Knock-out of Tpm4.2/Actin Filaments Alters Neuronal Signaling, Neurite Outgrowth, and Behavioral Phenotypes in Mice.

ABSTRACT: Tropomyosins (Tpm) are master regulators of actin dynamics through forming co-polymers with filamentous actin. Despite the well-understood function of muscle Tpms in the contractile apparatus of muscle cells, much less is known about the diverse physiological function of cytoplasmic Tpms in eukaryotic cells. Here, we investigated the role of the Tpm4.2 isoform in neuronal processes including signaling, neurite outgrowth, and receptor recycling using primary neurons from Tpm4.2 knock-out mice. Live imaging of calcium and electrophysiology data demonstrated increased frequency, yet reduced strength of single neuron spikes. Calcium imaging further showed an increase in neuronal networks. In vitro assays of Tpm4.2 knock-out neurons displayed impaired recycling of the AMPA neurotransmitter rece

SUBMITTER: Genoud S 

PROVIDER: S-EPMC12559059 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature