Tracy H A, Wayner M J, Armstrong D L
Division of Life Sciences, University of Texas at San Antonio 78249-0662, USA.
Alcohol. 1997 Sep-Oct;14(5):511-7. doi: 10.1016/s0741-8329(97)00041-4.
Results of previous research demonstrate that angiotensin II (Ang II) inhibits long-term potentiation (LTP) in medial perforant path-dentate gyrus granule cells and that the inhibition is mediated by the AT1 receptor because it can be blocked by losartan, a specific AT1 receptor antagonist. Ang II impairment of retention and ethanol inhibition of LTP can both be blocked by pretreatment with losartan. Because losartan pretreatment also prevents ethanol intoxication measured in terms of the aerial righting reflex, the purpose of the present study was to assess the effects of 2.0 g/kg ethanol administered by gavage on performance in an eight-arm radial maze, and then to determine the effectiveness of losartan in reducing the impairment of the learning and memory process. Results confirmed the general hypothesis that ethanol-induced cognitive deficits are mediated by Ang II and the AT1 receptor and that the impairment can be reduced by pretreatment with losartan.
先前的研究结果表明，血管紧张素II（Ang II）抑制内侧穿通通路-齿状回颗粒细胞中的长时程增强（LTP），并且这种抑制是由AT1受体介导的，因为它可以被特异性AT1受体拮抗剂氯沙坦阻断。氯沙坦预处理可同时阻断Ang II对记忆的损害和乙醇对LTP的抑制。由于氯沙坦预处理还可预防以空中翻正反射衡量的乙醇中毒，因此本研究的目的是评估经口灌胃给予2.0 g/kg乙醇对八臂放射状迷宫中行为表现的影响，然后确定氯沙坦在减轻学习和记忆过程损害方面的有效性。结果证实了一般假设，即乙醇诱导的认知缺陷由Ang II和AT1受体介导，并且氯沙坦预处理可减轻这种损害。
