Neuronal Actin Remodeling and Its Role in Higher Nervous Activity

The dynamic interaction of memory and forgetting processes determines the formation, stability, and specificity of the engram. While the molecular genetic processes of learning and memory have been intensively studied, the mechanisms of active forgetting have only recently attracted the attention of neuroscientists. The emergence and disappearance of memory traces in the brain are regulated by specific signaling cascades that influence the morphological and functional properties of synaptic connections. Actin remodeling is known to be the basis of neuroplasticity. Cofilin normally acts as an actin severing protein, allowing the actin cytoskeleton to locally change its structure. LIMK-dependent inactivation of cofilin stabilizes filamentous (F)-actin in dendritic spines, being crucial for engram consolidation. On the other hand, a lack of globular (G)-actin prevents actin remodeling, so inactivation of cofilin also stimulates forgetting after learning. The effects of cofilin-dependent signaling pathways on the engram depend on both the type of memory and the model object. In this review, I focus on the role of neuronal actin remodeling in learning, memory retention and forgetting processes, as well as the signal pathways that govern actin cytoskeleton dynamics. Parallels between neuroplasticity and learning in artificial neural networks (ANNs) are also discussed.