Johnson R A, Johnson S M, Mitchell G S
Department of Comparative Biosciences, School of Veterinary Medicine, University of Wisconsin, Madison, Wisconsin 53706, USA.
J Appl Physiol (1985). 1998 Jul;85(1):105-14. doi: 10.1152/jappl.1998.85.1.105.
An in vitro brain stem preparation from adult turtles was used to determine effects of dopamine (DA) and norepinephrine (NE) on the pattern of respiratory motor output recorded from hypoglossal nerve roots (XII). Bath-applied DA (10-200 microM) increased the frequency of respiratory bursts (peaks) from 0.9 +/- 0.2 to 2.4 +/- 0.3 (SE) peaks/min, resulting in a 99 +/- 9% increase in neural minute activity. R[+]-SCH-23390 (10 microM, D1 antagonist) and eticlopride (20 microM, D2 antagonist) attenuated the DA-mediated increase in peak frequency by 52 and 59%, respectively. On the other hand, the DA-receptor agonists apomorphine (D1, D2), quinelorane (D2), and SKF-38393 (D1) had no effect on peak frequency. Prazosin, an alpha1-adrenergic antagonist (250 nM) abolished the DA-mediated frequency increase. Although NE (10-200 microM) and phenylephrine (10-200 microM, alpha1-adrenergic agonist) increased peak frequency from 0.5 +/- 0.1 to 1.2 +/- 0.3 peaks/min and from 0.6 +/- 0.1 to 1. 0 +/- 0.2 peaks/min, respectively, these effects were not as large as that with DA alone. The data suggest that both dopaminergic and adrenergic receptor activation in the brain stem increase respiratory frequency in turtles, but the DA receptor-mediated increase is dependent on coactivation of alpha1-adrenergic receptors.
使用成年海龟的体外脑干制剂来确定多巴胺(DA)和去甲肾上腺素(NE)对舌下神经根(XII)记录的呼吸运动输出模式的影响。浴加DA(10 - 200微摩尔)使呼吸爆发(峰值)频率从0.9±0.2增加到2.4±0.3(标准误)次/分钟,导致神经每分钟活动增加99±9%。R[+]-SCH-23390(10微摩尔,D1拮抗剂)和依替必利(20微摩尔,D2拮抗剂)分别使DA介导的峰值频率增加减弱52%和59%。另一方面,DA受体激动剂阿扑吗啡(D1、D2)、喹那洛尔(D2)和SKF-38393(D1)对峰值频率无影响。哌唑嗪,一种α1肾上腺素能拮抗剂(250纳摩尔)消除了DA介导的频率增加。虽然NE(10 - 200微摩尔)和去氧肾上腺素(10 - 200微摩尔,α1肾上腺素能激动剂)分别使峰值频率从0.5±0.1增加到1.2±0.3次/分钟和从0.6±0.1增加到1.0±0.2次/分钟,但这些作用不如单独使用DA时大。数据表明,脑干中多巴胺能和肾上腺素能受体的激活均增加海龟的呼吸频率,但DA受体介导的增加依赖于α1肾上腺素能受体的共同激活。