Cohen Morton I, Shaw Chen-Fu
Department of Physiology and Biophysics, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Respir Physiol Neurobiol. 2004 Nov 15;143(2-3):127-40. doi: 10.1016/j.resp.2004.07.017.
Neurons of the pontine respiratory group (PRG) in the region of the nucleus parabrachialis medialis and the Kolliker-Fuse nucleus are believed to play an important role in promoting the inspiratory (I) off-switch (IOS). In decerebrate gallamine-paralyzed cats ventilated with a cycle-triggered pump system (lung inflation during the neural I phase), we studied the effects of vagal (V) afferent inputs on firing of I-modulated neurons (the most numerous population in PRG) and on I duration. The predominant V effect on unit activity was inhibitory, as shown by two types of test: (a) withholding of inflation during an I phase, which produced increase of unit firing and of its respiratory modulation (58/66 neurons in 14 cats), indicating disinhibition due to removal of phasic V input; (b) delivery of afferent V stimulus trains during a no-inflation I phase, which produced decrease of unit firing and of its respiratory modulation (20 neurons). In addition, application of V input during the neural expiratory (E) phase, which lengthened E phase duration, produced no effect on the neurons' firing, suggesting that the inhibition during I was presynaptic in origin. The results may be interpreted by the hypothesis that the medullary late-I presumptive IOS neurons receive excitatory inputs from the PRG I-modulated neurons as well as from V afferents.. With relatively strong V input, this pontine excitatory output is reduced by inhibition, whereas with relatively weak V input that excitatory output is increased due to reduction of inhibition. Thus the pontine and the V influences on the IOS can operate in a complementary manner dependent on state.
脑桥臂内侧核和柯利克-福斯核区域的脑桥呼吸组(PRG)神经元被认为在促进吸气(I)切断(IOS)中起重要作用。在用循环触发泵系统通气的去大脑加拉明麻痹猫(在神经I期肺充气)中,我们研究了迷走神经(V)传入输入对I调制神经元(PRG中数量最多的群体)放电和I持续时间的影响。对单位活动的主要V效应是抑制性的,如两种测试所示:(a)在I期停止充气,这导致单位放电及其呼吸调制增加(14只猫中的58/66个神经元),表明由于去除相位V输入而产生去抑制;(b)在无充气I期传递传入V刺激序列,这导致单位放电及其呼吸调制减少(20个神经元)。此外,在神经呼气(E)期应用V输入,这延长了E期持续时间,但对神经元放电没有影响,表明I期的抑制起源于突触前。这些结果可以用以下假设来解释:延髓晚期I期假定的IOS神经元接受来自PRG I调制神经元以及V传入神经的兴奋性输入。在相对较强的V输入下,这种脑桥兴奋性输出因抑制而降低,而在相对较弱的V输入下,由于抑制的减少,兴奋性输出增加。因此,脑桥和V对IOS的影响可以根据状态以互补的方式起作用。