کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4343931 | 1615143 | 2013 | 5 صفحه PDF | دانلود رایگان |
• Dendritic self-avoidance is critical for dendritic arborization neural circuits.
• DSCAML1 promotes dendritic self-avoidance in newborn mouse cortical neurons.
• Phosphorylation at Y1808 is essential in mediating the effects of DSCAML1.
• The results shed light on the regulation mechanisms of dendrite arborization.
Dendritic self-avoidance is critical for appropriate dendrite arborization. We herein examined the role of Down syndrome cell adhesion molecule like-1 (DSCAML1) in regulating dendritic self-avoidance and that of tyrosine phosphorylation in mediating the effects of DSCAML1. Knocking down DSCAML1 in newborn mouse cortical neurons compromised dendritic self-avoidance as evidenced by dendritic fasciculation and increased dendritic self-crossing. Introduction of a DSCAML1Y1808F mutant into the DSCAML1-knocked down neurons failed to reverse the abnormal dendritic arborization. These results suggest that DSCAML1 promotes dendritic self-avoidance in cortical neurons, and that phosphorylation at Y1808 is essential in mediating the effects of DSCAML1.
Journal: Neuroscience Letters - Volume 555, 25 October 2013, Pages 193–197