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. Author manuscript; available in PMC: 2021 Nov 1.
Published in final edited form as: J Physiol. 2020 Jul 24;598(21):4969–4994. doi: 10.1113/JP280243

Figure 13. Active expiration was induced by the antagonism of glycinergic receptors within the pFRG, which can be attenuated by an increase in the drive to expiratory populations of the BötC.

Figure 13.

Panels A and B: the reduction of the synaptic projection from the glycinergic post-inspiratory population [post-I (Gly)] to the late-expiratory population (late-E) induced active expiration. The transformation of the respiratory pattern during the late expiratory phase is emphasized by the orange shaded boxes. Panel C: In a simulation of this condition, an increase in the tonic excitatory conductances to the populations of the Bötzinger complex — the glycinergic and GABAergic post-I [post-I (GABA)], and the augmenting-expiratory (aug-E) populations – restrained active expiration during the interval emphasized by the orange shaded box.