Namba S, Shimizu Y, Wani T, Fujiwara N
Appl Neurophysiol. 1985;48(1-6):201-11. doi: 10.1159/000101128.
Deafferentation hyperactivity, produced unilaterally in the neurons of the subnucleus caudalis of the spinal trigeminal nucleus (STNcd) in cats by left Gasserian ganglionectomy, was studied neurochemically and electrophysiologically. Analysis of neuronal activities on both sides of the STNcd was done 11-63 days after the denervation. On the denervated side, 37 (57%) of the 65 neurons identified showed deafferentation hyperactivity. Continuous and spontaneous firing of these hyperactive neurons were inhibited neither by the intraventricular administration of morphine or enkephalinamide nor by the electrical stimulation of periaqueductal gray. In contrast, the facilitation of the pain perceptive neuronal activities in the STNcd of the nondenervated side was remarkably inhibited, both by the administration of the same drugs and by periaqueductal gray stimulation. The deafferentation hyperactivity produced in this experiment in the STNcd of the denervated side might have a close physiological relationship to the deafferented pain of clinical patients.
通过左侧半月神经节切除术在猫的三叉神经脊束核尾侧亚核（STNcd）神经元中单侧产生的去传入性活动亢进，进行了神经化学和电生理学研究。在去神经支配后11 - 63天对STNcd两侧的神经元活动进行分析。在去神经支配侧，65个被鉴定的神经元中有37个（57%）表现出去传入性活动亢进。这些活动亢进神经元的持续和自发放电既不被脑室内注射吗啡或脑啡肽酰胺所抑制，也不被导水管周围灰质的电刺激所抑制。相反，在未去神经支配侧的STNcd中，疼痛感受神经元活动的易化被相同药物的给药以及导水管周围灰质刺激均显著抑制。本实验在去神经支配侧的STNcd中产生的去传入性活动亢进可能与临床患者的去传入性疼痛有密切的生理关系。
