Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Barcelona, Spain; Department of Cell Biology, Physiology and Immunology and Neurosciences Institute, Universitat Autònoma de Barcelona, Barcelona, Spain.
Neurogastroenterol Motil. 2014 Mar;26(3):419-29. doi: 10.1111/nmo.12293. Epub 2013 Dec 25.
Inhibitory neuromuscular transmission in the human colon is due to nitrergic and purinergic (P2Y1 -mediated) inputs. The aim of this study was to determine the mechanisms of neuromuscular transmission in different regions of the human small intestine.
Ileal (n = 6) and jejunal (n = 6) samples underwent histological examination and were studied using sharp microelectrodes in smooth muscle cells and conventional muscle bath techniques. Electrical field stimulation (EFS) was used to stimulate inhibitory neurons.
No histological abnormalities were found. Resting membrane potential was -39.7 ± 1.5 and -45.5 ± 2.1 mV in the jejunum and ileum, respectively. Slow waves and spontaneous contractions were recorded at a frequency of about 8-9 and 6-7 cpm in the jejunum and ileum, respectively. In non-adrenergic, non-cholinergic conditions, EFS caused an inhibitory junction potential and mechanical relaxation. Both responses were blocked by tissue incubation with the nitric oxide synthase inhibitor (Nω-nitro-l-arginine 1 mM) and the P2Y1 receptor blocker 2'-deoxy-N(6) -methyladenosine 3',5'-bisphosphate tetrasodium salt (MRS2179; 10 μM). Both exogenous addition of sodium nitroprusside (1 μM) and the preferential P2Y1 receptor agonist ADPβS (1 μM) hyperpolarized and relaxed smooth muscle cells. MRS2179 (10 μM) blocked ADPβS-induced responses.
CONCLUSIONS & INFERENCES: Similar to colon, inhibitory neurotransmission in the human small intestine is mainly mediated by purinergic (via P2Y1 receptors) and nitrergic inhibitory neurotransmission. Similar mechanisms of inhibitory neurotransmission are present in different regions of the human intestine.
人类结肠的抑制性神经肌肉传递是由于氮能和嘌呤能（P2Y1 介导）输入。本研究的目的是确定人类小肠不同区域的神经肌肉传递机制。
回肠（n=6）和空肠（n=6）样本进行组织学检查，并使用锐性微电极在平滑肌细胞和常规肌肉浴技术中进行研究。电刺激（EFS）用于刺激抑制性神经元。
未发现组织学异常。空肠和回肠的静息膜电位分别为-39.7±1.5 mV 和-45.5±2.1 mV。在非肾上腺素能、非胆碱能条件下，EFS 引起抑制性突触后电位和机械松弛。两种反应均被组织孵育一氧化氮合酶抑制剂（Nω-硝基-L-精氨酸 1 mM）和 P2Y1 受体阻滞剂 2'-脱氧-N（6）-甲基腺苷 3'，5'-二磷酸四钠盐（MRS2179；10 μM）阻断。外源性添加硝普钠（1 μM）和优先 P2Y1 受体激动剂 ADPβS（1 μM）均可使平滑肌细胞超极化和松弛。MRS2179（10 μM）阻断 ADPβS 诱导的反应。
与结肠相似，人类小肠的抑制性神经传递主要由嘌呤能（通过 P2Y1 受体）和氮能抑制性神经传递介导。不同区域的人类肠道中存在相似的抑制性神经传递机制。
