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. 2020 Jan 23;9:e52572. doi: 10.7554/eLife.52572

Figure 7. Ablation of the catecholaminergic C1 neurons blunted the active expiration induced by hypoxia, but not by hypercapnia.

Figure 7.

(A) Experimental design. (B) Photomicrography showing the C1 regions after bilateral injection of saline or anti-DβH-SAP (2.4 ng/100 nL) into the RVLM. (C) Number of TH neurons into the RVLM of the saline and anti-DβH-SAP-treated groups. (D) Traces showing breathing parameters (diaphragm electromyography [DiaEMG] and abdominal electromyography [AbdEMG]) from a representative experiment in a rat treated with saline or anti-DβH-SAP into the C1 region in a condition of cytotoxic hypoxia (KCN) or hypercapnia (10% CO2). (E) Expanded traces showing the presence of active expiration (AE) (black arrow) after intravenous injection of KCN into a saline-treated rat and the absence of AE by KCN in an anti-DβH-SAP-treated rat. (F–I) Individual data for each parameter: (F) DiaEMG frequency (bpm), (G) DiaEMG amplitude (mV), (H) AbdEMG amplitude (mV) and (I) AP (mmHg) after bilateral injection of saline (white circles; N = 7) or anti-DβH-SAP (red circles; N = 6) into the RVLM under baseline KCN or 10% CO2. Lines show mean and SEM. *Different from saline; two-way ANOVA, p<0.05. Abbreviations: AbdEMG, abdominal electromyogram; Anti-DβH-SAP, immunotoxin anti-dopamine β-hydroxylase-saporin; AP, arterial pressure; bpm, breaths per minute; DiaEMG, diaphragm electromyogram; KCN, potassium cyanide; RVLM, rostral ventrolateral medulla; VII, facial motor nucleus. Scale bar in panel (B) = 25 μm.