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作者以前的研究曾显示：皮下注射福尔马林引起的背角伤害感受性单位长时程反应主要取决于周围传入。当阻断坐骨神经时可以使广动力型神经元的这种反应被完全抑制。为了进一步阐明福尔马林引起的伤害性感受的周围机制，本文用细胞外记录技术记录了在乌拉坦—氯醛糖麻醉下猫的Ｌ７背根神经节的初级传入单位．与背角完全一致，皮下注射福尔马林引起非伤害性感受性单位短时程的峰放电增加，例如Ａβ－毛囊型，Ａβ－快适应型，Ａβ－慢适应Ⅰ型，Ａβ－慢适应Ⅱ型，Ａδ－Ｄ毛发型以及Ｃ－低阈值机械感受性单位等，其放电均低于１０分钟；而使伤害感受性单位的放电有长时程的增加，例如Ａδ－高阈值机械伤害感受性单位放电为３０～７０分。令人感到意外的是，在单位放电终止时，检测实验中所有初级传入单位对其相应注射部位的任何机械刺激都失去反应．将此结果与以前的实验结果一起分析时可以得出结论；福尔马林引起的中枢神经改变主要取决于上传的周围传入影响，而福尔马林引起的背角单位放电的时程，则取决于外周传入纤维的分布．本文还提出和讨论了关于福尔马林引起伤害性感受机制的新见解。
Previous studies by the authors have shown that long-term response to nociception in the nociceptive area of the dorsal horn induced by subcutaneous injection of formalin mainly depends on the surrounding afferent. When blocking the sciatic nerve can make wide-energy-type neurons in this response was completely inhibited. To further elucidate the surrounding mechanisms of formalin-induced nociception, primary import units of L7 DRGs in cats under urethane-chloralose anesthesia were recorded using extracellular recording techniques. In full agreement with the dorsal horn, subcutaneous injection of formalin causes a short-term peak discharge increase in non-nociceptive units such as Aβ-hair follicle type, Aβ-fast adaptation type, Aβ-slow adaptation type I, Aβ-slow adaptation type II Aδ-D hair type and C-low threshold mechanosensitive units and the like, the discharge is less than 10 minutes; while the discharge of nociceptive units increases for a long time, for example, the Aδ-high threshold mechanical injury susceptibility unit discharge is 30 to 70 minutes. Surprisingly, at the end of unit discharge, all primary afferent units in the assay failed to respond to any mechanical stimulus at their respective injection site. Analysis of this result together with previous experimental results leads to the conclusion that central nervous system changes due to formalin mainly depend on the surrounding afferent effects of uploading and the time course of unit discharge due to formalin, Depends on the distribution of the peripherally introduced fibers. This article also presents and discusses new insights on the mechanisms responsible for nociception in formalin.