By Arnold M. Katz
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Additional info for Physiology of the Heart, 5th edition
2010). This problem has become even more interesting by the recent findings of Koizumi et al. (2013) that there are substantial subpopulations of inhibitory inspiratory neurons that are cophenotypic glycinergic and GABAergic neurons in the neonatal pre-Bo¨tC. Our model, which is based on available (but limited) information on the specific connectivity of glycinergic and GABAergic neurons, has attempted to assign potential roles to glycinergic and GABAergic neuron populations in the pre-Bo¨tC and Bo¨tC.
Specifically, during expiration, all four expiratory populations of Bo¨tC inhibit all inspiratory populations of pre-Bo¨tC and rVRG. The glycinergic post-I population of Bo¨tC stops firing in the postinspiratory phase because of inhibition provided by both aug-E populations of Bo¨tC. Before the end of expiration, the pre-I/I excitatory population of pre-Bo¨tC starts firing when released from the decreasing inhibition from the dec-E population, which exhibits spike frequency adaptation in the model and is progressively inhibited by the aug-E(1) population.
Later during hypoxia, aug-E neurons discharge almost tonically, producing expiratory apnea. Normal activity patterns are fully recovered shortly after restoration of normoxia. , 2010). The striking difference to the partial blockade of GlyRs, however, is the persistence of tonic expiratory discharges. The final disturbance of network activity during progressive hypoxia is shifting of late expiratory neuronal discharges into the period of long apneustic inspiratory bursts and their vanishing after-discharges (Fig.
Physiology of the Heart, 5th edition by Arnold M. Katz