Rörig B, Sutor B
Department of Physiology, University of Munich, Germany.
Neuroreport. 1996 Jan 31;7(2):569-72. doi: 10.1097/00001756-199601310-00046.
In the present study we demonstrate that gap junction coupling between developing layer II/III pyramidal cells in rat sensorimotor cortex is strongly modified by the nitric oxide (NO)/cyclic guanosine monophosphate (cGMP) system. Dye coupling was revealed by intracellular injection of the gap junction-permeable tracer neurobiotin into single neurones. Following incubation of slices with sodium nitroprusside, a source of NO, the size of dye-coupled cell clusters was significantly reduced. In many cases, 2-3 cells remained strongly dye-coupled. These effects were blocked by intracellular injection of the guanylyl cyclase inhibitor cystamine and mimicked by both application of the membrane-permeant cGMP analogue 8-Br-cGMP and intracellular injection of cGMP. cGMP injection also induced a 60% increase in neuronal input resistance. These results indicate that NO modulates gap junction coupling in the developing neocortex via stimulation of guanylyl cyclase.
在本研究中，我们证明大鼠感觉运动皮层发育中的II/III层锥体细胞之间的缝隙连接耦合受到一氧化氮（NO）/环磷酸鸟苷（cGMP）系统的强烈调节。通过将缝隙连接可通透的示踪剂神经生物素细胞内注射到单个神经元中来揭示染料耦合。在用NO供体硝普钠孵育切片后，染料耦合细胞簇的大小显著减小。在许多情况下，2 - 3个细胞仍保持强烈的染料耦合。这些效应被细胞内注射鸟苷酸环化酶抑制剂胱胺所阻断，并被膜通透性cGMP类似物8 - Br - cGMP的应用和cGMP的细胞内注射所模拟。cGMP注射还导致神经元输入电阻增加60%。这些结果表明，NO通过刺激鸟苷酸环化酶来调节发育中的新皮层中的缝隙连接耦合。
