Overexpression of tropomyosin isoform tpm3.1 does not alter synaptic function in hippocampal neurons

Chanchanok Chaichim, Tamara Tomanic, Holly Stefen, Esmeralda Paric, Lucy Gamaroff, Alexandra K. Suchowerska, Peter W. Gunning, Yazi D. Ke, Thomas Fath*, John Power

*Corresponding author for this work

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Tropomyosin (Tpm) has been regarded as the master regulator of actin dynamics. Tpms regulate the binding of the various proteins involved in restructuring actin. The actin cytoskeleton is the predominant cytoskeletal structure in dendritic spines. Its regulation is critical for spine formation and long‐term activity‐dependent changes in synaptic strength. The Tpm isoform Tpm3.1 is enriched in dendritic spines, but its role in regulating the synapse structure and function is not known. To determine the role of Tpm3.1, we studied the synapse structure and function of cultured hippocampal neurons from transgenic mice overexpressing Tpm3.1. We recorded hippocampal field excitatory postsynaptic potentials (fEPSPs) from brain slices to examine if Tpm3.1 overexpres-sion alters long‐term synaptic plasticity. Tpm3.1‐overexpressing cultured neurons did not show a significantly altered dendritic spine morphology or synaptic activity. Similarly, we did not observe altered synaptic transmission or plasticity in brain slices. Furthermore, expression of Tpm3.1 at the postsynaptic compartment does not increase the local F‐actin levels. The results suggest that alt-hough Tpm3.1 localises to dendritic spines in cultured hippocampal neurons, it does not have any apparent impact on dendritic spine morphology or function. This is contrary to the functional role of Tpm3.1 previously observed at the tip of growing neurites, where it increases the F‐actin levels and impacts growth cone dynamics.

Original languageEnglish
Article number9303
Pages (from-to)1-16
Number of pages16
JournalInternational Journal of Molecular Sciences
Issue number17
Publication statusPublished - 1 Sept 2021

Bibliographical note

Copyright the Author(s) 2021. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.


  • Actin cytoskeleton
  • Synapse function
  • Tropomyosin


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