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The Journal of Neuroscience, January 28, 2009, 29(4):1017-1033; doi:10.1523/JNEUROSCI.5528-08.2009

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Development/Plasticity/Repair
Synaptopodin Regulates Plasticity of Dendritic Spines in Hippocampal Neurons

Andreas Vlachos,1,2 * Eduard Korkotian,1 * Eldi Schonfeld,1 Ekaterini Copanaki,2 Thomas Deller,2 and Menahem Segal1

1Department of Neurobiology, The Weizmann Institute, Rehovot 76100, Israel, and 2Institute of Clinical Neuroanatomy, Goethe University Frankfurt, 60590 Frankfurt, Germany

Correspondence should be addressed to Menahem Segal, Department of Neurobiology, The Weizmann Institute, Rehovot 76100, Israel. Email: menahem.segal{at}weizmann.ac.il

The spine apparatus is an essential component of dendritic spines of cortical and hippocampal neurons, yet its functions are still enigmatic. Synaptopodin (SP), an actin-binding protein, is tightly associated with the spine apparatus and it may play a role in synaptic plasticity, but it has not yet been linked mechanistically to synaptic functions. We studied endogenous and transfected SP in dendritic spines of cultured hippocampal neurons and found that spines containing SP generate larger responses to flash photolysis of caged glutamate than SP-negative ones. An NMDA-receptor-mediated chemical long-term potentiation caused the accumulation of GFP-GluR1 in spine heads of control but not of shRNA-transfected, SP-deficient neurons. SP is linked to calcium stores, because their pharmacological blockade eliminated SP-related enhancement of glutamate responses, and release of calcium from stores produced an SP-dependent increase of GluR1 in spines. Thus, SP plays a crucial role in the calcium store-associated ability of neurons to undergo long-term plasticity.

Key words: GluR1; dendritic spines; synaptopodin; spine apparatus; LTP; glutamate uncaging


Received Nov. 18, 2008; revised Dec. 16, 2008; accepted Dec. 19, 2008.

Correspondence should be addressed to Menahem Segal, Department of Neurobiology, The Weizmann Institute, Rehovot 76100, Israel. Email: menahem.segal{at}weizmann.ac.il


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