Mellen Nicholas M, Roham Maryam, Feldman Jack L
Systems Neurobiology Laboratory, Department of Neurobiology, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, CA 90095-1763, USA.
J Physiol. 2004 May 1;556(Pt 3):859-74. doi: 10.1113/jphysiol.2004.060673. Epub 2004 Feb 6.
In mammals, expiration is lengthened by mid-expiratory lung inflation (Breuer-Hering Expiratory reflex; BHE). The central pathway mediating the BHE is paucisynaptic, converging on neurones in the rostral ventrolateral medulla. An in vitro neonatal rat brainstem-lung preparation in which mid-expiratory inflation lengthens expiration was used to study afferent modulation of respiratory neurone activity. Recordings were made from respiratory neurones in or near the pre-Bötzinger Complex (preBötC). Respiratory neurone membrane properties and BHE-induced changes in activity were characterized. Our findings suggest the following mechanisms for the BHE: (i) lung afferent signals strongly excite biphasic neurones that convey these signals to respiratory neurones in ventrolateral medulla; (ii) expiratory lengthening is mediated by inhibition of rhythmogenic and (pre)motoneuronal networks; and (iii) pre-inspiratory (Pre-I) neurones, some of which project to abdominal expiratory motoneurones, are excited during the BHE. These findings are qualitatively similar to studies of the BHE in vivo. Where there are differences, they can largely be accounted for by developmental changes and experimental conditions.
在哺乳动物中,呼气可通过呼气中期肺扩张(布雷尔 - 黑林呼气反射;BHE)而延长。介导BHE的中枢通路是少突触的,汇聚于延髓头端腹外侧的神经元。一种体外新生大鼠脑干 - 肺标本被用于研究呼吸神经元活动的传入调制,在该标本中呼气中期扩张会延长呼气时间。记录来自前包钦格复合体(preBötC)内或其附近的呼吸神经元的活动。对呼吸神经元的膜特性以及BHE诱导的活动变化进行了表征。我们的研究结果提示了BHE的以下机制:(i)肺传入信号强烈兴奋双相神经元,这些双相神经元将这些信号传递至延髓腹外侧的呼吸神经元;(ii)呼气延长是由对节律性和(前)运动神经元网络的抑制介导的;(iii)吸气前(Pre - I)神经元在BHE期间被兴奋,其中一些投射至腹部呼气运动神经元。这些结果在定性上与体内BHE的研究相似。存在差异的地方,很大程度上可由发育变化和实验条件来解释。