Pten, a gene associated with autism spectrum disorder, is an upstream regulator of receptor tyrosine kinase intracellular signaling pathways that mediate extracellular cues to inform cellular development and activity-dependent plasticity. We therefore hypothesized that Pten loss would interfere with activity dependent dendritic growth. We investigated the effects of this interaction on the maturation of retrovirally labeled postnatally generated wild-type and Pten knockout granule neurons in male and female mouse dentate gyrus while using chemogenetics to manipulate the activity of the perforant path afferents. We find that enhancing network activity accelerates the dendritic outgrowth of wild-type, but not Pten knockout, neurons. This was specific to immature neurons during an early developmental window. We also examined synaptic connectivity and physiological measures of neuron maturation. The input resistance, membrane capacitance, dendritic spine morphology, and frequency of spontaneous synaptic events were not differentially altered by activity in wild-type versus Pten knockout neurons. Therefore, Pten and its downstream signaling pathways regulate the activity-dependent sculpting of the dendritic arbor during neuronal maturation.

中文翻译：

---

依赖于活动的树突加工需要Pten。

Pten是一种与自闭症谱系障碍相关的基因，是受体酪氨酸激酶细胞内信号通路的上游调节剂，介导细胞外信号提示细胞发育和活动依赖性可塑性。因此，我们假设Pten丢失会干扰依赖于活性的树突状生长。我们调查了这种相互作用对雄性和雌性小鼠齿状回中逆转录病毒标记的产后生成的野生型和Pten敲除颗粒神经元成熟的影响，同时使用化学遗传学来操纵穿孔路径传入的活性。我们发现增强网络活动会加速野生型（而非Pten基因敲除）神经元的树突生长。这是在早期发育窗口期间对未成熟神经元所特有的。我们还检查了神经元成熟的突触连接性和生理指标。野生型和Pten基因敲除神经元的活性没有差异地改变输入电阻，膜电容，树突棘形态和自发突触事件的频率。因此，Pten及其下游信号通路调节神经元成熟过程中树突状乔木的活性依赖雕刻。