Jaspers R M, Cools A R
Department of Pharmacology, University of Nijmegen, The Netherlands.
Behav Brain Res. 1988 Mar;27(3):193-204. doi: 10.1016/0166-4328(88)90116-7.
During the ontogeny of many mammalian species there exists a remarkable resemblance with respect to the strict order in the appearance of distinct motor patterns during development. Moreover, along a cephalocaudal gradient more and more body parts become involved in these motor patterns. The same sequence in motor behaviour can be observed when adult animals start to explore a novel environment. On the other hand, s.c. injections of apomorphine result in a reversed 'ontogenetic' sequence of motor patterns: a 'breakdown' of motor behaviour. The present study investigated whether striatal injections of apomorphine produced a reversed 'breakdown' of a motor pattern sequence. Therefore, cats were tested in a paradigm in which they executed sequences of distinct motor patterns in order to collect food pellets when walking on the belt of a treadmill. As only one of the motor patterns in the sequence is caudate-specific, disturbances at the level of the caudate nucleus as well as disturbances at the level of other brain structures can be distinguished. In contrast to 0.6 and 2.5 micrograms, doses of 5.0 and 10.0 micrograms of apomorphine resulted in the successive breakdown of motor pattern sequences, whereby not only caudate-specific motor patterns were reduced, but also non-caudate-specific motor patterns. Moreover, this regression appeared in the reversed order compared to the order in which distinct patterns are executed during eating behaviour. The regression in motor behaviour following 5.0 micrograms apomorphine was induced via caudate dopamine receptors since it could be prevented by pretreatment with haloperidol. Because of the fact that 5.0 and 10.0 micrograms of apomorphine also affected motor patterns which are not caudate- and dopamine-specific, it is concluded that also brain structures receiving (in)directly caudate output signals are involved in the regression of the motor pattern sequence as observed in the present study. The clinical relevance of the presented data is discussed.
在许多哺乳动物物种的个体发育过程中，不同运动模式在发育过程中出现的严格顺序存在显著相似性。此外，沿着头尾梯度，越来越多的身体部位参与到这些运动模式中。当成年动物开始探索新环境时，也能观察到相同的运动行为序列。另一方面，皮下注射阿扑吗啡会导致运动模式出现反向的“个体发育”序列：运动行为的“崩溃”。本研究调查了纹状体注射阿扑吗啡是否会导致运动模式序列出现反向“崩溃”。因此，对猫进行了一项测试，在该测试中，当猫在跑步机皮带上行走时，它们执行不同的运动模式序列以获取食物颗粒。由于序列中的运动模式只有一种是尾状核特异性的，因此可以区分尾状核水平的干扰以及其他脑结构水平的干扰。与0.6微克和2.5微克剂量相比，5.0微克和10.0微克剂量的阿扑吗啡导致运动模式序列相继崩溃，不仅尾状核特异性运动模式减少，非尾状核特异性运动模式也减少。此外，这种退化出现的顺序与进食行为中不同模式执行的顺序相反。5.0微克阿扑吗啡后运动行为的退化是通过尾状核多巴胺受体诱导的，因为它可以被氟哌啶醇预处理所预防。由于5.0微克和10.0微克的阿扑吗啡也影响了非尾状核和多巴胺特异性的运动模式，因此得出结论，如本研究中所观察到的，接受（直接或间接）尾状核输出信号的脑结构也参与了运动模式序列的退化。本文讨论了所呈现数据的临床相关性。
