Rodríguez, J. J.; Dallérac, G. M.; Tabuchi, M.; Davies, H. A.; Colyer, F. M.; Stewart, M. G. and Doyère, V.
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|DOI (Digital Object Identifier) Link:||http://doi.org/10.1017/S1740925X09990159|
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Investigations examining the role of polysialic acid (PSA) on the neural cell adhesion molecule (NCAM) in synaptic plasticity have yielded inconsistent data. Here, we addressed this issue by determining whether homosynaptic long-term potentiation (LTP) and heterosynaptic long-term depression (LTD) induce changes in the distribution of PSA-NCAM in the dentate gyrus (DG) of rats in vivo. In addition, we also examined whether the observed modifications were initiated via the activation of N-methyl-d-aspartate (NMDA) receptors. Immunocytochemical analysis showed an increase in PSA-NCAM positive cells both at 2 and 24 h following high-frequency stimulation of either medial or lateral perforant paths, leading to homosynaptic LTP and heterosynaptic LTD, respectively, in the medial molecular layer of the DG. Analysis of sub-cellular distribution of PSA-NCAM by electron microscopy showed decreased PSA dendritic labelling in LTD rats and a sub-cellular relocation towards the spines in LTP rats. Importantly, these modifications were found to be independent of the activation of NMDA receptors. Our findings suggest that strong activation of the granule cells up-regulates PSA-NCAM synthesis which then incorporates into activated synapses, representing NMDA-independent plastic processes that act synergistically on LTP/LTD mechanisms without participating in their expression.
|Item Type:||Journal Article|
|Copyright Holders:||2009 Cambridge University Press|
|Keywords:||Adhesion molecules; hippocampus; synaptic plasticity|
Science > Life, Health and Chemical Sciences
|Interdisciplinary Research Centre:||Biomedical Research Network (BRN)|
|Depositing User:||Users 9108 not found.|
|Date Deposited:||18 Aug 2009 10:50|
|Last Modified:||23 Feb 2016 21:55|
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