Effect of Thyroxie and Propylthiouracil on the Responses of Plasma Corticosterone and Brain Norepinephrine to Swim-Stress

국문 초록 (Abstract)

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-${\alpha}_2-adrenoceptor\;agonist$ 작용에 기인되는 것으로 사료된다.

다국어 초록 (Multilingual Abstract)

The circadian rhythm of spontaneous motor activity was not significantly altered by $T_4$(4mg/kg, i.p. inj. once a day for 5 days: $T_4$) and PTU (fed ad lib in 0.01% drinking water for 5 weeks: PTU). The plasma thyroxine level was markedly increased by $T_4$ but reduced by PTU, and the plasma thyrotropin level was markedly increased by PTU but moderately increased by $T_4$. Clonidine slightly increased the plasma CS level, but the clonidine effect was significantly enhanced by $T_4-pretreatment$. The brain NE and MHPG contents were little affected by $T_4$ 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 $T_4$. However, clonidine significantly inhibited the SS-induced increase, and the inhibitory effect of clonidine was not significantly affected by PTU and $T_4$, 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 $T_4$. 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 $T_4$ 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 ${\alpha}_2-adrenoceptor$.