| Literature DB >> 3358858 |
Abstract
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.Entities:
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Year: 1988 PMID: 3358858 DOI: 10.1016/0166-4328(88)90116-7
Source DB: PubMed Journal: Behav Brain Res ISSN: 0166-4328 Impact factor: 3.332