Anisomycin selectively inhibits orientation tuning shifts in mouse visual cortex.

Abstract

Neural plasticity-the ability of nervous system to adapt its structure, function, or connections in response to stimuli-can be induced in adulthood through specific protocols, such as visual adaptation, referring to the imposition of a preferred/nonpreferred stimulus to a neuron(s) under investigation. Neuronal orientation selectivity-the preference for specific stimulus orientations-is fundamental to visual cortex organization across species and can be modified using adaptation or pharmacological protocols. Structural, molecular, and physiological properties of neurons, including activity-dependent protein synthesis, play a pivotal role during adaptation. In this study, we investigated the effect of anisomycin, an antibiotic that inhibits protein synthesis by interfering with peptidyl transferase activity in eukaryotic ribosomes, on neuroplastic changes in the mouse visual cortex. We first confirm that adaptation induces shifts in orientation tuning; however, anisomycin prevents these adaptation-induced shifts. Thus, as expected, anisomycin altered the relationship between orientation selectivity and amplitude of shifts, reflecting a stabilization of preferred orientation rather than a biological decoupling of these features. This suggests that protein synthesis is necessary for the OSI-dependent modulation of tuning properties, not merely for preventing tuning shifts. Overall, our findings demonstrate that anisomycin obstructs cortical neuroplasticity, suggesting its potential for suppressing unwanted plasticity in therapeutic applications.NEW & NOTEWORTHY We demonstrate that anisomycin, a protein synthesis inhibitor, blocks adaptation-induced shifts in neuronal orientation tuning in the mouse visual cortex. Although adaptation typically reshapes orientation selectivity, anisomycin disrupts this process and alters the relationship between selectivity and shift amplitude. These findings suggest that anisomycin interferes with neural signal transmission and cortical plasticity. Our results highlight anisomycin's potential to suppress maladaptive plasticity, offering insights into mechanisms of experience-dependent cortical reorganization and possible therapeutics for aberrant plasticity.