Molecular mechanisms of sensory svstem from urinary bladder

对膀胱的自主控制进行了研究。感觉神经末梢的激活主要是由于膀胱壁的膨胀。使用醋酸和炎症相关物质interluikin 1 β (il1 β)的化学刺激通过激活高阈纤维改变排尿反射的阈值。前列腺素E激活沉默C纤维单元，改变高阈值纤维的阈值。低阈值纤维的活性没有改变。吲哚美辛可消除il - 1 β和PGE的作用。正常排尿反射中不使用的高阈纤维被炎症相关物质激活，排尿频率增加，膀胱容量降低。根据长时间（300ms）去极化电流脉冲的放电特性，将副交感神经节前神经元（PGN）分为强直性和相性两种。4-氨基吡啶（4-AP）降低了强直性和相性PGN的峰激活阈值，揭示了相性PGN的强直性放电，增加了强直性PGN的放电频率。这些数据表明存在两种类型的PGN，并且可能对盆腔脏器的目标具有不同的神经支配。

Autonomic control of urinary bladder has been studied. Sensory nerve ending was activated primarily by distention of the bladder wall. Chemical irritation using acetic acid and inflammation related substance interluikin 1beta (IL1beta) changed the threshold for micturition reflex by activating the high threshold fibers. Prostaglandin E (PGE) activated silent C fiber unit and changed threshold of high threshold fiber. Activity was not changed in low threshold fiber. The effect of IL1 beta and PGE were abolished by indomethacin. High threshold fibers which is not used in normal micturition reflex was activated inflammation related substances and increased the frequency of micturition and reduced the capacity of the urinary bladder.Parasympathetic preganglionic neurons (PGN) were divided into tonic PGN and phasic PGN on the basis of firing properties during prolonged (300ms) depolarizing current pulses. 4-Aminopyridine (4-AP) reduced the threshold for spike activation in tonic and phasic PGN.4-AP unmasked tonic firing in phasic PGN and increased firing frequency in tonic PGN.These data indicated that two types of PGN were present and may have different innervation to the targets in the pelvic viscera.