수영-스트레스로 나타나는 뇌 catecholamine대사 및 혈장 corticosterone 함량의 변동에 대한 clonidine(500 ug/kg)의 억제작용을 propylthiouracil(0.01% 용액으로 5주간 마시게함) 및 1-thyrorine(4 mg/kg/day로 5일간 복강내에 주사)로 처치한 웅성-마우스에서 실험관찰하여 다음과 같은 성적을 얻었다. 마우스의 일과성 자발운동량의 변동은 갑상선-홀몬의 변동에 영향을 받지 않았고, 수영스트레스(SS)로 나타나는 혈장 corticosterone(CS)의 증가가 propylthiouracil 전처치 (PTU) 및 1-thyroxine 전처치 (T4)로 각각 다소의 감소 및 증강됨을 보였으나, SS에 의한 혈장 CS증가에 대한 clonidine의 억제작용은 PTU 및 T4의 영향을 받지 않았다. SS부하로 뇌 3-methoxy-4-hydroxyphenylglycol 함량(MHPG)가 유의하게 증가되고 clonidine에 의하여는 MHPG가 현저히 감소되었으나 뇌 norepinephrine 함량(NE)은 별 변동을 보이지 않아서 MHPG/NE비는 SS와 clonidine에 의하여 각각 현저한 증가 및 감소를 나타내었다. 아울러, PTU및 T4은 각각 뇌NE을 유의하게 감소 또는 증가시켰으나 뇌 MHPG에는 별 영향을 미치지 않았다. Clonidine은 SS에 의한 뇌 MHPG 및 MHPG/NE비의 증가를 모두 현저히 억제하였으며 그 억제작용은 PTU 및 T4에 의하여 별 영향을 받지 않았다. 이상의 성적으로 미루어서, 마우스의 일과성 자발운동양상 및 스트레스반응으로 나타나는 혈장 corticosterone의 증가현상등이 갑상선-홀몬의 변동에 별 영향을 받지 않으며, 시상하부-뇌하수체-부신계의 활성화가 시상하부의 norepinephrine성 신경-흥분에 매게되어 나타나는 바, 스트레스성 혈장 corticosterone 증가에 대한 clonidine의 억제작용이 그의 절전-α2-adrenoceptor agonist 작용에 기인되는 것으로 사료된다.
The circadian rhythm of spontaneous motor activity was not significantly altered by T4(4mg/kg, i.p. inj. once a day for 5 days: T4) and PTU (fed ad lib in 0.01% drinking water for 5 weeks: PTU). The plasma thyroxine level was markedly increased by T4 but reduced by PTU, and the plasma thyrotropin level was markedly increased by PTU but moderately increased by T4. Clonidine slightly increased the plasma CS level, but the clonidine effect was significantly enhanced by T4-pretreatment. The brain NE and MHPG contents were little affected by T4 but the NE content was significantly decreased by PTU. The SS-induced increase of plasma CS level was moderately decreased by PTU but increased by T4. However, clonidine significantly inhibited the SS-induced increase, and the inhibitory effect of clonidine was not significantly affected by PTU and T4, respectively. The brain MHPG content and MHPG/NE ratio were significantly decreased by clonidine but increased by SS. The clonidine- and SS-induced changes of brain MHPG content and MHPG/NE ratio were not altered by T4. PTU did not affect the SS-induced increase of brain NE turnover but significantly attenuated the clonidine-induced decrease. The SS-induced increases of brain MHPG content and MHPG/NE rtatio were markedly inhibited by clonidine, and the inhibitory effect of clonidine was not affected by T4 and PTU, respectively. These results suggest that the responses to swim-stress is not signigicantly affected by the alteration of thyroid function and that the hypothalamo-adenohypophysis-adrenocortical stimulation in response to swim-stress seems to be mediated via hypothalamic noradrenergic activation, and the stress response may be inhibited by the agonistic activity of clonidine on the presynaptic α2-adrenoceptor.
