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本文引用的文献

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The neural cell adhesion molecule promotes FGFR-dependent phosphorylation and membrane targeting of the exocyst complex to induce exocytosis in growth cones.神经细胞黏附分子促进 FGFR 依赖性磷酸化和外泌体复合物的膜靶向，以诱导生长锥中的胞吐作用。
J Neurosci. 2011 Mar 9;31(10):3522-35. doi: 10.1523/JNEUROSCI.3109-10.2011.
2
Opioids for cancer pain: the challenge of optimizing treatment.癌症疼痛的阿片类药物治疗：优化治疗的挑战。
Metabolism. 2010 Oct;59 Suppl 1:S47-52. doi: 10.1016/j.metabol.2010.07.010.
3
The role of mitogen-activated protein kinase (MAPK) in morphine tolerance and dependence.丝裂原活化蛋白激酶（MAPK）在吗啡耐受性和依赖性中的作用。
Mol Neurobiol. 2009 Oct;40(2):101-7. doi: 10.1007/s12035-009-8074-z. Epub 2009 May 26.
4
Deficiency of neural cell adhesion molecule or its polysialylation modulates pharmacological effects of the AMPA receptor antagonist NBQX.神经细胞黏附分子或其多唾液酸化的缺乏会调节α-氨基-3-羟基-5-甲基-4-异恶唑丙酸（AMPA）受体拮抗剂NBQX的药理作用。
Neuroscience. 2008 Apr 9;152(4):1093-8. doi: 10.1016/j.neuroscience.2007.09.027. Epub 2007 Sep 20.
5
Selective targeting of different neural cell adhesion molecule isoforms during motoneuron myotube synapse formation in culture and the switch from an immature to mature form of synaptic vesicle cycling.在培养过程中运动神经元与肌管突触形成期间对不同神经细胞黏附分子同种型的选择性靶向作用以及从突触小泡循环的不成熟形式向成熟形式的转变。
J Neurosci. 2007 Dec 26;27(52):14481-93. doi: 10.1523/JNEUROSCI.3847-07.2007.
6
Polysialic acid in the plasticity of the developing and adult vertebrate nervous system.多唾液酸在发育中和成年脊椎动物神经系统可塑性中的作用
Nat Rev Neurosci. 2008 Jan;9(1):26-35. doi: 10.1038/nrn2285.
7
When it comes to opiates, just say NO.说到鸦片类药物，一定要说“不”。
J Clin Invest. 2007 Nov;117(11):3185-7. doi: 10.1172/JCI34035.
8
Regulation of neuronal PLCgamma by chronic morphine.慢性吗啡对神经元磷脂酶Cγ的调节
Brain Res. 2007 Jul 2;1156:9-20. doi: 10.1016/j.brainres.2007.04.059. Epub 2007 May 4.
9
Drug-related side effects of long-term intrathecal morphine therapy.长期鞘内注射吗啡治疗的药物相关副作用。
Pain Physician. 2007 Mar;10(2):357-66.
10
NCAM promotes assembly and activity-dependent remodeling of the postsynaptic signaling complex.神经细胞黏附分子（NCAM）促进突触后信号复合体的组装及活性依赖性重塑。
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去除多涎酸化神经细胞黏附分子可增强吗啡镇痛作用并干扰小鼠的耐受。

Removal of polysialylated neural cell adhesion molecule increases morphine analgesia and interferes with tolerance in mice.

机构信息

Department of Cell Biology, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA.

出版信息

Brain Res. 2011 Aug 2;1404:55-62. doi: 10.1016/j.brainres.2011.06.021. Epub 2011 Jun 14.

DOI:10.1016/j.brainres.2011.06.021
PMID:21704981
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4041115/
Abstract

Neurons that express high levels of polysialylated neural cell adhesion molecule (PSA-NCAM) in adult spinal substantia gelatinosa also express the μ-opioid receptor. While PSA removal from NCAM by spinal intrathecal injection of endoneuraminidase-N (endo-N) did not detectably change opioid receptor expression, morphine-induced analgesia was significantly increased. This analgesic strengthening was detected as early as 15 min after endo-N treatment and persisted for at least 7 days. In addition, the tolerance that develops with chronic morphine treatment was overcome in the absence of PSA. Interestingly, the same effects on analgesia and tolerance were also produced by selective deletion of the NCAM-180 isoform.

摘要

成年脊髓胶状质中表达高水平多聚唾液酸神经细胞黏附分子（PSA-NCAM）的神经元也表达μ-阿片受体。虽然通过鞘内注射神经氨酸酶-N（endo-N）从 NCAM 上去除 PSA 并没有明显改变阿片受体的表达，但吗啡诱导的镇痛作用显著增强。这种镇痛增强早在 endo-N 处理后 15 分钟就被检测到，并持续至少 7 天。此外，在没有 PSA 的情况下，慢性吗啡治疗产生的耐受也被克服了。有趣的是，选择性删除 NCAM-180 同工型也产生了相同的镇痛和耐受效果。