Matsuyama Hayato, El-Mahmoudy AbuBakr, Shimizu Yasutake, Takewaki Tadashi
Department of Pathogenetic Veterinary Science, The United Graduate School, Gifu University, Yanagido 1-1, Japan.
J Neurophysiol. 2003 May;89(5):2346-53. doi: 10.1152/jn.00686.2002.
Neurogenic ATP and nitric oxide (NO) may play important roles in the physiological control of gastrointestinal motility. However, the interplay between purinergic and nitrergic neurons in mediating the inhibitory neurotransmission remains uncertain. This study investigated whether neurogenic NO modulates the purinergic transmission to circular smooth muscles of the hamster proximal colon. Electrical activity was recorded from circular muscle cells of the hamster proximal colon by using the microelectrode technique. Intramural nerve stimulation with a single pulse evoked a fast purinergic inhibitory junction potential (IJP) followed by a slow nitrergic IJP. The purinergic component of the second IJP evoked by paired stimulus pulses at pulse intervals between 1 and 3 s became smaller than that of the first IJP. This purinergic IJP depression could be observed at pulse intervals <3 s, but not at longer ones, and failed to occur in the presence of NO synthase inhibitor. Exogenous NO (0.3-1 microM), at which no hyperpolarization is produced, inhibited purinergic IJPs, without altering the nitrergic IJP and exogenously applied ATP-induced hyperpolarization. In the presence of both purinoceptor antagonist and nitric oxide synthase (NOS) inhibitor, intramural nerve stimulation with 5 pulses at 20 Hz evoked vasoactive intestinal peptide (VIP)-associated IJPs, suggesting that VIP component may be masked in the IJPs of the hamster proximal colon. Our results suggest that neurogenic NO may modulate the purinergic transmission to circular smooth muscles of the hamster proximal colon via a prejunctional mechanism. In addition, VIP may be involved in the neurotransmitter in the hamster proximal colon.
神经源性三磷酸腺苷（ATP）和一氧化氮（NO）可能在胃肠动力的生理控制中发挥重要作用。然而，嘌呤能神经元与一氧化氮能神经元在介导抑制性神经传递过程中的相互作用仍不明确。本研究调查了神经源性NO是否调节嘌呤能向仓鼠近端结肠环形平滑肌的传递。采用微电极技术记录仓鼠近端结肠环形肌细胞的电活动。用单个脉冲进行壁内神经刺激可诱发快速的嘌呤能抑制性接头电位（IJP），随后是缓慢的一氧化氮能IJP。在1至3秒的脉冲间隔下，成对刺激脉冲诱发的第二个IJP的嘌呤能成分比第一个IJP的小。这种嘌呤能IJP抑制在脉冲间隔<3秒时可观察到，但在更长间隔时则未出现，并且在一氧化氮合酶抑制剂存在时不会发生。外源性NO（0.3 - 1 microM），在此浓度下不会产生超极化，可抑制嘌呤能IJP，而不改变一氧化氮能IJP和外源性应用ATP诱导的超极化。在嘌呤受体拮抗剂和一氧化氮合酶（NOS）抑制剂均存在的情况下，以20 Hz频率进行5次脉冲的壁内神经刺激可诱发血管活性肠肽（VIP）相关的IJP，这表明VIP成分可能在仓鼠近端结肠的IJP中被掩盖。我们的结果表明，神经源性NO可能通过一种节前机制调节嘌呤能向仓鼠近端结肠环形平滑肌的传递。此外，VIP可能参与仓鼠近端结肠的神经递质传递。
