Révész E, van der Zypen E
Acta Anat (Basel). 1979;105(2):198-208. doi: 10.1159/000145123.
The paper describes the ultrastructural changes of the sympathetic neurons following guanethidine administration in mice. The main characteristics changes, after prolonged administration (1-10 weeks) of guanethidine (Ismelin, Ciba-Geigy, Basel, Switzerland) at doses of 30-50 mg/kg/day i.p. and i.m. were: (1) Mitochondrial damages: swelling and deformation of the mitochondria, with disruption and dispersion of the cristae and condensation or dissolution of the matrix. Membranolysis of the outer and inner mitochondrial membranes. (2) Neural processes: swelling and disorganization of the internal architecture in the postganglionic axonal and dendritic synaptic varicosities. (3) Adrenergic vesicles: disappearance of the granular vesicles in the early stage of the experiment, increase of the coated vesicles in the later stage of treatment. The effect of guanethidine is specific for the postganglionic adrenergic neurons, but the observed destruction is not caused solely by guanethidine; other chemical substances induce the same or similar degeneration in the sympathetic ganglion.
本文描述了小鼠给予胍乙啶后交感神经元的超微结构变化。以30 - 50mg/kg/天的剂量腹腔注射和肌肉注射胍乙啶(依斯美林,瑞士巴塞尔汽巴 - 嘉基公司),持续给药(1 - 10周)后的主要特征性变化为:(1)线粒体损伤:线粒体肿胀、变形,嵴断裂、分散,基质凝聚或溶解。线粒体外膜和内膜发生膜溶解。(2)神经突起:节后轴突和树突突触膨大处内部结构肿胀、紊乱。(3)肾上腺素能小泡:实验早期颗粒小泡消失,治疗后期包被小泡增加。胍乙啶的作用对节后肾上腺素能神经元具有特异性,但观察到的破坏并非仅由胍乙啶引起;其他化学物质在交感神经节中也可诱导相同或相似的变性。