M1 muscarinic receptor plays a fundamental role in memory and is closely associated with Alzheimer's disease (AD); it has long been assumed as a therapeutic goal. By activating of the cholinergic receptor vitamin E helps with memory retention. But effects of vitamin E on density of M1 muscarinic receptor-immunoreactive (ir) neurons remain poorly understood. The present research aimed to examine the chronic administration effect of vitamin E against scopolamine-induced memory loss and the number of M1 muscarinic receptor-ir neurons of the hippocampus in male rats. Randomly, 42 adult male Wistar rats were divided to six groups: control, Sham-saline: receiving scopolamine + saline, Sham-sesame oil: receiving scopolamine + sesame oil and three experimental groups: receiving scopolamine + vitamin E with different doses (25, 50, and 100 mg/kg/day, i.p.) for 14 days. The passive avoidance task was used for the memory test. Twenty-four hours after behavioral tests, rats' brains were taken and fixed, and after tissue processing, sections were stained using the immunohistochemical technique for M1 muscarinic receptor-ir neurons and cresyl violet for neurons. The injection of scopolamine to rats caused memory impairment and vitamin E treatment could ameliorate it. In the scopolamine-treated groups, the number of CA1 and CA3 pyramidal and dentate gyrus (DG) granular neurons was decreased significantly as compared to the control group. Vitamin E treatment significantly increased neuron numbers in the CA1 and CA3 areas of the hippocampus and DG area. Treatment with vitamin E for 14 days could compensate the loss of M1 muscarinic receptor-immunoreactive neuron numbers induced by scopolamine in the hippocampus. The most effective vitamin E dose was 50 mg/kg/day in this study. In conclusion, vitamin E can compensate the neuronal loss in the hippocampal formation and also it can raise the density of M1 receptor-ir muscarinic neurons after an injection of scopolamine.

中文翻译：

---

维生素E可以补偿东pol碱治疗的大鼠海马中M1受体的密度。

M1毒蕈碱受体在记忆中起基本作用，并与阿尔茨海默氏病（AD）密切相关；长期以来一直将其视为治疗目标。通过激活胆碱能受体，维生素E有助于记忆力的保持。但是，维生素E对M1毒蕈碱受体免疫反应性（ir）神经元密度的影响仍然知之甚少。本研究旨在检查维生素E对东pol碱所致记忆丧失的长期给药作用以及雄性大鼠海马M1毒蕈碱受体-ir神经元的数量。将42只成年雄性Wistar大鼠随机分为六组：对照组，深盐水：接受东pol碱+生理盐水；深芝麻油：接受东pol碱+芝麻油；三组实验组：接受不同剂量的东sco碱+维生素E（25， 50和100 mg / kg /天，即 第14页）。被动回避任务用于内存测试。行为测试后二十四小时，将大鼠的大脑固定并固定，在组织处理后，使用免疫组织化学技术对M1毒蕈碱受体-ir神经元进行染色，对神经元使用甲酚紫。向大鼠注射东pol碱可导致记忆力减退，维生素E治疗可改善这种记忆力。在东pol碱治疗组中，与对照组相比，CA1和CA3锥体和齿状回（DG）颗粒神经元的数量明显减少。维生素E处理可显着增加海马CA1和CA3区以及DG区的神经元数量。维生素E治疗14天可以补偿东碱在海马中引起的M1毒蕈碱受体免疫反应性神经元数量的损失。在这项研究中，最有效的维生素E剂量为50 mg / kg /天。总之，维生素E可以补偿东compensate碱注射后海马结构中神经元的损失，并且还可以提高M1受体-毒蕈碱性神经元的密度。