Belai A, Burnstock G
Department of Anatomy and Developmental Biology, University College London, UK.
J Auton Nerv Syst. 1996 Apr 20;58(1-2):56-62. doi: 10.1016/0165-1838(95)00117-4.
The effect of acrylamide intoxication (a widely used model for autonomic neuropathy) on the fluorescence intensity and density of catecholamine- and peptide-containing nerve fibres and tissue content of noradrenaline and the peptides vasoactive intestinal polypeptide, calcitonin gene-related peptide, substance P and neuropeptide Y in the enteric nerves of rat ileum was examined. Histochemical and immunohistochemical techniques were used to localize catecholamine- and peptide-containing nerve fibres. The tissue content of noradrenaline was measured using high-performance liquid chromatography, and an enzyme-linked immunosorbent assay technique was used to determine the tissue content of the peptides investigated. Acrylamide intoxication caused a significant decrease in the density of catecholamine-containing nerve fibres and tissue content of noradrenaline in the myenteric plexus of rat ileum. A decrease in tissue content and immunoreactivity of calcitonin gene-related peptide and an increase in vasoactive intestinal polypeptide was seen in the myenteric plexus of ileum from acrylamide-intoxicated rats. In the submucous plexus, the acrylamide treatment caused a decrease in calcitonin gene-related peptide immunoreactivity and an increase in vasoactive intestinal polypeptide and neuropeptide Y immunoreactivity. There was no change in either tissue content or immunoreactivity of substance P in both myenteric and submucous plexuses of the treated rat ileum. These changes have a striking similarity with those found in the enteric nerves of streptozotocin-diabetic rat ileum, suggesting the possible presence of an underlying common mechanism(s) in the development of neuropathic changes in the autonomic nerves of acrylamide-intoxicated and streptozotocin-diabetic rats.
研究了丙烯酰胺中毒(一种广泛应用的自主神经病变模型)对大鼠回肠肠神经中含儿茶酚胺和肽的神经纤维的荧光强度和密度、去甲肾上腺素的组织含量以及血管活性肠肽、降钙素基因相关肽、P物质和神经肽Y的影响。采用组织化学和免疫组织化学技术对含儿茶酚胺和肽的神经纤维进行定位。使用高效液相色谱法测定去甲肾上腺素的组织含量,并采用酶联免疫吸附测定技术测定所研究肽的组织含量。丙烯酰胺中毒导致大鼠回肠肌间神经丛中含儿茶酚胺神经纤维的密度和去甲肾上腺素的组织含量显著降低。在丙烯酰胺中毒大鼠回肠的肌间神经丛中,降钙素基因相关肽的组织含量和免疫反应性降低,而血管活性肠肽增加。在黏膜下神经丛中,丙烯酰胺处理导致降钙素基因相关肽免疫反应性降低,血管活性肠肽和神经肽Y免疫反应性增加。在处理过的大鼠回肠的肌间和黏膜下神经丛中,P物质的组织含量和免疫反应性均无变化。这些变化与链脲佐菌素诱导的糖尿病大鼠回肠肠神经中的变化惊人地相似,提示在丙烯酰胺中毒和链脲佐菌素诱导的糖尿病大鼠自主神经病变发展过程中可能存在潜在的共同机制。