Morphine의 血漿 Corticosterone增加作用에 對한 Clonidine의 抑制性 效果에 있어서 Monoamine性 神經系의 關聯性에 關한 硏究 = Monoaminergic Influences on the Inhibitory Effect of Clonidine on the Morphine-induced Increase of Plasma Corticosterone Level

다국어 초록 (Multilingual Abstract)

Buckingham suggested that the effects of opioid substances on CRF secretion are probably-due partially to direct actions on the hypothalamus and partially to alterations in the ratio of stimulatory and inhibitory signals received from higher centers i3 the brain. And there are several reports supporting that the inhibitory effect of clonidine on the morphine-induced increase of plasma corticosterone level may be mediate3 by its property as an alpha₂-adrenoceptor agonist.
In this paper, tire influences of alteration of moncaminergic neuoronal activities on the inhibitory effect of clonidine on the morphine-induced increase of plasma corticosterone level were studied in male mice.
The results obtained were summarized as follows;
1. Clonidine(100 and 500 ㎍/kg) slightly increased plasma corticosterone level in normal mice, and the increasing effect of clonidine was not affected by iproniazid(100 mg/kg) and p-chlorophenylalanine (400 mg/kg) but significantly enhanced by reserpine(2 mg/kg) and alpha-methyl-p-tyrosine(250 mg/kg).
2. Clonidine(100 and 50 0㎍/kg) showed the dose-depeiident inhibitory effect on the morphine-induced increase of plasma corticosterone level.
3. The inhibitory effect of clonidine(100 ㎍/kg) on the morphine-induced increase of plasma corticosterone level was not affected by iproniazid but moderately suppressed by reserpine, alpha-methyl-p-tyrosine, and p-chlorophenylalanine.
4. The inhibitory effect of clonidine(500 ㎍/kg) on the morphine-induced increase of plasma corticosterone level was cot affected by reserpine, iproniazid, alpha-methyl-p-tyrosine, and p-chlorophenylalanine.
These results suggest that the inhibitory effect of clonidine on the morphine-induced increase of plasma corticosterone level are probably due partially to its direct action on the hypothalamo-adenohypophyseal system rather than due to its indirect (presynaptic) action on the morphine-induced changes of central moncaminergic neuronal activities.