Markus H, Pomeranz B, Krushelnycky D
Brain Res. 1984 Mar 26;296(1):27-39. doi: 10.1016/0006-8993(84)90508-0.
The left sciatic nerve was cut and ligated in adult rats (chronic denervation). Twenty-one days later the right sciatic nerve was cut and ligated (acute denervation). The somatotopic maps of the surviving intact saphenous nerves (left and right) were compared on day 21 by recording from single interneurons in the dorsal horn of the spinal cord. On the acute side saphenous mediated natural responses were observed only as far caudally as L3, while no natural responses were found in L4 and 5 (this silent zone in L4 and 5 had previously been sciatic territory). In contrast, after chronic sciatic denervation, L4 and L5 were not silent to natural stimulation as the saphenous natural responses had spread into the sciatic territory. Saphenous inputs always won the sciatic territory in L4 and L5 over competing thigh afferents after chronic sciatic denervation. Electrical stimulation of the saphenous nerve on the acute side produced unit responses all the way down to S1 (with no silent areas in L4 and 5). These electrically evoked unit responses in L4 to S1 of the acute side were called 'long range' pathways. There were no differences in 'long range' electrical responses in the acutely and chronically denervated cord. The caudal boundary for electrically evoked saphenous responses was S1 on both sides of the cord, and post stimulus histograms of unit responses were not statistically different on the two sides. Thus after chronic sciatic denervation natural responses mediated by saphenous spread caudally into sciatic territory, but electrically evoked responses did not change. Behaviorally, there was the expected spread of saphenous mediated responses from the medial toe and foot to more lateral regions after chronic sciatic denervation. Unexpectedly, there was an increase in sensitivity (hyperalgesia) of the medial toe and foot. We postulate that this increased sensitivity might be mediated by the spread of saphenous projections into L4 and L5 of the cord after chronic sciatic denervation. Perhaps post traumatic neuralgia in humans could be due to increased number of spinal cord cells responding to stimulation of the receptive field of the surviving nerve.
在成年大鼠中切断并结扎左侧坐骨神经(慢性去神经支配)。21天后,切断并结扎右侧坐骨神经(急性去神经支配)。在第21天,通过记录脊髓背角中的单个中间神经元,比较了存活的完整隐神经(左右)的躯体定位图。在急性侧,仅在L3尾侧观察到隐神经介导的自然反应,而在L4和L5中未发现自然反应(L4和L5中的这个沉默区以前是坐骨神经支配区域)。相比之下,在慢性坐骨神经去神经支配后,L4和L5对自然刺激并不沉默,因为隐神经的自然反应已扩散到坐骨神经支配区域。在慢性坐骨神经去神经支配后,隐神经输入在L4和L5中总是在竞争的大腿传入神经中赢得坐骨神经支配区域。在急性侧对隐神经进行电刺激可产生一直到S1的单位反应(L4和L5中无沉默区)。急性侧L4至S1中的这些电诱发单位反应被称为“长程”通路。急性和慢性去神经支配的脊髓中“长程”电反应没有差异。脊髓两侧电诱发隐神经反应的尾侧边界均为S1,两侧单位反应的刺激后直方图无统计学差异。因此,在慢性坐骨神经去神经支配后,由隐神经介导的自然反应向尾侧扩散到坐骨神经支配区域,但电诱发反应没有改变。行为上,在慢性坐骨神经去神经支配后,隐神经介导的反应如预期的那样从内侧脚趾和足部扩散到更外侧区域。出乎意料的是,内侧脚趾和足部的敏感性增加(痛觉过敏)。我们推测,这种敏感性增加可能是由于慢性坐骨神经去神经支配后隐神经投射扩散到脊髓的L4和L5所致。也许人类创伤后神经痛可能是由于脊髓中对存活神经感受野刺激作出反应的细胞数量增加所致。