Neurons require a well-coordinated intercellular transport system to maintain their normal cellular function and morphology. The kinesin family of proteins (KIFs) fills this role by regulating the transport of a diverse array of cargos in post-mitotic cells. On the other hand, in mitotic cells, KIFs facilitate the fidelity of the cellular division machinery. Though certain mitotic KIFs function in post-mitotic neurons, little is known about them. We studied the role of a mitotic KIF (KIF3B) in neuronal architecture. We find that the RNAi mediated knockdown of KIF3B in primary cortical neurons resulted in an increase in spine density; the number of thin and mushroom spines; and dendritic branching. Consistent with the change in spine density, we observed a specific increase in the distribution of the excitatory post-synaptic protein, PSD-95 in KIF3B knockdown neurons. Interestingly, overexpression of KIF3B produced a reduction in spine density, in particular mushroom spines, and a decrease in dendritic branching. These studies suggest that KIF3B is a key determinant of cortical neuron morphology and that it functions as an inhibitory constraint on structural plasticity, further illuminating the significance of mitotic KIFs in post-mitotic neurons.

神经元需要协调良好的细胞间转运系统来维持其正常的细胞功能和形态。驱动蛋白家族（KIFs）通过调节有丝分裂后细胞中多种货物的运输来填补这一作用。另一方面，在有丝分裂细胞中，KIF促进了细胞分裂机制的保真度。尽管某些有丝分裂KIF在有丝分裂后神经元中起作用，但对其知之甚少。我们研究了有丝分裂KIF（KIF3B）在神经元结构中的作用。我们发现，在初级皮层神经元中，RNAi介导的KIF3B的敲低导致了脊柱密度的增加。稀薄和蘑菇刺的数量；和树枝状分支。与脊柱密度的变化一致，我们观察到兴奋性突触后蛋白的分布有特定的增加，KIF3B敲低神经元的PSD-95 有趣的是，KIF3B的过度表达导致脊椎密度（尤其是蘑菇棘）的减少和树突分支的减少。这些研究表明，KIF3B是皮质神经元形态的关键决定因素，并且它对结构可塑性具有抑制作用，进一步阐明了有丝分裂后神经元中有丝分裂KIF的重要性。