Dendritic spines form typical excitatory synapses in the brain and their shapes vary depending on synaptic inputs. It has been suggested that the morphological changes of dendritic spines play an important role in synaptic plasticity. Dendritic spines contain a high concentration of actin, which has a central role in supporting cell motility, and polymerization of actin filaments (F-actin) is most likely involved in spine shape changes. Drebrin is an actin-binding protein that forms stable F-actin and is highly accumulated within dendritic spines. Drebrin has two isoforms, embryonic-type drebrin E and adult-type drebrin A, that change during development from E to A. Inhibition of drebrin A expression results in a delay of synapse formation and inhibition of postsynaptic protein accumulation, suggesting that drebrin A has an important role in spine maturation. In mature synapses, glutamate stimulation induces rapid spine-head enlargement during long-term potentiation (LTP) formation. LTP stimulation induces Ca^2 + entry through N-methyl-d-aspartate (NMDA) receptors, which causes drebrin exodus from dendritic spines. Once drebrin exits from dendritic spine heads, the dynamic actin pool increases in spine heads to facilitate F-actin polymerization. To maintain enlarged spine heads, drebrin-decorated F-actin is thought to reform within the spine heads. Thus, drebrin plays a pivotal role in spine plasticity through regulation of F-actin.

树突棘在大脑中形成典型的兴奋性突触，其形状根据突触输入而变化。已经提出，树突棘的形态变化在突触可塑性中起重要作用。树突棘含有高浓度的肌动蛋白，在支持细胞运动中起着核心作用，肌动蛋白丝的聚合（F-肌动蛋白）最有可能参与脊柱形状的改变。Drebrin是一种肌动蛋白结合蛋白，可形成稳定的F-actin，并在树突棘中高度积累。Drebrin具有两种同工型，即胚胎型drebrin E和成人型drebrin A，它们在从E到A的发育过程中会发生变化。抑制Drebrin A的表达会导致突触形成的延迟并抑制突触后蛋白的积累，提示Drebrin A在脊柱成熟中起重要作用。在成熟的突触中，谷氨酸刺激在长期增强（LTP）形成过程中引起快速的脊柱头部增大。LTP刺激诱导钙^{2 +}通过条目Ñ甲基d天冬氨酸（NMDA）受体，这导致从drebrin树突棘外流。一旦脑残蛋白从树突状脊柱头部脱离，则动态肌动蛋白池在脊柱头部增加，以促进F-肌动蛋白的聚合。为了维持脊柱头部的扩大，人们认为在脑脊柱内重新修饰了脑膜修饰的F-肌动蛋白。因此，脑啡肽通过调节F-肌动蛋白在脊柱可塑性中起关键作用。