English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

Balance and stability of synaptic structures during synaptic plasticity

MPS-Authors
/persons/resource/persons85340

Meyer,  Daniel
Department: Synapses-Circuits-Plasticity / Bonhoeffer, MPI of Neurobiology, Max Planck Society;

/persons/resource/persons38769

Bonhoeffer,  Tobias
Department: Synapses-Circuits-Plasticity / Bonhoeffer, MPI of Neurobiology, Max Planck Society;

/persons/resource/persons15762

Scheuss,  Volker
Department: Synapses-Circuits-Plasticity / Bonhoeffer, MPI of Neurobiology, Max Planck Society;

External Resource
No external resources are shared
Fulltext (restricted access)
There are currently no full texts shared for your IP range.
Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available
Citation

Meyer, D., Bonhoeffer, T., & Scheuss, V. (2014). Balance and stability of synaptic structures during synaptic plasticity. Neuron, 82(2), 430-443. doi:10.1016/j.neuron.2014.02.031.


Cite as: https://hdl.handle.net/11858/00-001M-0000-0019-8C8B-3
Abstract
Subsynaptic structures such as bouton, active zone, postsynaptic density (PSD) and dendritic spine, are highly correlated in their dimensions and also correlate with synapse strength. Why this is so and how such correlations are maintained during synaptic plasticity remains poorly understood. We induced spine enlargement by two-photon glutamate uncaging and examined the relationship between spine, PSD, and bouton size by two-photon time-lapse imaging and electron microscopy. In enlarged spines the PSD-associated protein Homer1c increased rapidly, whereas the PSD protein PSD-95 increased with a delay and only in cases of persistent spine enlargement. In the case of nonpersistent spine enlargement, the PSD proteins remained unchanged or returned to their original level. The ultrastructure at persistently enlarged spines displayed matching dimensions of spine, PSD, and bouton, indicating their correlated enlargement. This supports a model in which balancing of synaptic structures is a hallmark for the stabilization of structural modifications during synaptic plasticity.