genomics and proteomics > genetics & nucleic acid processing > protein structure, function, modification > protein types > enzymes > kinase > CaMKII
organism description > animal behavior > learning
organs, tissues, organelles, cell types and functions > cell types and functions > cell functions > synaptic transmission
CSHL Authors:
Communities: CSHL labs > Mainen lab
CSHL labs > Tully lab
Depositing User: Kathleen Darby
Date Deposited: 13 May 2014 13:40
Last Modified: 13 May 2014 13:40
Related URLs:
URI: http://repository.cshl.edu/id/eprint/30110

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