Neuroblast migration and P2Y1 receptor mediated calcium signalling depend on 9-O-acetyl GD3 ganglioside

被引：12

作者：

Santiago, Marcelo F. ^{[1
,2
]}

Scemes, Eliana ^{[1
]}

机构：

[1] Albert Einstein Coll Med, Dominick P Purpura Dept Neurosci, Bronx, NY 10461 USA

[2] Univ Fed Rio de Janeiro, Inst Biofis Carlos Chagas Filho, BR-21941 Rio De Janeiro, Brazil

来源：

ASN NEURO | 2012年 / 4卷 / 06期

关键词：

cerebellar granule cell; Jones antibody; GD3; synthase; P2Y(1) receptor; calcium signalling and neuronal migration; OLIGODENDROCYTE PROGENITOR MIGRATION; CEREBELLAR GRANULE CELLS; NEURONAL MIGRATION; EXPRESSION; MICE; ASTROTACTIN; ATP; DIFFERENTIATION; NEUROTROPHIN-3; MAINTENANCE;

D O I：

10.1042/AN20120035

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Previous studies indicated that a ganglioside 9acGD3 (9-O-acetyl GD3) antibody [the J-Ab (Jones antibody)] reduces GCP (granule cell progenitor) migration in vitro and in vivo. We here investigated, using cerebellar explants of postnatal day (P) 6 mice, the mechanism by which 9acGD3 reduces GCP migration. We found that immunoblockade of the ganglioside with the J-Ab or the lack of GD3 synthase reduced GCP in vitro migration and the frequency of Ca2+ oscillations. Immunocytochemistry and pharmacological assays indicated that GCPs expressed P2Y(1)Rs (P2Y(1) receptors) and that deletion or blockade of these receptors decreased the migration rate of GCPs and the frequency of Ca2+ oscillations. The reduction in P2Y(1)-mediated calcium signals seen in Jones-treated and GD3 synthase-null GCPs were paralleled by P2Y(1)R internalization. We conclude that 9acGD3 controls GCP migration by influencing P2Y(1)R cellular distribution and function.

引用

页码：357 / 369

页数：13

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