RESPONSES OF NIGROSTRIATAL DOPAMINE NEURONS TO HIGH-INTENSITY SOMATOSENSORY STIMULATION IN THE ANESTHETIZED MONKEY
RESPONSES OF NIGROSTRIATAL DOPAMINE NEURONS TO HIGH-INTENSITY SOMATOSENSORY STIMULATION IN THE ANESTHETIZED MONKEY
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DOI：
10.1152/jn.1987.57.1.201
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发表时间：
1987-01-01
影响因子：
2.5
通讯作者：
ROMO, R
中科院分区：
文献类型：
--
作者：
SCHULTZ, W;ROMO, R
哺乳动物中脑黑质纹状体多巴胺（DA）神经元在行为反应中起重要作用。在帕金森病患者和实验损伤的动物中，它们的破坏导致运动减少和减慢以及其他运动、认知和动机缺陷。我们测试了DA神经元对体感刺激的反应，以深入了解到达这些神经元的外周信息的性质。实验在两只长期植入记录室的麻醉猴子中重复进行，从而减少了实验所需的灵长类动物的数量。中脑DA神经元的特征在于其组织学位置，由细胞外记录的形式，持续时间和频率，自发发生的冲动，从尾状核和壳核的逆向激活，并通过减少冲动率后，全身给药低剂量的DA自身受体激动剂阿扑吗啡。一半的中脑DA神经元（145个神经元中的65个，45%）从尾状核（35个神经元），壳核（47个神经元），或两种结构（其中17个）的长期植入刺激电极逆向激活。传导速度范围为0.7至2.5米/秒，中位数为1.2和1.5米/秒的神经元投射到尾状核和壳核，分别。一半的中脑DA神经元被压抑（72 140个神经元，51%）和不到四分之一的激活（24 140个神经元，17%），强烈的伤害性捏刺激身体表面。无害的，甚至强烈的，表面或深层的躯体感觉刺激是无效的。在大多数DA神经元中，在整个几秒钟的刺激期间，捏缩反应持续。反复刺激无反应习惯化。脊髓和三叉神经之间的收敛输入，并从身体两侧被视为几乎所有的伤害性捏反应。因此，DA神经元通常以相同的方向响应于捏刺激的手，脚，脸，尾巴，和背部的两侧。DA受体拮抗剂氟哌啶醇（0.33或0.50 mg/kg）的全身给药强烈减少捏反应在所有7个DA神经元测试。这为DA能神经传递参与大脑中外感受性输入的表征提供了证据。结果表明，在麻醉猴中脑DA能神经元投射到纹状体对伤害性躯体感觉输入的反应。双边nontopographic性质的反应不支持的作用，在精确的刺激识别，而是它表明一种机制，参与基本的神经元过程的行为反应。
Nigrostriatal dopamine (DA) neurons of the mammalian midbrain play an important role in behavioral reactions. Their destruction in Parkinsonian patients and experimentally lesioned animals leads to a reduction and slowing of movements as well as other motor, cognitive, and motivational deficits. We tested the responses of DA neurons to somatosensory stimulation to gain insight into the nature of peripheral information reaching these neurons. Experiments were performed as repeated sessions in two anesthetized monkeys having chronically implanted recording chambers, thereby reducing the number of primates required for experimentation. Midbrain DA neurons were characterized by their histological location, by the form, duration, and frequency of extracellularly recorded, spontaneously occurring impulses, by antidromic activation from caudate and putamen, and by the reduction of impulse rate following systemic administration of low doses of the DA autoreceptor agonist apomorphine. Half of the midbrain DA neurons (65 of 145 neurons, 45%) were antidromically activated from chronically implanted stimulating electrodes in caudate (35 neurons), putamen (47 neurons), or both structures (17 of them). Conduction velocities ranged from 0.7 to 2.5 m/s, with medians of 1.2 and 1.5 m/s for neurons projecting to caudate and putamen, respectively. Half of the midbrain DA neurons were depressed (72 of 140 neurons, 51%) and less than a quarter activated (24 of 140 neurons, 17%) by intense noxious pinch stimulation to the body surface. Innocuous, even intense, surface or deep somatosensory stimuli were ineffective. Pinch responses continued during the whole stimulating period of several seconds in most DA neurons. There was no response habituation during repeated stimulation. Convergence between spinal and trigeminal input and from both body sides was seen for virtually all noxious pinch responses. Thus DA neurons typically responded in the same direction to pinch stimulation of hand, foot, face, tail, and dorsum of both sides. Systemic administration of the DA receptor antagonist haloperidol (0.33 or 0.50 mg/kg) strongly reduced pinch responses in all seven DA neurons tested. This provides evidence for an involvement of DAergic neurotransmission in the representation of exteroceptive input in the brain. The results show that midbrain DA neurons projecting to the striatum respond to noxious somatosensory input in the anesthetized monkey. The bilateral nontopographic nature of the responses does not support a role in precise stimulus recognition, rather it suggests a mechanism involved in basic neuronal processes underlying behavioral responsiveness.