Activity-dependent plasticity of synaptic structure and function plays an essential role in neuronal development and in cognitive functions including learning and memory. The formation, maintenance and modulation of dendritic spines are mainly controlled by the dynamics of actin filaments (F-actin) through interaction with various actin-binding proteins (ABPs) and postsynaptic signaling messengers. Induction of long-term potentiation (LTP) triggers a cascade of events involving Ca²⁺ signaling, intracellular pathways such as cAMP and cGMP, and regulation of ABPs such as CaMKII, Cofilin, Aip1, Arp2/3, α-actinin, Profilin and Drebrin. We review here how these ABPs modulate the rate of assembly, disassembly, stabilization and bundling of F-actin during LTP induction. We highlight the crucial role that CaMKII exerts in both functional and structural plasticity by directly coupling Ca²⁺ signaling with F-actin dynamics through the β subunit. Moreover, we show how cAMP and cGMP second messengers regulate postsynaptic structural potentiation. Brain disorders such as Alzheimer's disease, schizophrenia or autism, are associated with alterations in the regulation of F-actin dynamics by these ABPs and signaling messengers. Thus, a better understanding of the molecular mechanisms controlling actin cytoskeleton can provide cues for the treatment of these disorders.

突触结构和功能的活动依赖性可塑性在神经元发育和包括学习和记忆在内的认知功能中起着至关重要的作用。树突棘的形成，维持和调节主要受肌动蛋白丝（F-肌动蛋白）与各种肌动蛋白结合蛋白（ABP）和突触后信号传递蛋白相互作用的控制。长期增强（LTP）的诱导触发了一系列涉及Ca ²⁺的事件信号传导，细胞内途径（例如cAMP和cGMP）以及ABP的调节（例如CaMKII，Cofilin，Aip1，Arp2 / 3，α-肌动蛋白，Profilin和Drebrin）。我们在这里回顾这些ABP如何在LTP诱导过程中调节F-肌动蛋白的组装，拆卸，稳定化和成束速率。我们着重指出了CaMKII通过直接偶联Ca ²⁺在功能和结构可塑性中发挥的关键作用通过β亚基具有F-肌动蛋白动力学的信号转导。此外，我们展示了cAMP和cGMP第二信使如何调节突触后结构增强。这些ABP和信号信使对诸如阿尔茨海默氏病，精神分裂症或自闭症等脑部疾病与F-肌动蛋白动力学调节的改变有关。因此，对控制肌动蛋白细胞骨架的分子机制的更好理解可以为这些疾病的治疗提供线索。