新生儿浦肯野细胞功能障碍是与损伤相关的学习缺陷的基础。

Disruption of neonatal Purkinje cell function underlies injury-related learning deficits.

机构信息

Center for Neuroscience Research, Children's National Research Institute, Children's National Hospital, Washington, DC, 20010;

Center for Neuroscience Research, Children's National Research Institute, Children's National Hospital, Washington, DC, 20010.

出版信息

Proc Natl Acad Sci U S A. 2021 Mar 16;118(11). doi: 10.1073/pnas.2017876118.

DOI:10.1073/pnas.2017876118

PMID:33688045

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7980280/

Abstract

It is hypothesized that perinatal cerebellar injury leads to long-term functional deficits due to circuit dysmaturation. Using a novel integration of GCaMP6f fiber photometry with automated measurement of cerebellar behavior using the ErasmusLadder, we causally link cerebellar injury to altered Purkinje cell responses during maladaptive behavior. Chemogenetic inhibition of neonatal Purkinje cells is sufficient to phenocopy the effects of perinatal cerebellar injury. Our results uncover a direct link between perinatal cerebellar injury and activity-dependent maturation of cerebellar cortex.

摘要

据推测，围产期小脑损伤会导致回路发育不良，从而导致长期的功能缺陷。我们通过将 GCaMP6f 光纤光度法与使用 ErasmusLadder 自动测量小脑行为的新技术相结合，因果地将小脑损伤与适应不良行为期间浦肯野细胞反应的改变联系起来。新生浦肯野细胞的化学遗传抑制足以模拟围产期小脑损伤的影响。我们的研究结果揭示了围产期小脑损伤与小脑皮层的活动依赖性成熟之间的直接联系。