Chitravanshi V C, Sapru H N
Section of Neurological Surgery, MSB H-586, New Jersey Medical School, 185 South Orange Avenue, Newark, NJ, 07103-2757, USA.
Brain Res. 1999 Aug 7;837(1-2):298-300. doi: 10.1016/s0006-8993(99)01634-0.
Microinjections (50 nl) of carbachol (2.5-500 microM) into the phrenic motor nucleus (PMN) of anesthetized rats caused a dose-dependent decrease in the phrenic nerve (PN) burst-amplitude. Prior microinjections of pirenzepine and methoctramine (1 mM, each) into the PMN, in separate experiments, significantly attenuated the carbachol-induced inhibition of PN activity. These results suggest that inhibition of PN activity induced by microinjections of carbachol into the PMN is mediated via M(1) and M(2) receptors. Since pirenzepine and methoctramine microinjections into the PMN did not alter the control PN activity, it was concluded that in anesthetized rats cholinergic inputs to the PMN, if any, are not tonically active. It is possible that muscarinic receptors in the PMN come into play only under specific conditions such as activation of a reflex mechanism which alters PN activity. These hypotheses remain to be tested.
向麻醉大鼠的膈神经运动核(PMN)微量注射(50微升)卡巴胆碱(2.5 - 500微摩尔)会导致膈神经(PN)爆发幅度呈剂量依赖性降低。在单独的实验中,事先向PMN微量注射哌仑西平和甲溴东莨菪碱(各1毫摩尔)可显著减弱卡巴胆碱诱导的PN活动抑制。这些结果表明,向PMN微量注射卡巴胆碱所诱导的PN活动抑制是通过M(1)和M(2)受体介导的。由于向PMN微量注射哌仑西平和甲溴东莨菪碱并未改变对照PN活动,因此得出结论,在麻醉大鼠中,向PMN的胆碱能输入(如果有的话)并非持续性活跃。有可能PMN中的毒蕈碱受体仅在特定条件下发挥作用,例如改变PN活动的反射机制激活时。这些假设仍有待检验。