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

我们利用大鼠胚胎脑干-脊髓标本，分析了胎儿晚期(E16-21)呼吸中枢的发育。[1]在胎儿发育后期，除第四颈前根呼吸神经放电频率和幅度增加外，爆发模式也发生了显著变化。也就是说，E19-20之后的吸气相持续时间比E19之前的短爆发持续时间(100-200ms)增加了2-3倍或更多(&gt；400ms)。E21/20大鼠延髓腹外侧区和部分E19大鼠延髓腹外侧区可见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，这种呼吸神经元亚型的存在尚不清楚(胎儿型网络)。胎儿型网络中的许多呼吸神经元具有内源性猝发的特性，可分为吸气神经元和吸气…时受抑制神经元。更多的阶段。[2]胺(肾上腺素、5-羟色胺、多巴胺)或cAMP相关物质(Forsklin、PACAP)可延长C4吸气活动的爆发持续时间，并使C4吸气活动的网络性可逆地从新生儿型转变为胎儿型。早在E17就发现了突发性或非突发性的I型吸气神经元的原型。吸气期抑制的内源性突触神经元被认为是吸气前神经元的一个候选原型。[3]延髓呼吸神经元的氯离子依赖突触电位即使在胚胎16岁时也能引起膜超极化。沐浴应用GABA(0.2-1 mM)主要引起胎儿呼吸神经元在高或低氯离子/甘草酸记录中的去极化。在低氯离子/全细胞记录中，GABA对74%的神经元有膜去极化作用。大多数对GABA的反应伴随着膜电阻的显著降低和膜兴奋性的丧失。GABA0.5-1 mM的作用可被100μM荷包牡丹碱阻断。在无CO_2/HCO3^-HEPES缓冲溶液中，GABA引起的去极化降低30-40%。较少

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