Clarke K A, Djouhri L
Department of Biomedical Science, University of Sheffield, UK.
Neuropeptides. 1991 Sep;20(1):9-15. doi: 10.1016/0143-4179(91)90034-g.
Previous behavioural and electrophysiological studies have indicated an antinarcotic action of thyrotropin-releasing hormone (TRH) and its analogues in antagonizing the action of CNS depressant drugs, including baclofen and a variety of anesthetics. While beta-adrenergic receptors are implicated in the level of anaesthesia/arousal, whether the analeptic action of TRH involves adrenergic systems for its expression is uncertain. The object of the present experiments, therefore, was to examine interactions between adrenergic systems and the anti-anaesthetic effects of TRH analogue CG3703. It was found that pretreatment with the beta-block (+/-)propranolol did not abolish or reduce the ability of CG3703 to antagonize urethane-induced depression of VBT transmission. These results suggest therefore, that beta-adrenergic systems are unlikely to be involved in the anti-anaesthetic effect of the tripeptide.
以往的行为学和电生理学研究表明,促甲状腺激素释放激素(TRH)及其类似物在拮抗中枢神经系统抑制药物(包括巴氯芬和多种麻醉剂)的作用方面具有抗麻醉作用。虽然β-肾上腺素能受体与麻醉/觉醒水平有关,但TRH的苏醒作用是否通过肾上腺素能系统来表达尚不确定。因此,本实验的目的是研究肾上腺素能系统与TRH类似物CG3703的抗麻醉作用之间的相互作用。结果发现,用β-阻滞剂(±)普萘洛尔预处理并不能消除或降低CG3703拮抗氨基甲酸乙酯诱导的VBT传递抑制的能力。因此,这些结果表明,β-肾上腺素能系统不太可能参与该三肽的抗麻醉作用。