Department of Pharmacology, University of Virginia, Charlottesville, VA 22908-0735, USA.
Respir Physiol Neurobiol. 2010 Oct 31;173(3):244-55. doi: 10.1016/j.resp.2010.02.005. Epub 2010 Feb 25.
The rat retrotrapezoid nucleus (RTN) contains about 2000 Phox2b-expressing glutamatergic neurons (ccRTN neurons; 800 in mice) with a well-understood developmental lineage. ccRTN neuron development fails in mice carrying a Phox2b mutation commonly present in the congenital central hypoventilation syndrome. In adulthood, ccRTN neurons regulate the breathing rate and intensity, and may regulate active expiration along with other neighboring respiratory neurons. Prenatally, ccRTN neurons form an autonomous oscillator (embryonic parafacial group, e-pF) that activates and possibly paces inspiration. The pacemaker properties of the ccRTN neurons probably vanish after birth to be replaced by synaptic drives. The neonatal parafacial respiratory group (pfRG) may represent a transitional phase during which ccRTN neurons lose their group pacemaker properties. ccRTN neurons are activated by acidification via an intrinsic mechanism or via ATP released by glia. In summary, throughout life, ccRTN neurons seem to be a critical hub for the regulation of CO(2) via breathing.
大鼠梯形核后区（RTN）含有约 2000 个表达 Phox2b 的谷氨酸能神经元（ccRTN 神经元；小鼠中约 800 个），其发育谱系已有明确的研究。在携带先天性中枢性通气不足综合征中常见的 Phox2b 突变的小鼠中，ccRTN 神经元的发育失败。在成年期，ccRTN 神经元调节呼吸频率和强度，并可能与其他相邻呼吸神经元一起调节主动呼气。在产前，ccRTN 神经元形成一个自主振荡器（胚胎面旁核群，e-pF），激活并可能调节吸气。ccRTN 神经元的起搏器特性可能在出生后消失，取而代之的是突触驱动。新生儿面旁呼吸核群（pfRG）可能代表一个过渡阶段，在此期间，ccRTN 神经元失去其群组起搏器特性。ccRTN 神经元通过内在机制或通过胶质细胞释放的 ATP 酸化而被激活。综上所述，在整个生命过程中，ccRTN 神经元似乎是通过呼吸调节 CO2 的关键枢纽。
