Changes in the expression of P2X1 and P2X2 purinergic receptors in facial motoneurons after nerve lesions in rodents and correlation with motoneuron degeneration

被引：18

作者：

Kassa, Roman M. ^{[1
]}

Bentivoglio, Marina ^{[1
]}

Mariotti, Raffaella ^{[1
]}

机构：

[1] Dept Morphol & Biomed Sci, Fac Med, I-37134 Verona, Italy

来源：

NEUROBIOLOGY OF DISEASE | 2007年 / 25卷 / 01期

关键词：

ATP; neurodegeneration; axotomy; nerve crush injury; motoneuron disease; amyotrophic lateral sclerosis; SOD-1; mutation; Bcl-2; nitric oxide synthase; Glia; mouse; rat;

D O I：

10.1016/j.nbd.2006.08.020

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Involvement of P2X(1) and P2X(2) purinergic receptors in motoneuron response to injury was investigated with Western blotting and immunohistochemistry and correlated with motoneuron loss, Bcl-2 expression, nitric oxide synthase induction and glial activation. P2X(1) was highly induced in rat facial motoneurons after nerve resection, which causes slowly occurring neurodegeneration. P2X(1) induction was lower and less persistent after nerve crush, permissive for fiber regeneration. P2X(2) expression was found in nuclei of rat facial motoneurons, with nuclear export in the cytoplasm after nerve resection. P2X(1) induction in axotomized facial motoneurons was impaired in superoxide dismutase (SOD)1-G93A-mutant mice, a model of motoneuron disease. The data in rats point to a correlation of P2X(1) induction with motoneuron degeneration, which also involves P2X(2) intracellular changes, rather than with axon regeneration effort. The data in mice show that the SOD1 mutation interferes with injury-elicited P2X(1) induction, suggesting alterations of ATP release from mutant motoneurons after damage. (c) 2006 Elsevier Inc. All rights reserved.

引用

页码：121 / 133

页数：13

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