Stepanichev M Iu, Zdobnova I M, Zarubenko I I, Lazareva N A, Guliaeva N V
Zh Vyssh Nerv Deiat Im I P Pavlova. 2004 Sep-Oct;54(5):705-11.
A possible relationship between the amnesia induced by central administration of beta-amyloid (25-35) [Abeta(25-35)] and neurodegeneration in the hippocampus was studied. Male Wistar rats received a single intracerebroventricular injection of Abeta(25-35) at a dose of 15 nmol. One month after the administration, animals were trained in an eight-arm radial maze. After the training, a histopathological investigation of the hippocampus was carried out using brain slices stained with hematoxylin/eosin. Abeta(25-35) induced impairments in reference and working memory in the eight-arm radial maze. A moderate decrease in neuronal cell number was demonstrated in the CA1, but not in the CA3 subfield of the hippocampus. The number of both reference and working errors negatively correlated with the number of neurons in hippocampal CA1. The results are the first evidence for a specific relationship between neurodegeneration in the CA1 subfield of rat hippocampus and impairments of learning and memory induced by Abeta(25-35).
研究了中枢给予β-淀粉样蛋白(25-35)[Aβ(25-35)]诱导的失忆与海马体神经退行性变之间的可能关系。雄性Wistar大鼠接受了一次剂量为15 nmol的脑室内注射Aβ(25-35)。给药一个月后,动物在八臂放射状迷宫中接受训练。训练后,使用苏木精/伊红染色的脑切片对海马体进行组织病理学研究。Aβ(25-35)在八臂放射状迷宫中诱导了参考记忆和工作记忆的损伤。海马体CA1区神经元细胞数量有适度减少,但CA3亚区未出现这种情况。参考错误和工作错误的数量与海马体CA1区的神经元数量呈负相关。这些结果首次证明了大鼠海马体CA1亚区神经退行性变与Aβ(25-35)诱导的学习和记忆损伤之间存在特定关系。