Hypercapnia promotes an increase in pulmonary ventilation due to the stimulation of brainstem chemosensory cells that are connected to the respiratory network. Among these cells are the raphe serotonergic neurons which widely send projections to distinct central respiratory compartments. Nevertheless, the physiological role of specific raphe serotonergic projections to other chemosensitive sites on the emergence of hypercapnia ventilatory response in vivo still remains to be elucidated. Here we investigated whether the ventilatory response to hypercapnia requires serotonergic inputs to the chemosensitive cells of the retrotrapezoid nucleus (RTN) in the ventrolateral medulla. To test this, pulmonary ventilation was evaluated under baseline conditions and during hypercapnia (7% CO₂) in unanesthetized juvenile Holtzman rats (60–90 g) that received bilateral microinjections of either vehicle (control) or anti-SERT-SAP (0.1 mM, 10 pmol/100 nl) toxin in the RTN to retrogradely destroy serotonergic afferents to this region. Fifteen days after microinjections, baseline ventilation was not different between anti-SERT-SAP (n = 8) and control animals (n = 9). In contrast, the ablation of RTN-projecting serotonergic neurons markedly attenuated the hypercapnia-induced increase in respiratory frequency which was correlated with reduced numbers of serotonergic neurons in the raphe obscurus and magnus, but not in the raphe pallidus. The increase in tidal volume during hypercapnia was not significantly affected by anti-SERT-SAP microinjections in the RTN. Our data indicate that serotoninergic neurons that send projections to the RTN region are required for the processing of ventilatory reflex response during exposure to high CO₂ in unanesthetized conditions.

由于刺激连接到呼吸网络的脑干化学感应细胞，高碳酸血症促进肺通气的增加。在这些细胞中，是裂口血清素能神经元，其广泛地将投射信号发送至不同的中央呼吸区室。然而，在体内高碳酸血症通气反应出现时，特定的缝隙性5-羟色胺能神经投射对其他化学敏感性部位的生理作用仍待阐明。在这里，我们调查了对高碳酸血症的通气反应是否需要在腹外侧延髓中向后梯形核（RTN）的化学敏感性细胞输入血清素能。为了测试这一点，在基线条件下和高碳酸血症（7％CO ₂）在未麻醉的Holtzman幼鼠（60-90 g）中，接受了RTN中双侧微量注射溶媒（对照）或抗SERT-SAP（0.1 mM，10 pmol / 100 nl）毒素以逆向破坏该区域的血清素能传入分子。显微注射15天后，抗SERT-SAP（n = 8）和对照动物（n = 9）的基线通气没有差异。相比之下，RTN投射的血清素能神经元的消融显着减弱了高碳酸血症诱导的呼吸频率的增加，这与暗纹中和大核的血清素能神经元数量的减少有关，而在睑裂中则没有。RTN中的抗SERT-SAP显微注射对高碳酸血症期间的潮气量增加没有显着影响。₂在未麻醉的条件下。