Jortner B S, Perkins S K, Ehrich M
Laboratory for Neurotoxicity Studies, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Tech, Blacksburg 24061-0442, USA.
Neurotoxicology. 1999 Dec;20(6):971-5.
Organophosphorus ester-induced delayed neuropathy (OPIDN) is manifest by delayed degeneration of distal levels of long myelinated fibers following an appropriate neurotoxic exposure. We investigated the dynamics of cytoskeletal changes during nerve fiber degeneration in this condition, focusing on the immunohistochemistry of axonal phosphorylated neurofilaments. OPIDN was produced in 5-month-old White Leghorn hens using a single 2.5 mg/kg intramuscular dose of phenyl saligenin phosphate. Hens were sacrificed on days 4, 7, 9, 15, and 20, and the tibial nerve branch to the gastrocnemius muscle was studied by light microscopy and immunohistochemistry (using the SMI 31 monoclonal primary antibody to phosphorylated neurofilaments). At post-dosing days 9, 15, and 20 various stages of OPIDN lesions were noted, including axonal swelling and myelinated nerve fiber degeneration. These were associated with intra-axonal cytoskeletal lysis, manifest by loss of immunolabeled phosphorylated neurofilaments, a process consistent with proteolysis. Aggregations of excess axonal phosphorylated neurofilaments were not observed.
有机磷酸酯诱导的迟发性神经病（OPIDN）表现为在适当的神经毒性暴露后，长有髓纤维远端水平的迟发性变性。我们研究了这种情况下神经纤维变性过程中细胞骨架变化的动态，重点是轴突磷酸化神经丝的免疫组织化学。使用2.5mg/kg的苯基水杨基磷酸单剂量肌肉注射，在5月龄的白来航鸡中诱发OPIDN。在第4、7、9、15和20天处死母鸡，并通过光学显微镜和免疫组织化学（使用针对磷酸化神经丝的SMI 31单克隆一抗）研究腓肠肌的胫神经分支。在给药后第9、15和20天，观察到OPIDN病变的各个阶段，包括轴突肿胀和有髓神经纤维变性。这些与轴突内细胞骨架溶解有关，表现为免疫标记的磷酸化神经丝丢失，这一过程与蛋白水解一致。未观察到过量轴突磷酸化神经丝的聚集。
