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. 2009 Jun 2;587(Pt 14):3539–3559. doi: 10.1113/jphysiol.2008.167502

Figure 10. Extended model of the brainstem respiratory network.

Figure 10

(See detailed description in Smith et al. 2007.) A, schematic diagram of the extended model showing interactions between specific populations of respiratory neurones within major brainstem respiratory compartments (pons, RTN/vlPF, BötC, pre-BötC, rVRG and cVRG). Each population (shown as a sphere) consists of 50 neurons described in the Hodgkin–Huxley style. This model incorporates an additional late-E population in the RTN/vlPF. This population is identical to the pre-I/I population in the pre-BötC and consists of 50 neurones containing persistent sodium current and interconnected with mutually excitatory connections (Smith et al. 2007). Most connections are based on previously published experimental data (for references see Smith et al. 2007) and some are suggested (ibid). The model includes proposed interactions between the late-E neuronal population in the RTN/vlPF, activated by hypercapnia, and other populations of respiratory neurones. Interactions between late-E and pre-I/I populations are similar to those proposed by Wittmeier et al. (2008). B and Ca–e show activity of selected neuronal populations in the model (B) and motor outputs (AbN, HN, PN in Ca–e). Activity of each population is represented by a histogram of average neuronal spiking frequency within the population (spikes s–1 neurone–1, bin size 30 ms). Hypercapnia was simulated by an additional ‘hypercapnia-evoked’ drive to the late-E population of RTN/vlPF. In B and Cb, the value of this drive was 0.27 (arbitrary units). In Ca–d/e, this drive progressively increased (indicated above each diagram). The late-E activity was expressed and increased frequency with the increase of this drive (Ca–c). Increasing drive above 0.35 converted the late-E pattern in the late-E population and AbN output to biphasic-E, containing a rebound post-I component (Cd, see also Wittmeier et al. 2008). Also similar to the Wittmeier et al. model, suppression of the pre-I/I population in the pre-BötC (by direct inhibition) to simulate the effects of opioids (Janczewski & Feldman, 2006a) eliminates inspiratory inhibition of the late-E population by the early-I population of pre-BötC, and converts the biphasic-E bursts in AbN to prolonged monophasic discharges lacking the rebound post-I component (Ce).