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酒精戒断点燃大鼠海马齿状回门区中生长抑素免疫反应性神经元无丢失。

No loss of somatostatin-immunoreactive neurons in the hippocampal dentate hilus of alcohol-withdrawal-kindled rats.

作者信息

Ulrichsen J, Woldbye D P, Olsen C H, Haugbøl S, Bolwig T G, Hemmingsen R

机构信息

Department of Psychiatry, Rigshospitalet, Copenhagen, Denmark.

出版信息

Alcohol Alcohol. 1996 Jul;31(4):411-9. doi: 10.1093/oxfordjournals.alcalc.a008171.

Abstract

The neuropeptide somatostatin has been suggested to play a role in seizure genesis, electrical kindling and the neurotoxic effects of alcohol. The purpose of the present experiment was to study somatostatin-immunoreactive (SS-IR) neurons in hippocampus during alcohol-withdrawal kindling. Alcohol-withdrawal kindling was performed by subjecting male Wistar rats to seven weekly episodes consisting of 2 days of severe alcohol intoxication and 5 days of alcohol withdrawal. Then the kindled animals (multiple withdrawal group) and a single withdrawal group, which was fed isocalorically with the kindled animals during episodes 1-7, were exposed to 4 days of severe alcohol intoxication (episode 8). During the following withdrawal, the seizure activity was observed 9-15 h after last alcohol dose, in order to subdivide the animals from these two groups into groups with and without seizures. Subsequently, SS-IR neurons were visualized immunocytochemically and counted in the hilus of the dentate gyrus (hippocampus). The number of SS-IR neurons per unit area of the hilus was neither affected by a single nor by multiple episodes of alcohol withdrawal. We therefore concluded that a loss of these neurons is not involved in the development of alcohol-withdrawal-kindled seizures.

摘要

神经肽生长抑素被认为在癫痫发作的发生、电点燃以及酒精的神经毒性作用中发挥作用。本实验的目的是研究酒精戒断点燃过程中海马体中生长抑素免疫反应性(SS-IR)神经元。通过对雄性Wistar大鼠进行为期七周的实验来诱导酒精戒断点燃,每周包括2天的严重酒精中毒和5天的酒精戒断。然后,将点燃的动物(多次戒断组)和单次戒断组(在第1-7阶段与点燃动物摄入等热量食物)暴露于4天的严重酒精中毒(第8阶段)。在接下来的戒断期间,在最后一次给予酒精后9-15小时观察癫痫活动,以便将这两组动物细分为有癫痫发作和无癫痫发作的组。随后,通过免疫细胞化学方法对SS-IR神经元进行可视化并在齿状回(海马体)的门区进行计数。门区单位面积内SS-IR神经元的数量既不受单次酒精戒断的影响,也不受多次酒精戒断的影响。因此,我们得出结论,这些神经元的丧失与酒精戒断点燃性癫痫的发展无关。

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