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GM1神经节苷脂治疗有助于单侧前庭损伤后的行为恢复。

Behavioural recovery from unilateral vestibular lesion is facilitated by GM1 ganglioside treatment.

作者信息

Petrosini L

出版信息

Behav Brain Res. 1987 Feb;23(2):117-26. doi: 10.1016/0166-4328(87)90049-0.

DOI:10.1016/0166-4328(87)90049-0
PMID:3566906
Abstract

Exogenously administered gangliosides function in vivo to facilitate survival and repair of damaged neurones in both central and peripheral nervous systems. These effects have been attributed to their neuritogenic and neuronotrophic properties. In this investigation the effects of ganglioside treatment have been studied on the compensation that follows a unilateral labyrinthectomy, considering that the vestibular recovery is supposed to be achieved through a mechanism of sprouting acting on the deafferented neurones. Hemilabyrinthectomized guinea pigs were given a daily injection of either GM1 ganglioside (30 mg/kg, i.p.) or saline for 21 days. As regards postural symptoms, the GM1 group more quickly restored a posture of the head non-deviated in the horizontal plane, while the remaining postural symptomatology was not significantly affected by the treatment. Furthermore, the GM1-treated group attained more rapidly an ocular position characterized by very slow drifts (or by no drift at all), directed towards the side of the intact labyrinth. Ganglioside treatment did not reduce the severity of the initial hemilabyrinthectomy impairments and the effect of the treatment became evident with time. This result is consistent with the hypothesis that also in this model of neuronal plasticity, gangliosides act by enhancing reactive synaptogenesis on the deafferented vestibular neurones.

摘要

外源性给予的神经节苷脂在体内发挥作用,促进中枢和外周神经系统中受损神经元的存活和修复。这些作用归因于它们的促神经突生长和神经营养特性。在本研究中,考虑到前庭恢复被认为是通过对去传入神经的神经元起作用的发芽机制来实现的,研究了神经节苷脂治疗对单侧迷路切除术后代偿的影响。对半侧迷路切除的豚鼠每天注射GM1神经节苷脂(30mg/kg,腹腔注射)或生理盐水,持续21天。关于姿势症状,GM1组更快地恢复了头部在水平面无偏斜的姿势,而其余姿势症状未受到治疗的显著影响。此外,GM1治疗组更快地达到了一种眼位,其特征是向完整迷路侧非常缓慢地漂移(或根本不漂移)。神经节苷脂治疗并未减轻最初半侧迷路切除术损伤的严重程度,且治疗效果随时间逐渐显现。这一结果与以下假设一致,即在这种神经元可塑性模型中,神经节苷脂通过增强去传入前庭神经元上的反应性突触形成而起作用。

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