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丁螺环酮对急性脊髓去大脑小鼠H反射的双相作用。

Biphasic Effect of Buspirone on the H-Reflex in Acute Spinal Decerebrated Mice.

作者信息

Develle Yann, Leblond Hugues

机构信息

Department of Anatomy, CogNAC Research Group, Université du Québec à Trois-Rivières, Trois-Rivières, QC, Canada.

出版信息

Front Cell Neurosci. 2020 Jan 15;13:573. doi: 10.3389/fncel.2019.00573. eCollection 2019.

DOI:10.3389/fncel.2019.00573
PMID:32009904
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6974439/
Abstract

Pharmacological treatment facilitating locomotor expression will also have some effects on reflex expression through the modulation of spinal circuitry. Buspirone, a partial serotonin receptor agonist (5-HT ), was recently shown to facilitate and even trigger locomotor movements in mice after complete spinal lesion (Tx). Here, we studied its effect on the H-reflex after acute Tx in adult mice. To avoid possible impacts of anesthetics on H-reflex depression, experiments were performed after decerebration in un-anesthetized mice ( = 20). The H-reflex in plantar muscles of the hind paw was recorded after tibial nerve stimulation 2 h after Tx at the 8th thoracic vertebrae and was compared before and every 10 min after buspirone (8 mg/kg, i.p.) for 60 min ( = 8). Frequency-dependent depression (FDD) of the H-reflex was assessed before and 60 min after buspirone. Before buspirone, a stable H-reflex could be elicited in acute spinal mice and FDD of the H-reflex was observed at 5 and 10 Hz relative to 0.2 Hz, FDD was still present 60 min after buspirone. Early after buspirone, the H-reflex was significantly decreased to 69% of pre-treatment, it then increased significantly 30-60 min after treatment, reaching 170% 60 min after injection. This effect was not observed in a control group (saline, = 5) and was blocked when a 5-HT antagonist (NAD-299) was administered with buspirone ( = 7). Altogether results suggest that the reported pro-locomotor effect of buspirone occurs at a time where there is a 5-HT receptors mediated reflex depression followed by a second phase marked by enhancement of reflex excitability.

摘要

促进运动表达的药物治疗也会通过调节脊髓回路对反射表达产生一些影响。丁螺环酮是一种5-羟色胺受体部分激动剂(5-HT),最近的研究表明,在小鼠完全脊髓损伤(Tx)后,它能够促进甚至触发运动。在此,我们研究了其对成年小鼠急性Tx后H反射的影响。为避免麻醉剂对H反射抑制产生可能的影响,实验在未麻醉的去大脑小鼠(n = 20)中进行。在第8胸椎水平进行Tx 2小时后,刺激胫神经,记录后爪足底肌肉的H反射,并在注射丁螺环酮(8 mg/kg,腹腔注射)前及注射后每10分钟记录一次,共记录60分钟(n = 8)。在丁螺环酮给药前及给药60分钟后评估H反射的频率依赖性抑制(FDD)。在丁螺环酮给药前,急性脊髓损伤小鼠能够引出稳定的H反射,相对于0.2 Hz,在5 Hz和10 Hz时观察到H反射的FDD,丁螺环酮给药60分钟后FDD仍然存在。丁螺环酮给药后早期,H反射显著降低至治疗前的69%,然后在治疗后30 - 60分钟显著增加,注射后60分钟达到170%。在对照组(生理盐水,n = 5)中未观察到这种效应,当5-HT拮抗剂(NAD - 299)与丁螺环酮联合给药时(n = 7),这种效应被阻断。总体结果表明,丁螺环酮促进运动的作用发生在5-HT受体介导反射抑制之后,随后是反射兴奋性增强的第二阶段。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c59c/6974439/31cadb03352d/fncel-13-00573-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c59c/6974439/8793a60bf164/fncel-13-00573-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c59c/6974439/2dfd431a93eb/fncel-13-00573-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c59c/6974439/31cadb03352d/fncel-13-00573-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c59c/6974439/8793a60bf164/fncel-13-00573-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c59c/6974439/2dfd431a93eb/fncel-13-00573-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c59c/6974439/31cadb03352d/fncel-13-00573-g003.jpg

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本文引用的文献

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Neurosci Lett. 2019 Jan 18;690:36-41. doi: 10.1016/j.neulet.2018.10.005. Epub 2018 Oct 4.
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Facilitation of Locomotor Spinal Networks Activity by Buspirone after a Complete Spinal Cord Lesion in Mice.在小鼠完全性脊髓损伤后,丁螺环酮促进运动性脊髓网络活动。
J Neurotrauma. 2018 Sep 15;35(18):2208-2221. doi: 10.1089/neu.2017.5476. Epub 2018 May 7.
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用于脊髓回路研究的去大脑小鼠模型
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