St-John Walter M, Paton Julian F R
Department of Physiology, Dartmouth Medical School, Dartmouth-Hitchcock Medical Center, Borwell Bldg., Lebanon, NH 03756, USA.
Respir Physiol Neurobiol. 2004 Nov 15;143(2-3):321-32. doi: 10.1016/j.resp.2004.05.010.
We have proposed a "switching concept" for the neurogenesis of ventilatory activity. Eupnea reflects the output of a pontomedullary neuronal circuit, whereas gasping is generated by medullary pacemaker mechanisms. Pontile mechanisms, then, are hypothesized to play a fundamental role in the neurogenesis of eupnea. If pontile mechanisms do play such a critical role, several criteria must be fulfilled. First, perturbations of pontile regions must alter eupnea under all experimental conditions. Second, neuronal activities that are consistent with generating the eupneic rhythm must be recorded in pons. Finally, medullary mechanisms alone cannot fully explain the neurogenesis of eupnea. Evidence from previous studies that support the validity of these criteria is presented herein. We conclude that pontile mechanisms play a critical role in the neurogenesis of eupnea.
我们提出了一种关于通气活动神经发生的“转换概念”。平静呼吸反映了脑桥延髓神经回路的输出,而喘息则由延髓起搏器机制产生。据此推测,脑桥机制在平静呼吸的神经发生中起基本作用。如果脑桥机制确实发挥如此关键的作用,那么必须满足几个标准。首先,在所有实验条件下,脑桥区域的扰动都必须改变平静呼吸。其次,必须在脑桥中记录到与产生平静呼吸节律一致的神经元活动。最后,仅延髓机制无法完全解释平静呼吸的神经发生。本文展示了先前研究中支持这些标准有效性的证据。我们得出结论,脑桥机制在平静呼吸的神经发生中起关键作用。