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链脲佐菌素处理大鼠的肠肌丛。肠道糖尿病神经病变的神经化学和组织化学证据。

Myenteric plexus in streptozotocin-treated rats. Neurochemical and histochemical evidence for diabetic neuropathy in the gut.

作者信息

Lincoln J, Bokor J T, Crowe R, Griffith S G, Haven A J, Burnstock G

出版信息

Gastroenterology. 1984 Apr;86(4):654-61.

PMID:6698366
Abstract

Adrenergic, cholinergic, and serotoninergic nerves were studied in the myenteric plexus of ileum and colon from streptozotocin-treated rats, an animal model of juvenile-onset diabetes. In view of clinical reports implicating diabetic autonomic neuropathy as the cause of gastrointestinal dysfunction in diabetes mellitus, neurochemical and histochemical techniques were used to study changes in the innervation of the gut. In the myenteric plexus of the ileum from diabetic animals, adrenergic nerves displayed signs of degeneration and the brightness of fluorescence in serotoninlike immunoreactive nerves was lower. Cholinergic nerves, however, did not display any signs of reduction in the ileum, and both choline acetyltransferase and acetylcholinesterase activities per centimeter were increased. In contrast, in the proximal colon 8 wk after induction of diabetes, neurochemical assays revealed significant increases in noradrenaline and serotonin levels as well as choline acetyltransferase activity, although no obvious changes in the pattern of innervation could be detected histochemically. The results indicate that changes do occur in the innervation of the gut of the streptozotocin-diabetic model shortly after the induction of diabetes, although they differ significantly in the ileum and colon; these may be of relevance to the types of gastrointestinal dysfunction displayed in human diabetes.

摘要

在链脲佐菌素诱导的幼年型糖尿病动物模型(即经链脲佐菌素处理的大鼠)的回肠和结肠肌间神经丛中,对肾上腺素能、胆碱能和5-羟色胺能神经进行了研究。鉴于临床报告表明糖尿病自主神经病变是糖尿病患者胃肠功能障碍的病因,因此采用神经化学和组织化学技术来研究肠道神经支配的变化。在糖尿病动物的回肠肌间神经丛中,肾上腺素能神经出现了退变迹象,5-羟色胺样免疫反应性神经的荧光亮度降低。然而,胆碱能神经在回肠中未显示出任何减少的迹象,每厘米的胆碱乙酰转移酶和乙酰胆碱酯酶活性均有所增加。相比之下,在糖尿病诱导8周后的近端结肠中,神经化学分析显示去甲肾上腺素和5-羟色胺水平以及胆碱乙酰转移酶活性显著增加,尽管组织化学检查未发现神经支配模式有明显变化。结果表明,在链脲佐菌素诱导的糖尿病模型中,糖尿病诱导后不久肠道神经支配确实会发生变化,尽管回肠和结肠中的变化差异显著;这些变化可能与人类糖尿病中出现的胃肠功能障碍类型有关。

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