Actin Cytoskeleton Role in the Maintenance of Neuronal Morphology and Long-Term Memory.

Raphael Lamprecht

doi:10.3390/cells10071795

Abstract

Evidence indicates that long-term memory formation creates long-lasting changes in neuronal morphology within a specific neuronal network that forms the memory trace. Dendritic spines, which include most of the excitatory synapses in excitatory neurons, are formed or eliminated by learning. These changes may be long-lasting and correlate with memory strength. Moreover, learning-induced changes in the morphology of existing spines can also contribute to the formation of the neuronal network that underlies memory. Altering spines morphology after memory consolidation can erase memory. These observations strongly suggest that learning-induced spines modifications can constitute the changes in synaptic connectivity within the neuronal network that form memory and that stabilization of this network maintains long-term memory. The formation and elimination of spines and other finer morphological changes in spines are mediated by the actin cytoskeleton. The actin cytoskeleton forms networks within the spine that support its structure. Therefore, it is believed that the actin cytoskeleton mediates spine morphogenesis induced by learning. Any long-lasting changes in the spine morphology induced by learning require the preservation of the spine actin cytoskeleton network to support and stabilize the spine new structure. However, the actin cytoskeleton is highly dynamic, and the turnover of actin and its regulatory proteins that determine and support the actin cytoskeleton network structure is relatively fast. Molecular models, suggested here, describe ways to overcome the dynamic nature of the actin cytoskeleton and the fast protein turnover and to support an enduring actin cytoskeleton network within the spines, spines stability and long-term memory. These models are based on long-lasting changes in actin regulatory proteins concentrations within the spine or the formation of a long-lasting scaffold and the ability for its recurring rebuilding within the spine. The persistence of the actin cytoskeleton network within the spine is suggested to support long-lasting spine structure and the maintenance of long-term memory.

Highlights

Manipulation of the long-lasting spines morphology can affect long-term memory. These results strongly suggest that spines formation and their particular morphology are involved in encoding the long-term memory trace
The prevailing hypothesis is that the persistence of long-term memory requires a stable underlying neuronal network
Dendritic spines contain most of the excitatory synapses in excitatory neurons, and their morphology affects synaptic transmission

Summary

Introduction

The prevailing hypothesis is that memory is encoded by a neuronal circuit, and this circuit needs to be preserved to maintain the memory. It implies that if the neuronal circuit that encodes a lasting memory is preserved, the overall influence of the dendritic spines on the activity of the neurons, and their morphology and distribution within the circuit, needs to be maintained. Longlasting elimination of spines can play a role in shaping the neuronal circuit that forms the memory trace. These observations suggest that long-term memory maintenance is subserved by long-lasting dendritic spines. How is the structure of dendritic spines preserved by the actin cytoskeleton to maintain long-term memory? How is the structure of dendritic spines preserved by the actin cytoskeleton to maintain long-term memory? This review discusses this topic and suggests models that can resolve the issue

The Functions of Dendritic Spines in Neurons

Dendritic Spines and Memory Formation and Maintenance

Actin Is Involved in the Stabilization of Spines

Regulation of Actin Is Involved in Controlling the Retraction of Spines

The Role of Actin in Maintaining Spines and Long-Term Memory

Trafficking of Proteins into Spines

Findings

Conclusions and Future Directions