Zanoni J N, de Miranda Neto M H, Bazotte R B, de Souza R R
Departamento of Morphophysiological Science, State University of Maringá, Paraná, Brasil.
Arq Neuropsiquiatr. 1997 Dec;55(4):696-702. doi: 10.1590/s0004-282x1997000500004.
The purpose of this work was to study the neurons of the myenteric plexus of the cecum of rats with chronic streptozotocin-induced diabetes. We used four experimental groups of animals. In groups D2 and D8 animals were killed two and eight months, respectively, after diabetes induction and groups C2 and C8 were used as controls. We carried out whole-mount preparations stained with Giemsa and NADH-diaphorase. We verified that the diabetes did not alter the shape and disposition of the myenteric ganglia; it provoked decrease on the neuronal density and increase on the incidence of weakly basophilic neurons. The effects of streptozotocin caused dilatation of the cecum still evidenced two months after induction, but no more observed on the eight months after induction. The smaller incidence of neurons in group D8 relative to group C8 was due to the early loss related to the drug toxicity and later to the aging in diabetic condition.
这项工作的目的是研究慢性链脲佐菌素诱导的糖尿病大鼠盲肠肌间神经丛的神经元。我们使用了四组实验动物。在D2组和D8组中，动物分别在糖尿病诱导后两个月和八个月处死，C2组和C8组作为对照。我们进行了吉姆萨染色和NADH-黄递酶染色的整装标本制备。我们证实糖尿病并未改变肌间神经节的形状和分布；它导致神经元密度降低，弱嗜碱性神经元的发生率增加。链脲佐菌素的作用导致盲肠扩张，在诱导后两个月仍可观察到，但在诱导后八个月不再观察到。D8组相对于C8组神经元发生率较低是由于早期与药物毒性相关的损失，以及后期糖尿病状态下的衰老。
