VASOACTIVE INTESTINAL POLYPEPTIDE AND CHOLINERGIC MECHANISMS IN CAT NASAL-MUCOSA - STUDIES ON CHOLINE-ACETYLTRANSFERASE AND RELEASE OF VASOACTIVE INTESTINAL POLYPEPTIDE
VASOACTIVE INTESTINAL POLYPEPTIDE AND CHOLINERGIC MECHANISMS IN CAT NASAL-MUCOSA - STUDIES ON CHOLINE-ACETYLTRANSFERASE AND RELEASE OF VASOACTIVE INTESTINAL POLYPEPTIDE
复制标题
DOI：
10.1073/pnas.78.8.5255
复制
发表时间：
1981-01-01
期刊：
影响因子：
--
通讯作者：
HOKFELT, T
中科院分区：
文献类型：
--
作者：
LUNDBERG, JM;ANGGARD, A;HOKFELT, T
正常猫蝶腭神经节的定量免疫组织化学分析显示，几乎所有的神经节细胞（98.5%）的免疫反应血管活性肠多肽（VIP）。在手术切除该神经节后，VIP和胆碱乙酰转移酶（乙酰CoA：胆碱O-乙酰转移酶，EC 2.3.1.6）（胆碱能神经元的特异性标记）的含量均降低至约70-80%在鼻粘膜中。在动物进行交感神经切除术结合感觉（三叉神经）去神经支配，VIP或胆碱乙酰转移酶没有显着变化，发现在鼻粘膜。蝶腭神经节中的VIP神经元的很大比例显然含有胆碱乙酰转移酶。VIP可能存在于一个人口的自主胆碱能神经元支配外分泌腺的猫。睫状神经节含有高水平的胆碱乙酰转移酶，但没有VIP。副交感神经刺激（15 Hz）引起的最大血管舒张和500倍增加VIP输出从鼻粘膜。在凝胶渗透色谱上，血浆VIP免疫反应性在与猪VIP相同的位置洗脱。阿托品预处理，消除鼻分泌物，导致在神经刺激（15 Hz）过程中VIP输出进一步增加3倍。同时，观察到血管舒张反应的持续时间明显延长。在通过阿托品预处理的副交感神经刺激期间VIP的输出增加表明递质乙酰胆碱可以抑制共存肽的释放，即，VIP，通过毒蕈碱自动受体。
Quantitative immunohistochemical analysis of the sphenopalatine ganglion in normal cats revealed that virtually all ganglion cells (98.5%) were immunoreactive to vasoactive intestinal polypeptide (VIP). After surgical removal of this ganglion, the content of both VIP and choline acetyltransferase (acetylCoA:choline O-acetyltransferase, EC 2.3.1.6), a specific marker for cholinergic neurons, was decreased to .apprx. 70-80% in the nasal mucosa. In animals subjected to sympathectomy combined with sensory (trigeminal) denervation, no significant change in VIP or choline acetyltransferase was found in the nasal mucosa. A large proportion of the VIP neurons in the sphenopalatine ganglion apparently contains choline acetyltransferase. VIP may be present in a population of autonomic cholinergic neurons innervating exocrine glands in the cat. The ciliary ganglion contained high levels of choline acetyltransferase but no VIP. Parasympathetic nerve stimulation (15 Hz) caused a maximal vasodilation and a 500-fold increase in VIP output from the nasal mucosa. The plasma VIP immunoreactivity eluted at the same position as porcine VIP on gel permeation chromatography. Atropine pretreatment, which abolishes nasal secretion, caused a further 3-fold increase in VIP output during the nerve stimulation (15 Hz). Simultaneously, a markedly prolonged duration of the vasodilatory response was observed. The increased output of VIP during parasympathetic nerve stimulation by atropine pretreatment suggests that the transmitter acetylcholine may inhibit the release of the coexisting peptide, i.e., VIP, via muscarinic autoreceptors.