Modulation of cofilin 1 phosphorylation induces juvenile-like plasticity in the adult mouse visual cortex.

Cofilin 1 is an actin-depolymerizing protein that plays a fundamental role in actin dynamics, particularly within dendritic spines, where it has been implicated in both structural and functional plasticity. We recently demonstrated (by differential proteomics, western blot and immunohistochemistry) that the expression of cofilin 1 and its inactive phosphorylated form are dynamically regulated in the mouse visual cortex during postnatal development and by visual experience. Moreover, we found that cofilin 1 expression levels correlates with periods of heightened plasticity in the mouse visual cortex. In this study, we analyzed whether the pharmacological modulation of cofilin 1 activity affects plasticity processes in the visual cortex. Adult mice were treated with a synthetic peptide inhibitor of cofilin 1 activity (PCOF) or a control peptide (TAT) and then monocularly deprived of vision during 3 days. Following reopening of the deprived eye, structural plasticity was assessed by quantifying dendritic spine density using Golgi-like staining, and visual plasticity was evaluated by measuring visual acuity through the optomotor response test. Our results show that, in adult mice treated with the PCOF peptide - but not in controls - monocular deprivation led to a significant reduction in dendritic spine density in the contralateral visual cortex, as well as a decrease in visual acuity of the previously deprived eye. These findings indicate that cofilin 1 activity is crucial for the regulation of experience-dependent plasticity in the adult mouse visual cortex.