Niittykoski M, Lappalainen R, Jolkkonen J, Haapalinna A, Riekkinen P, Sirviö J
A.I. Virtanen Institute, University of Kuopio, Finland.
Neurosci Biobehav Rev. 1998 Oct;22(6):735-50. doi: 10.1016/s0149-7634(98)00002-5.
The present study used trimethyltin (TMT)-intoxicated rats as a model for the behavioural syndrome seen after neuronal damage to the limbic system. Behavioural assessments indicated increased locomotor activity and reduced number of groomings in an open-arena task in TMT-intoxicated (6.6 mg/kg as a free base) rats, as has been found previously. A novel finding was the severe deficit in swimming to a visible platform in the water maze task, with reduced swimming speed at the beginning of the training period. During the reacquisition phase of a radial arm maze task, TMT-intoxicated rats made more short-term and long-term memory errors, and their behavioural activity was increased in comparison with controls. The administration of atipamezole (300 micrograms/kg), a selective antagonist of alpha 2-adrenoceptors, enhanced locomotor activity compared to saline-treated rats, but these effects did not differ between the TMT group and their controls. Atipamezole did not enhance short-term or long-term memory in either TMT or control groups. Taken together, the present data indicate that TMT intoxication is a model for global dementia rather than for a specific loss of relational memory. Previous studies on the neurochemical effects of TMT and the alleviation or prevention of neurotoxicity of TMT are reviewed.
本研究使用三甲基锡（TMT）中毒的大鼠作为边缘系统神经元损伤后出现的行为综合征模型。行为评估表明，如先前发现的那样，在TMT中毒（游离碱形式为6.6 mg/kg）的大鼠的旷场任务中，运动活动增加，理毛次数减少。一个新发现是在水迷宫任务中向可见平台游泳时存在严重缺陷，在训练期开始时游泳速度降低。在放射状臂迷宫任务的重新获取阶段，TMT中毒的大鼠出现更多短期和长期记忆错误，并且与对照组相比其行为活动增加。给予阿替美唑（300微克/千克），一种α2肾上腺素能受体的选择性拮抗剂，与盐水处理的大鼠相比增强了运动活动，但这些效应在TMT组及其对照组之间没有差异。阿替美唑在TMT组或对照组中均未增强短期或长期记忆。综上所述，目前的数据表明TMT中毒是一种全面性痴呆模型，而非关系记忆的特异性丧失模型。本文回顾了先前关于TMT神经化学效应以及TMT神经毒性的缓解或预防的研究。
