Zhang A L, Hao J X, Seiger A, Xu X J, Wiesenfeld-Hallin Z, Grant G, Aldskogius H
Karolinska Institute, Department of Neuroscience, Stockholm, Sweden.
Brain Res. 1994 Sep 5;656(1):187-90. doi: 10.1016/0006-8993(94)91383-8.
The number of GABA-like immunoreactive (LI) cells in lamina I-III of the rat spinal cord was significantly decreased bilaterally 48-72 h after photochemical induction of transient spinal cord ischemia compared to sham-operated controls. No significant changes in the number of GABA-LI cells were observed at cervical level. The number of GABA-LI cells was restored 2 weeks after ischemia. These data, together with recent behavioral and electrophysiological findings, suggest that decreased intraneuronal GABA levels after spinal cord ischemia may underlie the development of the temporary pain-like response to innocuous mechanical stimuli (allodynia) in rats after transient spinal cord ischemia.
与假手术对照组相比,光化学诱导大鼠短暂性脊髓缺血后48 - 72小时,双侧脊髓I - III层中γ-氨基丁酸样免疫反应性(LI)细胞数量显著减少。在颈部水平未观察到γ-氨基丁酸-LI细胞数量的显著变化。缺血2周后γ-氨基丁酸-LI细胞数量恢复。这些数据,连同最近的行为学和电生理学研究结果表明,脊髓缺血后神经元内γ-氨基丁酸水平降低可能是大鼠短暂性脊髓缺血后对无害机械刺激产生暂时疼痛样反应(痛觉过敏)的基础。