MODULATION OF THE VAGAL DRIVE TO THE INTRAMURAL CHOLINERGIC AND NONCHOLINERGIC NEURONS IN THE FERRET STOMACH BY BACLOFEN
MODULATION OF THE VAGAL DRIVE TO THE INTRAMURAL CHOLINERGIC AND NONCHOLINERGIC NEURONS IN THE FERRET STOMACH BY BACLOFEN
复制标题
DOI：
10.1113/jphysiol.1987.sp016599
复制
发表时间：
1987-07-01
影响因子：
5.5
通讯作者：
WOOD, KL
中科院分区：
文献类型：
--
作者：
ANDREWS, PLR;BINGHAM, S;WOOD, KL
1.在麻醉的雪貂迷走神经切断术（颈部和腹部）和六烃季铵都产生了阿托品和乙啶，部分内脏大神经和肾上腺切除术治疗后，胃体压力增加。2.压力增加是由于中断紧张迷走神经驱动器的壁内非肾上腺素能，非胆碱能抑制神经元。3. GABAB受体激动剂巴氯芬（8 mg/kg s.c.）引起胃内压力增加，并增强节律性收缩的幅度。巴氯芬在切断迷走神经的动物中没有作用。4.在阿托品、乙啶、肾上腺切除术和内脏大神经切除术的存在下，巴氯芬仅产生轻微的节律性收缩增强，但仍存在胃压的大幅增加。在上述条件下，巴氯芬对整个胃的作用几乎与仅在胃体区观察到的作用相同。5.巴氯芬是没有影响的程度上产生的次最大迷走神经传出刺激阿托品的存在下，体松弛。6.这些结果表明，GABAB激动剂巴氯芬，可能作用于一个中央网站，通过增加迷走神经驱动壁内胆碱能神经元，增强胃的节律性活动。同时胃压力增加，主要是通过减少紧张迷走神经驱动器的壁内非肾上腺素能，非胆碱能抑制神经元在体部区域。巴氯芬和迷走神经切断术研究的结果进一步证明了迷走神经支配的非肾上腺素能、非胆碱能抑制性神经元在胃压力调节中的重要性。
1. In the urethane-anaesthetized ferret vagotomy (cervical and abdominal) and hexamethonium both produced an increase in gastric corpus pressure after treatment with atropine and guanethidine, section of the greater splanchnic nerves and adrenalectomy. 2. The pressure increase was due to an interruption of a tonic vagal drive to the intramural non-adrenergic, non-cholinergic inhibitory neurones. 3. The GABAB receptor agonist baclofen (8 mg/kg s.c.) produced an increase in gastric pressure and enhanced the amplitude of the rhythmic contractions. Baclofen was without effect in vagotomized animals. 4. In the presence of atropine, guanethidine, adrenalectomy and section of the greater splanchnic nerves, baclofen produced only a slight enhancement of rhythmic contractions but the large increase in gastric pressure was still present. Under the above conditions the effects of baclofen on the whole stomach were virtually identical to those observed in the corpus region alone. 5. Baclofen was without effect on the magnitude of the corpus relaxation produced by submaximal vagal efferent stimulation in the presence of atropine. 6. These results demonstrate that the GABAB agonist baclofen, probably acting at a central site, enhanced rhythmic gastric activity by increasing the vagal drive to the intramural cholinergic neurones. Simultaneously gastric pressure was increased primarily by a reduction in the tonic vagal drive to the intramural non-adrenergic, non-cholinergic inhibitory neurones in the corpus region. The results of both the baclofen and vagotomy studies further demonstrate the importance of the vagal innervation of the non-adrenergic, non-cholinergic inhibitory neurones in the regulation of gastric pressure.