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雄性大鼠沿腹下神经和盆神经与节前轴突一起投射的盆神经节细胞的递质分布及脊髓输入

Transmitter profile and spinal inputs of pelvic ganglion cells projecting with preganglionic axons along the hypogastric and pelvic nerves of the male rat.

作者信息

Kepper M E, Keast J R

机构信息

Department of Physiology and Pharmacology, University of Queensland, St. Lucia, Australia.

出版信息

Neurosci Lett. 2000 Feb 18;280(2):123-6. doi: 10.1016/s0304-3940(00)00771-0.

DOI:10.1016/s0304-3940(00)00771-0
PMID:10686393
Abstract

Pelvic autonomic ganglion cells receive spinal preganglionic inputs via the hypogastric (lumbar) or pelvic (sacral) nerves. Damage to these nerves stimulates axogenesis (sprouting) from pelvic ganglion cells and two possible triggers are deafferentation (decentralisation) or, if some ganglion cells project centrally in these nerves, axotomy. We have used a combination of retrograde tracing and immunohistochemistry in male rats to identify the number of pelvic ganglion cells that project centrally along these nerves, their transmitter type and the spinal level of their preganglionic inputs. Only a small number (<1%) of pelvic ganglion cells project along these nerves; 29-65 project in each hypogastric nerve and 41-71 in each pelvic nerve. These neurons comprise of both cholinergic and noradrenergic classes and the majority receive preganglionic inputs from the nerve in which they also project. These results suggest that damage of the hypogastric and pelvic nerves close to the pelvic ganglion is unlikely to cause axotomy of many pelvic ganglion cells. Therefore deafferentation rather than axotomy is likely to be the primary trigger of axogenesis occurring in pelvic ganglia after these lesions.

摘要

盆腔自主神经节细胞通过腹下(腰)神经或盆(骶)神经接收脊髓节前输入。这些神经的损伤会刺激盆腔神经节细胞发生轴突生成(发芽),两种可能的触发因素是传入神经阻滞(去神经支配),或者,如果一些神经节细胞在这些神经中向中枢投射,则是轴突切断术。我们在雄性大鼠中结合使用逆行追踪和免疫组织化学方法,以确定沿这些神经向中枢投射的盆腔神经节细胞的数量、它们的递质类型以及它们节前输入的脊髓节段。只有少数(<1%)盆腔神经节细胞沿这些神经投射;每条腹下神经中有29 - 65个投射,每条盆神经中有41 - 71个投射。这些神经元包括胆碱能和去甲肾上腺素能两类,并且大多数从它们也投射的神经接收节前输入。这些结果表明,靠近盆腔神经节的腹下神经和盆神经损伤不太可能导致许多盆腔神经节细胞的轴突切断。因此,传入神经阻滞而非轴突切断术可能是这些损伤后盆腔神经节中发生轴突生成的主要触发因素。

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