LESIONS OF THE TEGMENTAL PEDUNCULOPONTINE NUCLEUS - EFFECTS ON THE LOCOMOTOR-ACTIVITY INDUCED BY MORPHINE AND AMPHETAMINE
LESIONS OF THE TEGMENTAL PEDUNCULOPONTINE NUCLEUS - EFFECTS ON THE LOCOMOTOR-ACTIVITY INDUCED BY MORPHINE AND AMPHETAMINE
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DOI：
10.1016/0091-3057(92)90438-l
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发表时间：
1992-05-01
影响因子：
3.6
通讯作者：
VANDERKOOY, D
中科院分区：
文献类型：
--
作者：
BECHARA, A;VANDERKOOY, D
动机的神经生物学中的一个重要问题是，刺激对前脑边缘系统的激励影响如何最终转化为行动和接近行为。先前已经证明，损毁被盖脚桥核(TPP)(边缘系统的脑干输出，接受边缘前脑和中脑部位的神经元输入，被认为是精神活性药物奖励的主要部位)的双侧鹅膏藤酸可以阻止吗啡和苯丙胺条件性位置偏爱的获得，但不能阻止其保留。这些结果表明，这些药物的无条件奖赏效应在加工过程中存在缺陷。TPP投射到大脑和脊髓的广泛部位，参与各种躯体运动反应。因此，我们在野外研究了TPP在吗啡和苯丙胺诱导的运动中的作用。我们报告说，TPP损伤阻断了苯丙胺产生的运动兴奋和条件性多动。TPP损毁也阻止了吗啡产生的条件性运动增加，但不能阻止惊厥。TPP损毁是行为特异性的，因为在甩尾试验中吗啡的止痛特性不会减弱，也不会影响吗啡依赖动物纳洛酮催促戒断引起的运动。我们认为，调节作用于前脑部位的药物刺激的急性奖赏效应的神经回路离开了脑干TPP区域的边缘系统，在那里动机获得了启动接近和探索的运动系统(或与之同构)。
One of the important questions in the neurobiology of motivation asks how the incentive impact of stimuli acting on the limbic system of the forebrain are ultimately translated into action and approach behavior. Bilateral ibotenic acid lesions of the tegmental pedunculopontine nucleus (TPP) (a brainstem output of the limbic system that receives neuronal input from limbic forebrain and midbrain sites identified as primary sites for psychoactive drug reward) have been shown previously to block the acquisition, but not the retention, of morphine and amphetamine conditioned place preferences in formerly drug-naive rats. These results suggest a deficit in the processing of the unconditioned rewarding effects of these drugs. The TPP projects to widespread parts of the brain and spinal cord involved in various somatomotor responses. Thus, we investigated the role of the TPP in morphine- and amphetamine-induced locomotion as assessed in an open field. We report that TPP lesions blocked the locomotor excitation, as well as the conditioned hyperactivity, produced by amphetamine. TPP lesions also blocked the conditioned increase in locomotion, but not the catalepsy, produced by morphine. TPP lesions were behaviorally specific in that the analgesic properties of morphine in a tail-flick test were not attenuated, nor did the lesions affect the locomotion induced by naloxone-precipitated withdrawal in morphine-dependent animals. We suggest that the neural circuits mediating the acute rewarding effects of drug stimuli acting at forebrain sites exit the limbic system in the TPP region of the brainstem, where motivation gains access to (or is isomorphic with) motor systems that initiate approach and exploration.