Benabid A L, Henriksen S J, McGinty J F, Bloom F E
Brain Res. 1983 Dec 5;280(2):217-31. doi: 10.1016/0006-8993(83)90052-5.
These experiments investigated the role of a specific thalamic nucleus in the cellular response to noxious and non-noxious inputs. Single-unit extracellular responses to peripheral noxious stimuli were recorded with glass micropipettes in the nucleus parafascicularis (Pf) of the rat under chloral hydrate anesthesia. Bipolar stimulating/recording electrodes were inserted in the nucleus ventro-postero-lateralis (VPL) of the thalamus, in areas responsive to the peripheral noxious stimulation. Single-unit records in Pf and multi-unit records in VPL demonstrated that both these nuclei are differentially sensitive to noxious and non-noxious inputs: Pf was more sensitive to late (200-600 ms latency) high threshold noxious inputs, while VPL was more responsive to early (10-40 ms) low threshold non-noxious inputs. Late, high threshold inputs to VPL were selectively suppressed by systemic morphine and restored by naloxone. Trains of stimuli applied to VPL suppressed the response of 76% of Pf units, to peripheral noxious stimuli but did not inhibit the response of spinal cord dorsal horn units to the same stimuli. This inhibitory effect of VPL on Pf cells was not reversed by systemically administered naloxone. The neural pathways responsible for the VPL suppression of Pf nociception appear to be neither monosynaptic nor mediated through the spinal cord dorsal horn, nor through any single, naloxone-reversible, central opioid process. Nevertheless, this inhibitory effect of VPL stimulation on Pf nociception provides a physiological basis for the analgesic effects of thalamic stimulation on clinically observed deafferentation pain. It also supports the existence of a pain modulating system at the thalamic level comparable, at least in part, with the spinal Gate Control concept.
这些实验研究了特定丘脑核在细胞对有害和无害输入的反应中的作用。在水合氯醛麻醉下，用玻璃微电极在大鼠的束旁核（Pf）中记录对周围有害刺激的单单位细胞外反应。将双极刺激/记录电极插入丘脑腹后外侧核（VPL）中对周围有害刺激有反应的区域。Pf中的单单位记录和VPL中的多单位记录表明，这两个核团对有害和无害输入的敏感性不同：Pf对晚期（潜伏期200 - 600毫秒）高阈值有害输入更敏感，而VPL对早期（10 - 40毫秒）低阈值无害输入反应更强。全身应用吗啡可选择性抑制VPL的晚期高阈值输入，并可被纳洛酮恢复。施加于VPL的刺激串可抑制76%的Pf单位对周围有害刺激的反应，但不抑制脊髓背角单位对相同刺激的反应。VPL对Pf细胞的这种抑制作用不能被全身给予纳洛酮逆转。负责VPL抑制Pf伤害感受的神经通路似乎既不是单突触的，也不是通过脊髓背角介导的，也不是通过任何单一的、纳洛酮可逆的中枢阿片类过程介导的。然而，VPL刺激对Pf伤害感受的这种抑制作用为丘脑刺激对临床观察到的去传入性疼痛的镇痛作用提供了生理基础。它还支持在丘脑水平存在一个至少部分与脊髓门控理论相当的疼痛调制系统。
