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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 10. Active expiration induced by reducing drive to neurons active in the post-inspiratory phase was suppressed either by increasing drive to all populations in the Bötzinger complex or by reducing glycinergic transmission within the Bötzinger complex.

Figure 10.

Panel A: Active expiration was induced by decreasing tonic excitatory conductances on the GABAergic (GABA) and glycinergic (Gly) post-inspiratory populations (post-I) by 5%. Active expiration was then abolished by transiently increasing tonic excitatory conductances of the all populations in the Bötzinger complex [post-I and augmenting-expiratory (aug-E)] by 12% during the interval emphasized by the orange shaded box. Panel B and C: Active expiration was abolished by reducing the aug-E to post-I synaptic weight by 10%. Other abbreviations – early-I: early inspiratory population, and late-E: late expiratory population.