Synaptopodin-deficient mice lack a spine apparatus and show deficits in synaptic plasticity.
The spine apparatus is a cellular organelle that is present in many dendritic spines of excitatory neurons in the mammalian forebrain. Despite its discovery >40 years ago, the function of the spine apparatus is still unknown although calcium buffering functions as well as roles in synaptic plasticity have been proposed. We have recently shown that the 100-kDa protein synaptopodin is associated with the spine apparatus. Here, we now report that mice homozygous for a targeted deletion of the synaptopodin gene completely lack spine apparatuses. Interestingly, this absence of the spine apparatus is accompanied by a reduction in hippocampal long-term potentiation (LTP) in the CA1 region of the hippocampus and by an impairment of spatial learning in the radial arm maze test. This genetic analysis points to a role of the spine apparatus in synaptic plasticity.
Deller
Thomas
T
Institute of Anatomy, University of Freiburg, P.O. Box 111, D-79001 Freiburg, Germany.
Korte
Martin
M
Chabanis
Sophie
S
Drakew
Alexander
A
Schwegler
Herbert
H
Stefani
Giulia Good
GG
Zuniga
Aimee
A
Schwarz
Karin
K
Bonhoeffer
Tobias
T
Zeller
Rolf
R
Frotscher
Michael
M
Mundel
Peter
P
D000818:Animals; D003712:Dendrites / Q000473:pathology*; D006624:Hippocampus / Q000473:pathology*; D007859:Learning Disabilities / Q000209:etiology; D017774:Long-Term Potentiation; D008297:Male; D051379:Mice; D008840:Microfilament Proteins / Q000172:deficiency / Q000502:physiology*; D009473:Neuronal Plasticity; D013569:Synapses / Q000502:physiology*
D008840:Microfilament Proteins; C503968:Synpo protein, mouse