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Synaptic loss and retention of different classic cadherins with LTP‐associated synaptic structural remodeling in vivo
Author(s) -
Huntley George W.,
Elste Alice M.,
Patil Shekhar B.,
Bozdagi Ozlem,
Benson Deanna L.,
Steward Oswald
Publication year - 2012
Publication title -
hippocampus
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.767
H-Index - 155
eISSN - 1098-1063
pISSN - 1050-9631
DOI - 10.1002/hipo.20859
Subject(s) - synaptic plasticity , synapse , long term potentiation , neuroscience , synaptic augmentation , chemistry , postsynaptic density , synaptophysin , synaptic fatigue , synaptogenesis , dentate gyrus , metaplasticity , biology , excitatory postsynaptic potential , microbiology and biotechnology , hippocampus , receptor , immunology , inhibitory postsynaptic potential , biochemistry , immunohistochemistry
Cadherins are synaptic cell adhesion molecules that contribute to persistently enhanced synaptic strength characteristic of long‐term potentiation (LTP). What is relatively unexplored is how synaptic activity of the kind that induces LTP‐associated remodeling of synapse structure affects localization of cadherins, particularly in mature animals in vivo, details which could offer insight into how different cadherins contribute to synaptic plasticity. Here, we use a well‐described in vivo LTP induction protocol that produces robust synaptic morphological remodeling in dentate gyrus of adult rats in combination with confocal and immunogold electron microscopy to localize cadherin‐8 and N‐cadherin at remodeled synapses. We find that the density and size of cadherin‐8 puncta are significantly diminished in the potentiated middle molecular layer (MML) while concurrently, N‐cadherin remains tightly clustered at remodeled synapses. These changes are specific to the potentiated MML, and occur without any change in density or size of synaptophysin puncta. Thus, the loss of cadherin‐8 probably represents selective removal from synapses rather than overall loss of synaptic junctions. Together, these findings suggest that activity‐regulated loss and retention of different synaptic cadherins could contribute to dual demands of both flexibility and stability in synapse structure that may be important for synaptic morphological remodeling that accompanies long‐lasting plasticity. © 2010 Wiley Periodicals, Inc., Inc.