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Fig. 6. Effects of anoxia on rhythmic bursting of respiratory neurons in isolated medulla preparations from neonatal rats. (A) Bursting of rhythmogenic pre-Bötzinger complex (PBC) neurons is possibly caused by the cooperative interaction between regenerative intrinsic ion conductances such as persistent Na⁺ channels (Na_P) or intermediate-voltage-activated (P/Q-type) Ca²⁺ channels (Ca_P) with K_ir channels (including K_ATP channels) or leak (e.g. TASK-1 channels) that contribute to resting membrane potential (V_m) and are affected by various neuromodulators, CO₂/H⁺ and/or O₂. These neuromodulators may also indirectly affect PBC neurons via an action on K_ir (or TASK-1) channels of pacemaker cells within the reticular formation proposed to provide excitatory drive to rhythmogenic PBC cells. Spike firing during individual bursts is mediated by Hodgkin-Huxley-type Na⁺ channels (Na_HH) plus L- and N-type Ca²⁺ channels (Ca_L,N). (B) In a minor subpopulation of inspiratory (PBC) neurons in a brainstem–spinal cord preparation, a hyperpolarisation induced by anoxia does not block the rhythmic drive potential, as also evident from persistence of inspiratory-related cervical (C₄) nerve rootlet activity. (C) In other respiratory neurons, such as this inspiratory cell in a brainstem–spinal cord preparation, anoxia depresses the drive potential and abolishes spiking. This effect is antagonised by the K_ir and K_ATP channel antagonist Ba²⁺. The downward deflections on the membrane potential traces in B and C are responses to injection of dc current for measurement of membrane conductance. Data from K. Ballanyi.

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