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本文引用的文献

1
Administration of phosphodiesterase inhibitors and an adenosine A1 receptor antagonist induces phrenic nerve recovery in high cervical spinal cord injured rats.给予磷酸二酯酶抑制剂和腺苷A1受体拮抗剂可诱导高位颈脊髓损伤大鼠的膈神经恢复。
Exp Neurol. 2008 Apr;210(2):671-80. doi: 10.1016/j.expneurol.2007.12.021. Epub 2008 Jan 5.
2
Descending respiratory pathways in the cervical spinal cord.颈髓中的下行呼吸通路。
Am J Physiol. 1949 Jun;157(3):468-76. doi: 10.1152/ajplegacy.1949.157.3.468.
3
MK-801 upregulates NR2A protein levels and induces functional recovery of the ipsilateral hemidiaphragm following acute C2 hemisection in adult rats.MK-801上调成年大鼠急性C2半横断后同侧半膈肌的NR2A蛋白水平并诱导其功能恢复。
J Spinal Cord Med. 2007;30(4):346-54. doi: 10.1080/10790268.2007.11753950.
4
Spinal activation of serotonin 1A receptors enhances latent respiratory activity after spinal cord injury.脊髓损伤后，脊髓中5-羟色胺1A受体的激活可增强潜在呼吸活动。
J Spinal Cord Med. 2006;29(2):147-55. doi: 10.1080/10790268.2006.11753868.
5
Barrel map development relies on protein kinase A regulatory subunit II beta-mediated cAMP signaling.桶状图的形成依赖于蛋白激酶A调节亚基IIβ介导的环磷酸腺苷（cAMP）信号传导。
J Neurosci. 2006 Apr 19;26(16):4338-49. doi: 10.1523/JNEUROSCI.3745-05.2006.
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Protein kinase A regulates calcium permeability of NMDA receptors.蛋白激酶A调节N-甲基-D-天冬氨酸受体的钙通透性。
Nat Neurosci. 2006 Apr;9(4):501-10. doi: 10.1038/nn1664. Epub 2006 Mar 12.
7
Bidirectional behavioral plasticity of memory reconsolidation depends on amygdalar protein kinase A.记忆再巩固的双向行为可塑性取决于杏仁核蛋白激酶A。
Nat Neurosci. 2006 Feb;9(2):167-9. doi: 10.1038/nn1628. Epub 2006 Jan 15.
8
Theophylline stimulates cAMP-mediated signaling associated with growth regulation in human cells from pulmonary adenocarcinoma and small airway epithelia.茶碱刺激与肺腺癌和小气道上皮细胞生长调节相关的cAMP介导的信号传导。
Int J Oncol. 2005 Jul;27(1):155-60.
9
Adenosinergic mechanisms underlying recovery of diaphragm motor function following upper cervical spinal cord injury: potential therapeutic implications.上颈段脊髓损伤后膈肌运动功能恢复的腺苷能机制：潜在的治疗意义
Neurol Res. 2005 Mar;27(2):195-205. doi: 10.1179/016164105X21977.
10
Long-lasting synapse formation in cultured rat hippocampal neurons after repeated PKA activation.反复激活蛋白激酶A后，培养的大鼠海马神经元中形成持久的突触。
Brain Res. 2005 Apr 25;1042(1):6-16. doi: 10.1016/j.brainres.2005.01.102.

环磷酸腺苷-蛋白激酶A信号通路的脊髓激活可诱导高位颈髓损伤后呼吸运动功能恢复。

Spinal activation of the cAMP-PKA pathway induces respiratory motor recovery following high cervical spinal cord injury.

作者信息

Kajana S, Goshgarian H G

机构信息

Department of Anatomy and Cell Biology, Wayne State University School of Medicine, 540 East Canfield, Detroit, MI 48201, USA.

出版信息

Brain Res. 2008 Sep 26;1232:206-13. doi: 10.1016/j.brainres.2008.07.012. Epub 2008 Jul 12.

DOI:10.1016/j.brainres.2008.07.012
PMID:18656458
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2573999/
Abstract

The present study investigated the involvement of the adenosine 3'5'-cyclic monophosphate-dependent protein kinase A (cAMP-PKA) pathway in the activation of the crossed-phrenic pathways after left C2 spinal cord hemisection. Experiments were conducted on left C2 spinal cord hemisected, anesthetized, vagotomized, pancuronium paralyzed, and artificially ventilated male Sprague-Dawley rats. One week post-injury, the ipsilateral phrenic nerve exhibited no respiratory-related activity indicating a functionally complete hemisection. Intrathecal spinal cord administration of the cAMP analog, 8-Br-cAMP at the level of the phrenic nucleus resulted in an enhancement of contralateral phrenic nerve output and a restoration of respiratory-related activity in the phrenic nerve ipsilateral to the hemisection. Furthermore, pre-treatment with Rp-8-Br-cAMP, a PKA inhibitor, abolished the effects of 8-Br-cAMP. These results suggest that PKA activation is necessary for the cAMP-mediated respiratory recovery following high cervical spinal cord injury and that activation of intracellular signaling cascades may represent an important strategy for improving respiratory function after spinal cord injury.

摘要

本研究调查了3',5'-环磷酸腺苷依赖性蛋白激酶A（cAMP-PKA）通路在左侧C2脊髓半横断后膈神经交叉通路激活中的作用。实验在左侧C2脊髓半横断、麻醉、迷走神经切断、泮库溴铵麻痹并人工通气的雄性Sprague-Dawley大鼠身上进行。损伤后一周，同侧膈神经未表现出与呼吸相关的活动，表明半横断在功能上是完全的。在膈神经核水平鞘内注射cAMP类似物8-Br-cAMP，可增强对侧膈神经输出，并恢复半横断同侧膈神经的呼吸相关活动。此外，用PKA抑制剂Rp-8-Br-cAMP预处理可消除8-Br-cAMP的作用。这些结果表明，PKA激活对于高位颈脊髓损伤后cAMP介导的呼吸恢复是必要的，并且细胞内信号级联的激活可能是改善脊髓损伤后呼吸功能的重要策略。