Axonal degeneration and axonal caliber alterations following combined beta,beta'-iminodipropionitrile (IDPN) and acrylamide administration.
Axonal degeneration and axonal caliber alterations following combined beta,beta'-iminodipropionitrile (IDPN) and acrylamide administration.
复制标题
联合使用 β,β-亚氨基二丙腈 (IDPN) 和丙烯酰胺后轴突变性和轴突口径改变。
DOI：
10.1097/00005072-198911000-00007
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发表时间：
1989
影响因子：
3.2
通讯作者：
Halleck,MM
中科院分区：
文献类型：
--
作者：
Gold,BG;Halleck,MM
本文报道了一种新的神经纤维轴突异常模型，该模型采用β，β′-亚氨基二丙腈（IDPN）和丙烯酰胺（AC）联合给药。该模型被开发来测试IDPN诱导的肿胀增加远端轴突对第二次神经毒性化学损伤的脆弱性的假设。在接受单次注射AC（75 mg/kg，IP）之前一周，对大鼠单次腹腔内（IP）注射IDPN（1.5 g/kg）。在两周时沿坐骨神经在多个水平沿着观察到轴突变性（参照IDPN给药），并且在长达五周时没有进展。变性纤维的定量表明，变性的程度增加远端沿着坐骨神经。IDPN或AC单次给药均未引起变性。因此，IDPN诱导的神经丝鞘改变了轴突对AC神经毒性的易感性。还研究了该模型的两种变体。首先，大鼠给予AC（30毫克/公斤，IP）开始IDPN给药后一个星期，每天注射5次，在IDPN诱导的微管通道的快速轴突运输材料的积累。第二，大鼠长期注射AC（30 mg/kg，IP，5天/周，持续4周），以减少神经丝向近端轴突的输送，当用IDPN攻击时，轴突扩大不太明显。因此，轴突萎缩可以掩盖神经丝轴突萎缩的发展。
A new model of neurofilamentous axonal abnormality is described which employs combined administration of β,β′-iminodipropionitrile (IDPN) and acrylamide (AC). The model was developed to test the hypothesis that IDPN-induced swelling increases the vulnerability of the distal axon to a second neurotoxic chemical insult. Rats were given a single intraperitoneal (IP) injection of IDPN (1.5 g/kg) one week before receiving a single injection of AC (75 mg/kg, IP). Axonal degeneration was observed at multiple levels along the sciatic nerve at two weeks (with reference to IDPN administration), and was not progressive up to five weeks. Quantitation of degenerating fibers demonstrated that the extent of degeneration increased distally along the sciatic nerve. Single administration of either IDPN or AC did not produce degeneration. Thus, IDPN-induced neurofilamentous swellings alter the susceptibility of the axon to AC neurotoxicity. Two variations of this model were also studied. First, rats given five daily injections of AC (30 mg/kg, IP) beginning one week following IDPN administration developed accumulations of fast axonally transported materials in IDPN-induced microtubule channels. Second, rats given chronic injections of AC (30 mg/kg, IP, five days/week, for four weeks), to reduce the delivery of neurofilaments to the proximal axon, developed less prominent axonal enlargements when challenged with IDPN. Thus, axonal atrophy can mask the development of neurofilamentous axonal swellings.