Kometiani P A, Aleksidze N G, Kleĭn E E
Fiziol Zh SSSR Im I M Sechenova. 1976 Jan;62(1):10-21.
The first series of experiments showed that inhibition of the proteins synthesis followed by memory disorders, was reflected in decrease of the synaptosomal proteins fraction which was identified as the cholinoreceptor protein. Another series of experiments: training of rats to use unpreferred paw, showed the system acetylcholine-acetylcholinesterase to be directly connected with memory phenomena, and the synthesis of this enzyme to be induced by genetic apparatus. The third series of experiments showed that feeding of rats with small doses of aminoacids for a long time leads to regular shifts in distribution of both the aminoacids and the monoamines. The aminoacids increasing the brain activity were found to activate the production of cycle-adenyl acid. Those aminoacids which inhibit the brain activity, decrease the production of cyclic-AMP. Tranquilizers which decrease the level of monoamines and inhibit the brain activity, also decrease the production of cyclic-AMP. Antidepressants inhibiting MAO and increasing the level of monoamines in the brain, activate the production of cyclic-AMP. As the monoamines act via cyclic-AMP and the latter participates in suppression of DNA, the mechanism of involvement of the genetic apparatus in regulation of memory phenomena and learning, becomes more apparent.
第一组实验表明,蛋白质合成受到抑制并伴有记忆障碍,这表现为被鉴定为胆碱受体蛋白的突触体蛋白部分减少。另一组实验:训练大鼠使用非偏好爪,结果显示乙酰胆碱 - 乙酰胆碱酯酶系统与记忆现象直接相关,且该酶的合成由遗传机制诱导。第三组实验表明,长期给大鼠喂食小剂量氨基酸会导致氨基酸和单胺的分布规律发生变化。发现能增强大脑活动的氨基酸会激活环磷酸腺苷的产生。而那些抑制大脑活动的氨基酸会降低环磷酸腺苷的产生。降低单胺水平并抑制大脑活动的镇静剂也会降低环磷酸腺苷的产生。抑制单胺氧化酶并提高大脑中单胺水平的抗抑郁药会激活环磷酸腺苷的产生。由于单胺通过环磷酸腺苷起作用,且后者参与对DNA的抑制,遗传机制参与记忆现象和学习调节的机制变得更加明显。