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甘丙肽受体-1和-2在大鼠腰段脊髓中的差异分布及调控

Differential distribution and regulation of galanin receptors- 1 and -2 in the rat lumbar spinal cord.

作者信息

Brumovsky Pablo, Mennicken Françoise, O'donnell Dajan, Hökfelt Tomas

机构信息

Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden.

出版信息

Brain Res. 2006 Apr 26;1085(1):111-20. doi: 10.1016/j.brainres.2006.02.088. Epub 2006 Apr 13.

DOI:10.1016/j.brainres.2006.02.088
PMID:16626647
Abstract

The expression of the galanin receptor-1 and -2 (Gal(1) and Gal(2)) messenger ribonucleic acids (mRNAs) was studied in the lower spinal cord of rat by means of in situ hybridization, using ribonucleic acid probes (riboprobes). Naïve rats as well as rats with unilateral axotomy of the sciatic nerve or unilateral inflammation of the hindpaw were analyzed. In naïve rats, numerous Gal(1) mRNA-positive (+) neurons were detected in lamina (L) I-III. In addition, several Gal(1) mRNA(+) neurons were seen in deeper layers, including the ventral horns, area X, and the lateral spinal nucleus. In contrast, few and comparatively weakly labeled Gal(2) mRNA(+) neurons were observed, mostly in the ventral horns and in area X, with fewer in the dorsal horn and in the sympathetic and parasympathetic intermediate lateral cell columns. Axotomy induced a strong increase in intensity and number of Gal(2) mRNA(+) motoneurons ipsilateral to the lesion. In contrast, nerve cut or hindpaw inflammation did not alter the expression of Gal(1) or Gal(2) in the dorsal horn. The present (and previous) results suggest that galanin, acting through Gal(1) and Gal(2) receptors, has a modulatory role on spinal excitability, not only via interneurons in superficial dorsal horn, but also on neurons in deep layers and area X, as well as on the sympathetic and parasympathetic outflow. Furthermore, the nerve injury-induced Gal(2) upregulation in motor neurons suggests a role for galanin in survival/regeneration mechanisms.

摘要

利用核糖核酸探针(核糖探针),通过原位杂交技术研究了大鼠脊髓下部中甘丙肽受体-1和-2(Gal(1)和Gal(2))信使核糖核酸(mRNA)的表达。分析了未处理的大鼠以及坐骨神经单侧轴突切断或后爪单侧炎症的大鼠。在未处理的大鼠中,在I-III层检测到大量Gal(1) mRNA阳性(+)神经元。此外,在更深层,包括腹角、X区和外侧脊髓核中也可见到一些Gal(1) mRNA(+)神经元。相比之下,观察到很少且标记相对较弱的Gal(2) mRNA(+)神经元,主要在腹角和X区,背角以及交感和副交感中间外侧细胞柱中的较少。轴突切断导致损伤同侧Gal(2) mRNA(+)运动神经元的强度和数量显著增加。相比之下,神经切断或后爪炎症并未改变背角中Gal(1)或Gal(2)的表达。目前(以及之前)的结果表明,甘丙肽通过Gal(1)和Gal(2)受体发挥作用,不仅通过浅背角中的中间神经元,而且对深层和X区的神经元以及交感和副交感传出神经,对脊髓兴奋性具有调节作用。此外,神经损伤诱导运动神经元中Gal(2)上调表明甘丙肽在存活/再生机制中发挥作用。

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