Spinal cord injury causes plasticity in a subpopulation of lamina I GABAergic interneurons
Spinal cord injury causes plasticity in a subpopulation of lamina I GABAergic interneurons
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DOI：
10.1152/jn.01104.2007
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发表时间：
2008-07-01
影响因子：
2.5
通讯作者：
Hochman, Shawn
中科院分区：
文献类型：
--
作者：
Dougherty, Kimberly J.;Hochman, Shawn
脊髓GABA能系统的功能障碍与脊髓损伤（SCI）后的疼痛综合征有关。由于板层I参与伤害性和热信号传导，我们表征了慢性SCI对GAD 67-GFP转基因小鼠脊髓切片中荧光鉴定的GABA能神经元细胞特性的影响。从13至17日龄小鼠的腰髓获得全细胞记录，包括在实验前6-9天切除胸段（T8-11）的小鼠。在慢性SCI后，GFP（+）细胞的分布、发生率和放电类别与对照组相似，并且对电流注射有单一尖峰反应的细胞的膜特性变化最小。与此相反，显示强直/初始爆发放电的细胞有更多的去极化膜电位，增加稳态外向电流，并增加尖峰高度。此外，更高的放电频率和自发平台电位在慢性SCI后更为普遍，这些变化主要发生在显示紧张性放电模式的细胞中。持续性内向电流（PIC）中观察到一个类似的分数的细胞从脊髓横断面，并可能有助于这些高原。持久性Na+和L-型Ca 2+通道可能对电流有贡献，因为两者均被鉴定为双稳态。总之，慢性脊髓损伤诱导一个亚群的板层GABA能中间神经元的可塑性反应。改变是针对放大神经元的反应。这些变化如何改变脊髓感觉整合，以及它们是否有助于感觉功能障碍仍有待阐明。
Dysfunction of the spinal GABAergic system has been implicated in pain syndromes following spinal cord injury (SCI). Since lamina I is involved in nociceptive and thermal signaling, we characterized the effects of chronic SCI on the cellular properties of its GABAergic neurons fluorescently identified in spinal slices from GAD67-GFP transgenic mice. Whole cell recordings were obtained from the lumbar cord of 13- to 17-day-old mice, including those having had a thoracic segment (T8-11) removed 6-9 days prior to experiments. Following chronic SCI, the distribution, incidence, and firing classes of GFP(+) cells remained similar to controls, and there were minimal changes in membrane properties in cells that responded to current injection with a single spike. In contrast, cells displaying tonic/initial burst firing had more depolarized membrane potentials, increased steady-state outward currents, and increased spike heights. Moreover, higher firing frequencies and spontaneous plateau potentials were much more prevalent after chronic SCI, and these changes occurred predominantly in cells displaying a tonic firing pattern. Persistent inward currents (PICs) were observed in a similar fraction of cells from spinal transects and may have contributed to these plateaus. Persistent Na+ and L-type Ca2+ channels likely contributed to the currents as both were identified pharmacologically. In conclusion, chronic SCI induces a plastic response in a subpopulation of lamina I GABAergic interneurons. Alterations are directed toward amplifying neuronal responsiveness. How these changes alter spinal sensory integration and whether they contribute to sensory dysfunction remains to be elucidated.