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海马交感神经长入和胆碱能去神经支配对海马M2胆碱能受体的影响。

The effect of hippocampal sympathetic ingrowth and cholinergic denervation on hippocampal M2 cholinergic receptors.

作者信息

Kolasa K, Harrell L E, Parsons D S

机构信息

Department of Neurology, Veterans Administration Medical Center, Birmingham, AL 35294, USA.

出版信息

Brain Res. 1995 Jul 3;684(2):201-5. doi: 10.1016/0006-8993(95)00386-5.

DOI:10.1016/0006-8993(95)00386-5
PMID:7583223
Abstract

After cholinergic denervation of the hippocampus, via medial septal (MS) lesions, peripheral sympathetic fibers, originating from the superior cervical ganglia, grow into the hippocampus. In this study, we sought to determine the effect of hippocampal sympathetic ingrowth (HSI) on the M2 subtype of muscarinic cholinergic receptors, by examining the membrane binding of [3H]AF-DX 384 in hippocampal tissue from control rats, rats with HSI and rats with MS lesions + concurrent ganglionectomy (CD group). In dorsal hippocampus, Kd was found to be increased while Bmax was decreased in the CD group as compared with both the HSI and control group which did not differ from one another. In ventral hippocampus, Kd was found to be increased while Bmax was decreased in the CD group when compared only with the control group. These results suggest that sympathetic ingrowth, which has its greatest concentration in dorsal hippocampus, can 'normalize' the M2 receptor in hippocampus.

摘要

通过内侧隔区(MS)损伤对海马进行胆碱能去神经支配后,起源于颈上神经节的外周交感神经纤维长入海马。在本研究中,我们试图通过检测[3H]AF-DX 384在对照大鼠、有海马交感神经长入(HSI)的大鼠以及有MS损伤+同期神经节切除术的大鼠(CD组)海马组织中的膜结合情况,来确定海马交感神经长入(HSI)对毒蕈碱胆碱能受体M2亚型的影响。在背侧海马中,与HSI组和对照组相比,CD组的解离常数(Kd)升高而最大结合容量(Bmax)降低,而HSI组和对照组之间无差异。在腹侧海马中,仅与对照组相比,CD组的Kd升高而Bmax降低。这些结果表明,在背侧海马中浓度最高的交感神经长入可以使海马中的M2受体“正常化”。

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The effect of hippocampal sympathetic ingrowth and cholinergic denervation on hippocampal M2 cholinergic receptors.海马交感神经长入和胆碱能去神经支配对海马M2胆碱能受体的影响。
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引用本文的文献

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Sympathetic sprouting drives hippocampal cholinergic reinnervation that prevents loss of a muscarinic receptor-dependent long-term depression at CA3-CA1 synapses.交感神经发芽驱动海马胆碱能再支配,从而防止CA3-CA1突触处毒蕈碱受体依赖性长时程抑制的丧失。
J Neurosci. 2006 Apr 5;26(14):3745-56. doi: 10.1523/JNEUROSCI.5507-05.2006.