Changes of Unit Discharge of the Medullary Respiratory Neurons during Apnea

Changes of the neuronal discharge of 128 medullary respiratory unitswere recorded and studied during the period of expiratory apnea induced reflexlyby intracarotid sinus injection of sodium citrate in rabbits.Generally,theneuronal discharge of inspiratory units began,stopped and recovered at the sametime with those of the phrenic nerve.But,about 5% the phase-spanninginspiratory units near the obex showed a different time course with the dischargeof the phrenic nerve.They fired continuously in a low frequency while thephrenic nerve was quiet.When increasing progressively and approaching to acertain level,the firing rate increased abruptly and at the same time phrenic nervebegan to fire.So it seemed that they acted as the pacemaker of inspiration.Comparison of the cycle-triggered histograms(CTH)of these inspiratory unitswith those of phrenic nerve showed clearly the above mentioned phasicrelationship.They started firing before the phrenic nerve,but they reached theirmaximal rate and then declined and stopped quite in accordance with the phrenicnerve.It is,therefore,reasonable to assume that the central mechanism of theswitch from expiratory apnea to inspiration may originate from this kind ofneurons.Most of the expiratory units show tonic discharges during the period of apneawith a higher discharge rate than normal and then the rate decreases just beforerecovery of phrenic firing.In addition,small portion of the expiratory units weredepressed as the phrenic discharge ceased.The function of these two differentkinds of neurons in the mechanism of development of respiratory rhythm is,apparently,different.     

损毁面神经后核内侧区神经元胞体对呼吸节律的影响

1％ procaine阻滞和电损毁面神经后核内侧区(mNRF)可消除动物节律性呼吸。红藻氨酸(Kainicacid)化学损毁mNRF,也引起动物不可逆性呼吸停止。结果提示,阻滞和电损毁面神经后核内侧区引起的呼吸停止是由于破坏了该区的神经元胞体所致。这些被破坏的神经元和呼吸节律的起源有关。     

延髓呼吸性神经元在呼吸暂停期间的放电变化

在向家兔颈动脉窦区注入枸橼酸钠反射性引起呼气性的呼吸暂停中,记录了128个延髓呼吸单位放电变化。一般吸气单位与膈神经放电同时停止,又同时恢复。但在延髓闩部附近的中间部及腹侧,发现约有5％的呼—吸跨时相神经元在膈神经放电停止期间呈连续的低频发放。其放电频率逐渐增高至一定水平后,转为急剧升高,同时膈神经恢复放电。由周期触发直方图显示的时相关系,可见它们放电频率骤增点早于膈神经放电的起始点,并和膈神经放电同时达到高峰频率,又同时衰减和停止放电。推测该类神经元可能与“中枢吸气性活动”(central inspiratory activity)有关。多数的呼气单位在呼吸暂停期间呈现紧张性发放,而且放电频率可高于正常的高峰频率;在膈神经放电恢复之前其放电频率又减低。而小部分的呼气单位,在膈神经放电停止时,其放电活动也受到抑制。根据呼气单位这两种不同的放电变化,推测它们在呼吸节律发生机制中可能起不同的作用.