Distinct cytoskeletal mechanisms in the maintenance of lysophosphatidic acid-produced retracted neurites in young cortical neurons

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Abstract

Young cortical neurons respond to a bioactive lipid lysophosphatidic acid (LPA) with not only neurite retraction but also actin microspike cap formation and collapse of non-actin components. These responses require the small GTPase Rho-dependent actin polymerization. However, when neurite retraction is completed, how rearranged cytoskeletal components are maintained for the retraction period remains unclear. Here I pharmacologically investigated the signaling mechanisms for the maintenance of rearranged cytoskeletal components. Actin caps disappeared when inhibitors for Rho and actomyosin pathways were added to neurons having actin microspikes induced by LPA. By contrast, these inhibitors failed to affect the maintenance of collapsed non-actin cytoskeleton. These results implicate distinct cytoskeletal mechanisms in the maintenance of retracted neurites induced by LPA.

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