Bowers C W, Kolton L
Howard Hughes Medical Institute Laboratories, San Francisco, CA.
Neuroscience. 1987 Dec;23(3):1157-68. doi: 10.1016/0306-4522(87)90189-8.
The neural input to the frog bladder was characterized in vitro. The nerve-evoked bladder contraction consists primarily of an early parasympathetic cholinergic component and a later, longer-lasting non-adrenergic non-cholinergic component. This slow non-adrenergic non-cholinergic contraction is not only resistant to cholinergic and adrenergic antagonists, but also to H1 and H2 histaminergic antagonists and to the serotoninergic antagonist, methysergide. It is concluded that the non-adrenergic non-cholinergic contraction is mediated by an efferent action of the sensory system because it is resistant to ganglionic nicotinic antagonists and because it is elicited specifically by stimulation of the peripheral cut end of the dorsal root. 5-Hydroxytryptamine is a potent and specific inhibitor of the sensory non-adrenergic non-cholinergic contraction. Although the bladder smooth muscle is innervated by terminals containing a somatostatin-like substance, somatostatin does not cause a bladder contraction. Luteinizing hormone-releasing hormone, enkephalin, histamine, 5-hydroxytryptamine, adenosine and adenosine 5 monophosphate are also unlikely candidates for the non-adrenergic non-cholinergic transmitter because they do not produce bladder contractions and/or their antagonists are ineffective on the nerve-evoked contraction. A putatively sensory network of fibers containing a substance P-like material is located within the wall of the bladder. Substance P produces bladder contractions at concentrations as low as 10(-9) M and so it, or a related substance, is a viable transmitter candidate in this system. Adenosine 5'-triphosphate (ATP)(10(-5) M) also causes a bladder contraction and remains a possible candidate as well. The data demonstrate that the bladder contraction resulting from electrical stimulation of the bladder nerves is due in large part to the "antidromic" stimulation of sensory axons. The likely presence therefore of potent and releasable substances in the peripheral sensory terminals of the bladder suggests that this sensory system may exert significant local, efferent control of bladder smooth muscle (i.e. independent from the central nervous system).
在体外对蛙膀胱的神经输入进行了特性分析。神经诱发的膀胱收缩主要由早期副交感胆碱能成分和后期持续时间更长的非肾上腺素能非胆碱能成分组成。这种缓慢的非肾上腺素能非胆碱能收缩不仅对胆碱能和肾上腺素能拮抗剂有抗性，而且对H1和H2组胺能拮抗剂以及5-羟色胺能拮抗剂麦角新碱也有抗性。得出的结论是，非肾上腺素能非胆碱能收缩是由感觉系统的传出作用介导的，因为它对神经节烟碱拮抗剂有抗性，并且是由刺激背根外周切断端特异性引发的。5-羟色胺是感觉性非肾上腺素能非胆碱能收缩的一种强效且特异性抑制剂。尽管膀胱平滑肌由含有生长抑素样物质的终末支配，但生长抑素不会引起膀胱收缩。促黄体生成素释放激素、脑啡肽、组胺、5-羟色胺、腺苷和腺苷5-单磷酸也不太可能是非肾上腺素能非胆碱能递质的候选物，因为它们不会引起膀胱收缩，和/或它们的拮抗剂对神经诱发的收缩无效。在膀胱壁内存在一个假定的含有P物质样物质的感觉纤维网络。P物质在低至10(-9)M的浓度下就能引起膀胱收缩，因此它或相关物质是该系统中一种可行的递质候选物。腺苷5'-三磷酸(ATP)(10(-5)M)也会引起膀胱收缩，仍然是一种可能的候选物。数据表明，电刺激膀胱神经引起的膀胱收缩在很大程度上是由于感觉轴突的“逆向”刺激。因此，膀胱外周感觉终末中可能存在强效且可释放的物质，这表明该感觉系统可能对膀胱平滑肌发挥显著的局部传出控制作用(即独立于中枢神经系统)。
