Andrews P L, Lawes I N
J Physiol. 1985 Jun;363:1-20. doi: 10.1113/jphysiol.1985.sp015692.
This paper reports a quantitative in vivo study on the vagal activation of the intramural non-adrenergic, non-cholinergic inhibitory nerves in the ferret gastric corpus. The nature of the inhibitory neurotransmitter was also investigated. In the atropinized, guanethidine-treated, urethane-anaesthetized ferret, electrical stimulation (10 s at 20 V, 1-20 Hz, 0.5 ms pulses) of the cervical vagi produced a prompt fall in intracorpus pressure that was related to the stimulus frequency. The maximal response was achieved at 10 Hz. The time taken for the intracorpus pressure to return to pre-stimulus levels after a 10 s period of stimulation was related to the stimulus frequency; at 10 Hz the pressure took approximately 11 min to recover. In contrast to studies in the cat (Martinson & Muren, 1963), there was no detectable difference in the electrical threshold for activation of the vagal excitatory and vagal inhibitory fibres. The nature of the vagal non-adrenergic, non-cholinergic inhibitory neurotransmitter was investigated using a variety of antagonists and agonists. Adenosine triphosphate (ATP), adenosine, alpha beta-methylene ATP and beta gamma-methylene ATP all contracted the corpus in the presence of vagotomy, atropine, guanethidine and indomethacin. The vagally induced fall in corpus pressure was not blocked by high doses of alpha beta-methylene ATP. A variety of peptides were investigated for their effects on corpus pressure in the presence of atropine, guanethidine and vagotomy. Bombesin, pentagastrin, substance P, cholecystokinin octapeptide (CCK-8) and bradykinin all produced an increase in intracorpus pressure. Neurotensin and vasoactive intestinal polypeptide (VIP) both decreased intracorpus pressure, and of the two VIP most closely mimicked the response to vagal activation of the non-cholinergic, non-adrenergic inhibitory neurones. The results provide support for the involvement of a peptide (possibly VIP) rather than a purine in the vagally driven decrease in intracorpus pressure in the ferret.
本文报道了一项关于雪貂胃体壁内非肾上腺素能、非胆碱能抑制性神经迷走神经激活的定量体内研究。同时也对抑制性神经递质的性质进行了研究。在阿托品化、胍乙啶处理、乌拉坦麻醉的雪貂中，电刺激（20V，1 - 20Hz，0.5ms脉冲，持续10s）颈迷走神经会使胃体内压迅速下降，且这种下降与刺激频率有关。最大反应在10Hz时达到。刺激10s后胃体内压恢复到刺激前水平所需的时间与刺激频率有关；在10Hz时，压力大约需要11分钟才能恢复。与猫的研究（Martinson & Muren，1963）不同，迷走神经兴奋性纤维和迷走神经抑制性纤维激活的电阈值没有可检测到的差异。使用多种拮抗剂和激动剂研究了迷走神经非肾上腺素能、非胆碱能抑制性神经递质的性质。在迷走神经切断、阿托品、胍乙啶和消炎痛存在的情况下，三磷酸腺苷（ATP）、腺苷、αβ - 亚甲基ATP和βγ - 亚甲基ATP都会使胃体收缩。高剂量的αβ - 亚甲基ATP并未阻断迷走神经诱导的胃体内压下降。研究了多种肽在阿托品、胍乙啶和迷走神经切断情况下对胃体内压的影响。蛙皮素、五肽胃泌素、P物质、八肽胆囊收缩素（CCK - 8）和缓激肽都会使胃体内压升高。神经降压素和血管活性肠肽（VIP）都能降低胃体内压，且在这两种物质中，VIP最接近模拟非胆碱能、非肾上腺素能抑制性神经元对迷走神经激活的反应。这些结果支持了在雪貂中，迷走神经驱动的胃体内压下降涉及一种肽（可能是VIP）而非嘌呤的观点。
