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树突棘的伯格曼胶质细胞包裹在不影响棘突运动性的情况下调节突触数量。

Bergmann glial ensheathment of dendritic spines regulates synapse number without affecting spine motility.

作者信息

Lippman Bell Jocelyn J, Lordkipanidze Tamar, Cobb Natalie, Dunaevsky Anna

机构信息

Department of Neuroscience, Brown University, Providence, RI, USA.

出版信息

Neuron Glia Biol. 2010 Aug;6(3):193-200. doi: 10.1017/S1740925X10000165. Epub 2010 Nov 2.

DOI:10.1017/S1740925X10000165
PMID:21044397
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3244562/
Abstract

In the cerebellum, lamellar Bergmann glial (BG) appendages wrap tightly around almost every Purkinje cell dendritic spine. The function of this glial ensheathment of spines is not entirely understood. The development of ensheathment begins near the onset of synaptogenesis, when motility of both BG processes and dendritic spines are high. By the end of the synaptogenic period, ensheathment is complete and motility of the BG processes decreases, correlating with the decreased motility of dendritic spines. We therefore have hypothesized that ensheathment is intimately involved in capping synaptogenesis, possibly by stabilizing synapses. To test this hypothesis, we misexpressed GluR2 in an adenoviral vector in BG towards the end of the synaptogenic period, rendering the BG α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) Ca2+-impermeable and causing glial sheath retraction. We then measured the resulting spine motility, spine density and synapse number. Although we found that decreasing ensheathment at this time does not alter spine motility, we did find a significant increase in both synaptic pucta and dendritic spine density. These results indicate that consistent spine coverage by BG in the cerebellum is not necessary for stabilization of spine dynamics, but is very important in the regulation of synapse number.

摘要

在小脑中,板层状的伯格曼胶质细胞(BG)附属物紧密包裹着几乎每一个浦肯野细胞的树突棘。这种对树突棘的胶质细胞包裹功能尚未完全明了。包裹的发育始于突触发生开始时,此时BG突起和树突棘的活动都很活跃。到突触发生期结束时,包裹完成,BG突起的活动减少,这与树突棘活动的减少相关。因此,我们推测包裹可能通过稳定突触密切参与突触发生的封顶过程。为了验证这一假设,我们在突触发生期末期,通过腺病毒载体在BG中错误表达GluR2,使BG的α-氨基-3-羟基-5-甲基-4-异恶唑丙酸受体(AMPARs)对Ca2+不渗透,并导致胶质鞘回缩。然后我们测量由此产生的树突棘活动、树突棘密度和突触数量。虽然我们发现此时减少包裹不会改变树突棘活动,但我们确实发现突触小体和树突棘密度都显著增加。这些结果表明,小脑中小脑伯格曼胶质细胞对树突棘的持续覆盖对于稳定树突棘动态并非必要,但在调节突触数量方面非常重要。

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