PACAP plays significant roles in dendritic spine morphology using optogenetics.

在本研究中，我们发现PSD-95标记的突触点数在PACAP-/-小鼠原代培养的海马神经元中减少，而在野生型小鼠海马神经元中PSD-95标记的突触点数增加，而PACAP增加了miR-132的表达，并降低了miR-132靶向的p250GAP的mRNA和蛋白表达水平。PACAP以剂量和时间依赖的方式诱导5-HT2A受体内化。VIP不能诱导5-HT2A受体内化，提示PAC1参与了PACAP诱导的5-HT2A受体内化。此外，我们观察到蛋白激酶C(PKC)抑制剂鞘氨醇可抑制5-HT2A受体内化。

In this study, we showed that the number of PSD-95-labeled synaptic puncta was decreased in primary cultured hippocampal neurons prepared from PACAP-/- mice while it was increased by PACAP in the neurons from wild-type mice, and PACAP increased miR-132 expression and decreased mRNA and protein expression levels of p250GAP which is involved in dendritic spine formation and targeted by miR-132.PACAP induced 5-HT2A receptor internalization in a dose-and time-dependent manner. VIP did not induce 5-HT2A receptor internalization, suggesting that PAC1 is involved in the PACAP-induced 5-HT2A receptor internalization. In addition, we observed that pretreatment with the protein kinase C (PKC) inhibitor sphingosineinhibited the 5-HT2A receptor internalization.