Superficial NK1-expressing neurons control spinal excitability through activation of descending pathways
Superficial NK1-expressing neurons control spinal excitability through activation of descending pathways
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DOI：
10.1038/nn966
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发表时间：
2002-12-01
影响因子：
25
通讯作者：
Dickenson, AH
中科院分区：
文献类型：
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作者：
Suzuki, R;Morcuende, S;Dickenson, AH
损伤后疼痛敏感性的增加由脊髓背角中表达神经激肽-1（NK 1）受体的表面定位投射神经元调节。在大鼠中选择性消融这些神经元后，我们确定了感受野大小、机械和热编码以及对痛觉和反射都很重要的深背角神经元的中枢敏化的变化。我们能够重现这些变化的药理学阻断下行多巴胺能易化途径。使用Fos组织化学，我们发现了脑干中多巴胺能神经元激活的变化，以及脊髓兴奋性下降控制丧失的证据。我们的结论是，NK 1阳性脊髓投射神经元，激活初级传入输入，项目更高的大脑区域，控制脊髓兴奋性，因此疼痛敏感性，主要是通过从脑干下行通路。
The increase in pain sensitivity that follows injury is regulated by superficially located projection neurons in the dorsal horn of the spinal cord that express the neurokinin-1 (NK1) receptor. After selective ablation of these neurons in rats, we identified changes in receptive field size, mechanical and thermal coding and central sensitization of deeper dorsal horn neurons that are important for both pain sensations and reflexes. We were able to reproduce these changes by pharmacological block of descending serotonergic facilitatory pathways. Using Fos histochemistry, we found changes in the activation of serotonergic neurons in the brainstem as well as evidence for a loss of descending control of spinal excitability. We conclude that NK1-positive spinal projection neurons, activated by primary afferent input, project to higher brain areas that control spinal excitability- and therefore pain sensitivity-primarily through descending pathways from the brainstem.