English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT
Add to Basket
  Local TagsRelease HistoryDetailsSummary

Released
Journal Article

Rac1 is a downstream effector of PKCα in structural synaptic plasticity

MPS-Authors

Tu,  Xun
Max Planck Florida Institute for Neuroscience, Max Planck Society;

Yasuda,  Ryohei
Max Planck Florida Institute for Neuroscience, Max Planck Society;

Colgan,  Lesley A.
Max Planck Florida Institute for Neuroscience, 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

Tu, X., Yasuda, R., & Colgan, L. A. (2020). Rac1 is a downstream effector of PKCα in structural synaptic plasticity. Scientific Reports, (1), 1-9. Retrieved from https://www.nature.com/articles/s41598-020-58610-6.


Cite as: https://hdl.handle.net/21.11116/0000-000C-DF91-5
Abstract
Structural and functional plasticity of dendritic spines is the basis of animal learning. The rapid remodeling of actin cytoskeleton is associated with spine enlargement and shrinkage, which are essential for structural plasticity. The calcium-dependent protein kinase C isoform, PKCα, has been suggested to be critical for this actin-dependent plasticity. However, mechanisms linking PKCα and structural plasticity of spines are unknown. Here, we examine the spatiotemporal activation of actin regulators, including small GTPases Rac1, Cdc42 and Ras, in the presence or absence of PKCα during single-spine structural plasticity. Removal of PKCα expression in the postsynapse attenuated Rac1 activation during structural plasticity without affecting Ras or Cdc42 activity. Moreover, disruption of a PDZ binding domain within PKCα led to impaired Rac1 activation and deficits in structural spine remodeling. These results demonstrate that PKCα positively regulates the activation of Rac1 during structural plasticity.