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乙醚应激和倍他米松治疗对大鼠脑不同区域去甲肾上腺素和多巴胺浓度的影响。

The effects of ether stress and betamethasone treatment on the concentrations of noradrenaline and dopamine in various regions of the rat brain.

作者信息

Vellucci S V

出版信息

Br J Pharmacol. 1977 Aug;60(4):601-5. doi: 10.1111/j.1476-5381.1977.tb07541.x.

Abstract
  1. The effects of ether stress on noradrenaline (NA) and dopamine levels in different regions of the rat brain were studied. 2. Exposure to ether vapour (90 s) caused a significant decrease in the concentration of hypothalamic NA but had no effect on catecholamine (CA) concentrations in the other regions studied. 3. Treatment with betamethasone alone (20 microgram/ml) given in the drinking water for 24 h, had no effect on CA levels in the cerebral cortex, midbrain or hypothalamus. However, pretreatment with this dose of steroid prevented the decreases in hypothalamic NA which were normally seen after ether stress and also induced significant increases in the concentration of midbrain NA. 4. The data provide further support for the involvement of NA in the regulation stress-induced corticotrophin (ACTH) release and indicate that centres other than the hypothalamus may be involved in mediating the inhibitory action of betamethasone on the response to ether stress.
摘要
  1. 研究了乙醚应激对大鼠脑不同区域去甲肾上腺素(NA)和多巴胺水平的影响。2. 暴露于乙醚蒸汽(90秒)导致下丘脑NA浓度显著降低,但对所研究的其他区域的儿茶酚胺(CA)浓度没有影响。3. 单独用倍他米松(20微克/毫升)处理,在饮用水中给予24小时,对大脑皮层、中脑或下丘脑的CA水平没有影响。然而,用该剂量的类固醇预处理可防止通常在乙醚应激后出现的下丘脑NA降低,并且还导致中脑NA浓度显著增加。4. 这些数据为NA参与调节应激诱导的促肾上腺皮质激素(ACTH)释放提供了进一步的支持,并表明除下丘脑外的其他中枢可能参与介导倍他米松对乙醚应激反应的抑制作用。

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本文引用的文献

1
PATHWAYS BY WHICH TRAUMATIC STRESS AND ETHER INDUCE INCREASED ACTH RELEASED IN THE RAT.
Endocrinology. 1964 Jun;74:981-5. doi: 10.1210/endo-74-6-981.
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BRAIN AMINES: RESPONSE TO PHYSIOLOGICAL STRESS.脑胺:对生理应激的反应
Biochem Pharmacol. 1963 Oct;12:1232-5. doi: 10.1016/0006-2952(63)90101-1.
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Neural control of ACTH secretion: effect of acute decerebration in the rat.
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Daily rhythm in the noradrenaline content of rat hypothalamus.
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The effect of injury on monoamine concentrations in the rat hypothalamus.
J Neurochem. 1971 Oct;18(10):1837-46. doi: 10.1111/j.1471-4159.1971.tb09589.x.

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