Berthoud H R
Pennington Biomedical Research Center, Louisiana State University, Baton Rouge 70808-4124, USA.
J Comp Neurol. 1995 Jul 31;358(3):428-39. doi: 10.1002/cne.903580309.
Recent pharmacological evidence suggests that the nonadrenergic, noncholinergic (NANC) vagal inhibitory input responsible for receptive relaxation of the fundic stomach is mediated by nitric oxide-synthesizing enteric neurons. To demonstrate anatomically such direct vagal inputs to neurochemically identified enteric neurons, we utilized the nicotinamide acetamide dinucleotide phosphate (NADPH)-diaphorase histochemical reaction in conjunction with selective anterograde labeling of vagal efferents or afferents. Approximately 30% of all myenteric neurons of the fundic myenteric plexus stained positive for NADPH diaphorase, and the principal recipient of axonal projections from NADPH diaphorase-positive neurons was the circular muscle layer. In a group of animals showing the most complete labeling of vagal efferent preganglionics with the carbocyanine dye DiA, quantitative analysis of the half of the ventral fundic wall closer to the greater curvature revealed that 46.8% +/- 4.4% of all myenteric neurons received some degree of vagal contacts and that 30.5% +/- 6.6% of such vagally contacted neurons were also NADPH diaphorase positive. In another group of rats with the most successful selective labeling of vagal afferents through DiI injections into the left nodose ganglion, analysis of select ganglia throughout the ventral fundic wall revealed that, of a total of 454 neurons with vagal afferent contacts, 34.8% +/- 2.8% were NADPH diaphorase positive. These findings support the view that, in the fundic stomach, some vagal preganglionic efferents terminate on nitric oxide-synthesizing neurons that, in turn, project to and relax the external smooth muscle layers. Furthermore, vagal afferent endings also contact NADPH diaphorase-positive neurons, suggesting the possibility of local axon reflexes originating from smooth muscular in-series tension receptors and terminating on nitrergic neurons of the myenteric plexus.
最近的药理学证据表明，负责胃底容受性舒张的非肾上腺素能、非胆碱能（NANC）迷走神经抑制性输入是由合成一氧化氮的肠神经元介导的。为了从解剖学上证明这种迷走神经对神经化学鉴定的肠神经元的直接输入，我们利用烟酰胺乙酰酰胺二磷酸（NADPH）-黄递酶组织化学反应结合迷走神经传出或传入纤维的选择性顺行标记。胃底肌间神经丛中约30%的肌间神经元对NADPH黄递酶染色呈阳性，NADPH黄递酶阳性神经元轴突投射的主要接受者是环行肌层。在一组用羰花青染料DiA对迷走神经节前传出纤维进行最完全标记的动物中，对靠近大弯侧的胃底前壁的一半进行定量分析发现，所有肌间神经元中有46.8%±4.4%接受了一定程度的迷走神经接触，并且这些与迷走神经接触的神经元中有30.5%±6.6%也对NADPH黄递酶呈阳性。在另一组通过将DiI注入左侧结状神经节对迷走神经传入纤维进行最成功选择性标记的大鼠中，对整个胃底前壁的选定神经节进行分析发现，在总共454个有迷走神经传入接触的神经元中，34.8%±2.8%对NADPH黄递酶呈阳性。这些发现支持了这样一种观点，即在胃底，一些迷走神经节前传出纤维终止于合成一氧化氮的神经元，这些神经元进而投射到外平滑肌层并使其舒张。此外，迷走神经传入末梢也与NADPH黄递酶阳性神经元接触，这表明存在源自平滑肌串联张力感受器并终止于肌间神经丛的氮能神经元的局部轴突反射的可能性。
