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首页> 外文期刊>American Journal of Physiology >Postnatal development of myenteric neurochemical phenotype and impact on neuromuscular transmission in the rat colon.
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Postnatal development of myenteric neurochemical phenotype and impact on neuromuscular transmission in the rat colon.

机译：产后肌性神经化学表型的发展及其对大鼠结肠神经肌肉传递的影响。

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Profound changes in intestinal motility occur during the postnatal period, but the involvement of the enteric nervous system (ENS), a key regulator of gastrointestinal (GI) motility, in these modifications remains largely unknown. We therefore investigated the postnatal development of the ENS phenotype and determined its functional repercussion on the neuromuscular transmission in the rat colon. Sprague-Dawley rats were euthanized at postnatal day (P) 1, P3, P5, P7, P14, P21, and P36. Whole mounts of colonic myenteric plexus were stained with antibodies against choline acetyltransferase (ChAT), neuronal nitric oxide synthase (nNOS), and HuC/D. Colonic contractile response induced by electrical field stimulation (EFS) was investigated in organ chambers in absence or presence of N-nitro-l-arginine methyl ester (l-NAME) and/or atropine. In vivo motility was assessed by measurement of the colonic bead latency time. Randomly occurring ex vivo contractions appeared starting at P5. Starting at P14, rhythmic phasic contractions occurred whose frequency and amplitude increased over time. In vivo, bead latency was significantly reduced between P14 and P21. Ex vivo, EFS-induced contractile responses increased significantly over time and were significantly reduced by atropine starting at P14 but were sensitive to l-NAME only after P21. The proportion of ChAT-immunoreactive (IR) neurons increased time dependently starting at P14. The proportion of nNOS-IR neurons increased as early as P5 compared with P1 but did not change afterward. Our data support a key role for cholinergic myenteric pathways in the development of postnatal motility and further identify them as putative therapeutic target for the treatment of GI motility disorders in the newborn.
机译：产后时期肠道蠕动发生了深刻变化，但是肠胃神经系统（ENS）（胃肠道（GI）运动的关键调节器）的参与在这些改变中仍然未知。因此，我们调查了ENS表型的产后发育，并确定了其对大鼠结肠神经肌肉传递的功能影响。在出生后第1天，P3，P5，P7，P14，P21和P36对Sprague-Dawley大鼠实施安乐死。用抗胆碱乙酰基转移酶（ChAT），神经元一氧化氮合酶（nNOS）和HuC / D的抗体对结肠肌层神经丛的整个部分进行染色。在不存在或存在N-硝基-1-精氨酸甲酯（l-NAME）和/或阿托品的情况下，在器官室内研究了由电场刺激（EFS）诱导的结肠收缩反应。通过测量结肠珠的潜伏时间来评估体内运动性。从P5开始出现随机发生的体外收缩。从P14开始，发生有节奏的相位收缩，其频率和幅度随时间增加。在体内，P14和P21之间的磁珠潜伏期显着减少。在离体时，EFS诱导的收缩反应随时间显着增加，并从阿托品开始于P14开始显着降低，但仅在P21之后对l-NAME敏感。 ChAT免疫反应（IR）神经元的比例从P14开始逐渐增加时间。与P1相比，nNOS-IR神经元的比例最早在P5之前就增加了，但之后没有变化。我们的数据支持胆碱能肠系膜通路在产后运动发展中的关键作用，并进一步将其确定为新生儿胃肠动力运动障碍的假定治疗靶标。

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