Protective effect of galanin on behavioral deficits in experimental traumatic brain injury.
Protective effect of galanin on behavioral deficits in experimental traumatic brain injury.
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甘丙肽对实验性脑外伤行为缺陷的保护作用。
DOI：
10.1089/neu.1994.11.73
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发表时间：
1994
影响因子：
4.2
通讯作者：
Hamm,RJ
中科院分区：
文献类型：
--
作者：
Liu,S;Lyeth,BG;Hamm,RJ
创伤性脑损伤（TBI）中行为缺陷的严重程度已被证明部分与兴奋性和抑制性神经递质释放之间平衡的改变有关。先前的研究表明，实验性 TBI 后细胞外兴奋性神经递质浓度急剧增加。我们研究了神经调节肽甘丙肽 (GAL) 对行为发病率的影响，通过与大鼠实验性 TBI 相关的感觉运动和记忆表现任务来测量。在大鼠中枢液体冲击 TBI 前 5 分钟，单次脑室内注射 GAL（1.0 μg，n= 8 或 10.0 μg，n= 10）或脑脊液（CSF）载体（n= 10）。在受伤前和 TBI 后 5 天内，通过平衡木、平衡木行走和旋转棒任务评估感觉运动任务的表现。 TBI 后第 11-15 天使用莫里斯水迷宫评估记忆表现。 TBI 在脑脊液治疗组中产生了显着的运动和记忆缺陷。与 CSF 治疗的大鼠相比，GAL 治疗的大鼠在平衡木、平衡木行走和旋转棒表现方面的缺陷程度明显较小。 1.0 μg GAL 剂量比 10.0 μg GAL 剂量产生的保护略强。 GAL 剂量均不会影响体重减轻或莫里斯水迷宫的表现。这些结果表明，GAL 的生理作用可能通过调节神经元兴奋性来降低 TBI 发病率的某些组成部分。
The magnitude of behavioral deficits in traumatic brain injury (TBI) has been shown to be partly related to alterations in the balance between excitatory and inhibitory neurotransmitter release. Previous studies have demonstrated that extracellular excitatory neurotransmitter concentrations dramatically increase following experimental TBI. We examined the effects of a neuromodulatory peptide, galanin (GAL), on behavioral morbidity, as measured by sensory motor and memory performance tasks, associated with experimental TBI in the rat. A single intraventricular injection of GAL (1.0 μg,n= 8 or 10.0 μg,n= 10) or cerebrospinal fluid (CSF) vehicle (n= 10) was administered 5 minutes prior to central fluid percussion TBI in rats. Performance on sensory motor tasks was assessed prior to injury and for 5 days after TBI with beam-balance, beam-walking, and rotarod tasks. Memory performance was assessed on days 11–15 after TBI with the Morris water maze. TBI produced significant motor and memory deficits in the CSF-treated group. GAL-treated rats had significantly less magnitude of deficits compared to CSF-treated rats on beam-balance, beam-walking, and rotarod performance. The 1.0 μg GAL dose produced slightly greater protection than the 10.0 μg GAL dose. Neither GAL dose affected body weight loss or Morris water maze performance. These results suggest that the physiologic effects of GAL may reduce certain components of TBI morbidity, possibly by modulating neuronal excitability.