Sheldon R J, Malarchik M E, Fox D A, Burks T F, Porreca F
Department of Pharmacology, University of Arizona Health Sciences Center, Tucson.
J Pharmacol Exp Ther. 1989 May;249(2):572-82.
Neural regulation of electrolyte transport in mouse jejunum was investigated in vitro using: 1) a full-thickness intestinal segment (intact preparation) and 2) a mucosal preparation, consisting of only mucosa, basement membrane and muscularis mucosa. In Ussing chambers, intact tissues exhibited high- and low-frequency oscillations of basal transmural potential difference (PD) and short-circuit current (Isc), whereas mucosal tissues exhibited only low-frequency oscillation of these parameters. High-frequency oscillations of PD and Isc were found to originate from muscle activity. Under basal conditions, intact tissues exhibited net Na+ absorption and net Cl- secretion, whereas mucosal tissues displayed greater net Na+ absorption and net Cl- absorption. When applied to the serosal medium of intact tissues, tetrodotoxin, a neurotoxin, and chlorisondamine, a ganglionic blocking agent, caused a concentration-dependent reduction of basal PD and Isc, whereas atropine produced no significant effect; these agents were without effect in mucosal tissues. Furthermore, in intact tissues, tetrodotoxin caused significant increases in net Na+ absorption and net residual flux, attaining values that were comparable to those seen in mucosal tissues. Carbachol, a muscarinic agonist, and 1,1-dimethyl-4-phenylpiperizinium, a ganglionic stimulant, elicited concentration-dependent, transient increases of basal PD and Isc when applied to the serosal medium of intact tissues; in mucosal preparations, carbachol elicited greater changes of basal PD and Isc, whereas 1,1-dimethyl-4-phenylpiperizinium produced no significant effect. In intact tissues, Isc responses elicited by carbachol were antagonized by atropine, but not tetrodotoxin or chlorisondamine; Isc responses induced by 1,1-dimethyl-4-phenylpiperizinium, however, were blocked by tetrodotoxin or chlorisondamine, but not atropine. These results support the existence of a multisynaptic, and tonically active neural pathway which serves to limit intestinal Na+ transport at some point below the maximal absorptive capacity of the mucosa. Furthermore, cholinergic muscarinic and nicotinic receptors are present in distinct neural pathways that influence intestinal electrolyte transport in the small intestine of the mouse.(ABSTRACT TRUNCATED AT 250 WORDS)
1）全层肠段（完整标本）和2）仅由黏膜、基底膜和黏膜肌层组成的黏膜标本。在尤斯灌流小室中，完整组织表现出基础跨膜电位差（PD）和短路电流（Isc）的高频和低频振荡，而黏膜组织仅表现出这些参数的低频振荡。发现PD和Isc的高频振荡源于肌肉活动。在基础条件下，完整组织表现出净Na⁺吸收和净Cl⁻分泌，而黏膜组织表现出更大的净Na⁺吸收和净Cl⁻吸收。当将神经毒素河豚毒素和神经节阻断剂氯异吲哚铵应用于完整组织的浆膜介质时，会导致基础PD和Isc浓度依赖性降低，而阿托品则无显著作用；这些药物对黏膜组织无作用。此外，在完整组织中，河豚毒素导致净Na⁺吸收和净残余通量显著增加，达到与黏膜组织中所见相当的值。毒蕈碱激动剂卡巴胆碱和神经节兴奋剂1,1 - 二甲基 - 4 - 苯基哌嗪鎓应用于完整组织的浆膜介质时，会引起基础PD和Isc浓度依赖性的短暂增加；在黏膜标本中，卡巴胆碱引起基础PD和Isc的变化更大，而1,1 - 二甲基 - 4 - 苯基哌嗪鎓无显著作用。在完整组织中，卡巴胆碱引起的Isc反应被阿托品拮抗，但不被河豚毒素或氯异吲哚铵拮抗；然而，1,1 - 二甲基 - 4 - 苯基哌嗪鎓诱导的Isc反应被河豚毒素或氯异吲哚铵阻断，但不被阿托品阻断。这些结果支持存在一条多突触且具有紧张性活动的神经通路，该通路在黏膜最大吸收能力以下的某个点限制肠道Na⁺转运。此外，毒蕈碱能和烟碱能胆碱能受体存在于影响小鼠小肠肠道电解质转运的不同神经通路中。（摘要截取自250字）
