Zanella Sebastien, Roux J C, Viemari J C, Hilaire Gérard
FRE CNRS 2722, Université de la Méditerranée, 280 Boulevard Sainte-Marguerite, 13009 Marseille, France.
Respir Physiol Neurobiol. 2006 Sep 28;153(2):126-38. doi: 10.1016/j.resp.2005.09.009. Epub 2005 Nov 22.
Although compelling evidence exist that the respiratory rhythm generator is modulated by endogenous noradrenaline released from pontine A5 and A6 neurones, we examined whether medullary catecholaminergic neurones also participated in respiratory rhythm modulation. Experiments were performed in neonatal (postnatal days 0-6, P0-P6) and young mice (P14-P18) using "en bloc" medullary preparations (pons resected) and transverse medullary slices. In "en bloc" preparations, blockade of medullary alpha2 adrenoceptors with yohimbine and activation of catecholamine biosynthesis with L-tyrosine significantly depresses and facilitates the respiratory rhythm, respectively. In slices from neonatal and young mice, blockade of medullary alpha2 adrenoceptors also depressed the respiratory rhythm. Yohimbine local applications and lesion-ablation experiments of the dorsal medulla revealed implication of A1/C1 neurones in the yohimbine depressing effect. Although the mechanisms responsible for the yohimbine-depressing effect remain to be elucidated, our in vitro results in neonatal and young mice suggest that endogenous catecholamines released from A1/C1 neurones participate in respiratory rhythm modulation via medullary alpha2 adrenoceptors.
尽管有确凿证据表明呼吸节律发生器受脑桥A5和A6神经元释放的内源性去甲肾上腺素调节,但我们研究了延髓儿茶酚胺能神经元是否也参与呼吸节律调节。实验在新生小鼠(出生后0 - 6天,P0 - P6)和幼鼠(P14 - P18)中进行,使用“整体”延髓制备物(切除脑桥)和横断延髓切片。在“整体”制备物中,用育亨宾阻断延髓α2肾上腺素能受体以及用L - 酪氨酸激活儿茶酚胺生物合成分别显著抑制和促进呼吸节律。在新生和幼鼠的切片中,阻断延髓α2肾上腺素能受体也会抑制呼吸节律。育亨宾局部应用和延髓背侧的损伤消融实验揭示了A1/C1神经元在育亨宾抑制作用中的作用。尽管育亨宾抑制作用的机制仍有待阐明,但我们在新生和幼鼠中的体外实验结果表明,A1/C1神经元释放的内源性儿茶酚胺通过延髓α2肾上腺素能受体参与呼吸节律调节。