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Impairment of in vivo theta‐burst long‐term potentiation and network excitability in the dentate gyrus of synaptopodin‐deficient mice lacking the spine apparatus and the cisternal organelle
Author(s) -
Jedlicka Peter,
Schwarzacher Stephan W.,
Winkels Raphael,
Kienzler Friederike,
Frotscher Michael,
Bramham Clive R.,
Schultz Christian,
Bas Orth Carlos,
Deller Thomas
Publication year - 2009
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.20489
Subject(s) - neuroscience , long term potentiation , population spike , dentate gyrus , perforant path , granule cell , dendritic spine , synaptopodin , synaptic plasticity , chemistry , biology , hippocampus , hippocampal formation , endocrinology , biochemistry , receptor , podocyte , proteinuria , kidney
The function of the spine apparatus in dendritic spines and the cisternal organelles in axon initial segments is little understood. The actin‐associated protein, synaptopodin, is essential for the formation of these organelles which are absent in synaptopodin −/− mice. Here, we used synaptopodin −/− mice to explore the role of the spine apparatus and the cisternal organelle in synaptic plasticity and local circuit excitability in response to activation of the perforant path input to the dentate gyrus in vivo. We found impaired long‐term potentiation following theta‐burst stimulation, whereas tetanus‐evoked LTP was unaffected. Furthermore, paired‐pulse inhibition of the population spike was reduced and granule cell excitability was enhanced in mutants, hence revealing an impairment of local network inhibition. In summary, our data represent the first electrophysiological evidence that the lack of the spine apparatus and the cisternal organelle leads to a defect in long‐term synaptic plasticity and alterations in local circuit control of granule cell excitability under adult in vivo conditions. © 2008 Wiley‐Liss, Inc.