Izumiyama K, Kogure K
Department of Neurology, Tohoku University School of Medicine, Sendai, Japan.
Acta Neurol Scand. 1988 Sep;78(3):214-20. doi: 10.1111/j.1600-0404.1988.tb03649.x.
The CA 1 neurons in the gerbil hippocampus exhibiting necrosis with delayed onset following 5 min ischemia were reduced markedly by the systemic administration of dihydroergotoxine mesylate (Hydergine; HYG). Immediately after 5 min of forebrain ischemia, the animals were injected intraperitoneally with HYG. Seven days after ischemia, perfusion-fixed brains were processed by conventional histology. The number of neurons per millimeter in the CA 1 pyramidal cell layer were calculated and they were labelled neuronal density. In the control group, the neuronal density was 66.03 +/- 7.37 (mean +/- SEM), in the vehicle group, it was 11.25 +/- 4.93. The neuronal density in the HYG group was 69.19 +/- 6.49. The difference in the neuronal density between the HYG group and the control group was not statistically significant. These data indicate that HYG protects on the CA 1 neurons, and this suggest that the suppression of adrenoceptors by this drugs may be the main mechanism of action. This morphologic outcome may explain the functional amelioration of mental impairment by HYG.
沙土鼠海马体中的CA1神经元在5分钟缺血后出现延迟性坏死，而系统性给予甲磺酸双氢麦角毒碱（喜得镇；HYG）可使其显著减少。在前脑缺血5分钟后，立即给动物腹腔注射HYG。缺血7天后，对灌注固定的大脑进行常规组织学处理。计算CA1锥体细胞层每毫米的神经元数量，并将其标记为神经元密度。对照组的神经元密度为66.03±7.37（平均值±标准误），溶剂对照组为11.25±4.93。HYG组的神经元密度为69.19±6.49。HYG组与对照组之间的神经元密度差异无统计学意义。这些数据表明HYG对CA1神经元具有保护作用，这表明该药物对肾上腺素能受体的抑制作用可能是主要作用机制。这一形态学结果可能解释了HYG对精神障碍的功能改善作用。
