Neuronal mechanisms of development of respiratory neuron network in the late fetal stage of rat

我们用大鼠胎脑脊髓标本分析了呼吸中枢在胚胎晚期（E16-21）的发育。[1]除了第四颈前根呼吸神经放电频率和幅度增加外，爆发模式在胎儿发育后期也发生了明显变化。也就是说，与E19之前的短爆发持续时间（100-200 ms）相比，E19-20之后的吸气相持续时间增加了2-3倍或更多（>400 ms）。在E21/20和部分E19大鼠的延髓腹外侧区发现了与新生大鼠相似的呼吸神经元亚型（吸气前、吸气、呼气三种类型;新生型网络）。在E18之前，这些呼吸神经元亚型的存在尚不清楚（胎儿型网络）。胎儿型神经网络中的许多呼吸神经元具有内在爆发器的特性，可分为吸气神经元和吸气时接受抑制的神经元 ...更多信息 相位[2]胺（肾上腺素，5-HT，多巴胺）或cAMP相关物质（毛喉素，PACAP）延长C4吸气活动的爆发持续时间和可逆地转换的网络性质从新生儿型到胎儿型。在E17时也发现了爆发型和非爆发型的I型吸气神经元原型。吸气相抑制的内源性爆发神经元被认为是吸气前神经元的原型。[3]延髓呼吸神经元的Cl^-依赖性突触电位甚至在E16时就引起了膜超极化。在高或低Cl^-/短杆菌肽记录中，GABA（0.2-1 mM）主要诱导胎儿呼吸神经元的去极化。在低Cl^-/全细胞记录中，GABA在74%的神经元中引起膜去极化。对GABA的大多数反应伴随着膜电阻的显著降低和膜兴奋性的丧失。GABA（0.5 - 1 mM）的作用可被100 μM荷包牡丹碱阻断。在无CO_2/HCO_3^-HEPES缓冲液中GABA诱导的去极化降低30-40%。少

We analyzed development of respiratory center in the late fetal stage (E16-21), using rat fetus brainstem-spinal cord preparations. [1] In addition to increase in frequency and amplitude of respiratory nerve discharge from fourth cervical ventral roots, the burst pattern changed markedly during the late fetal development. Namely, duration of inspiratory phase after E19-20 increased 2-3 times or more (>400 ms) compared with short burst duration (100-200 ms) before E19. Subtypes of respiratory neurons (pre-inspiratory, three types of inspiratory, expiratory ; neonatal type network) similar to those in newborn rats were found in the ventrolateral medulla of preparations from E21/20 and in some E19 rats. Before E18, the presence of such subtypes of respiratory neurons was not clear (fetal type network). Many respiratory neurons in fetal type network possess properties as intrinsic burster, and they were classified into inspiratory neurons and neurons receiving inhibition during inspiratory … More phase. [2] Amines (adrenaline, 5-HT, dopamine) or cAMP-related substances (forskolin, PACAP) prolonged the burst duration of C4 inspiratory activity and converted reversibly the network property from neonatal type to fetal type. Prototype of type-I inspiratory neurons which were burster or non-burster was found even in E17. Intrinsic burster neurons inhibited during inspiratory phase were proposed as a candidate of prototype of pre-inspiratory neurons. [3] Cl^--dependent synaptic potentials in medullary respiratory neurons caused a membrane hyperpolarization even at E16. Bath-applied GABA (0.2-1 mM) mainly induced a depolarization of fetal respiratory neurons in high or low Cl^-/gramicidin recordings. In low Cl^-/whole-cell recordings, GABA induced a membrane depolarization in 74% neurons. Most responses to GABA were accompanied by a marked reduction in the membrane resistance and a loss of membrane excitability. Effects of GABA (0.5 -1 mM) were blocked by 100 μM bicuculline. GABA-induced depolarization reduced by 30-40% in CO_2/HCO_3^- free-HEPES buffered solution. Less