Role of the spinal neural mechanism controlling the micturition in conjunction with descending pathways from Barrington's nucleus

利用神经元追踪技术，已证明巴林顿核或脑桥排尿中心直接投射到支配膀胱肌的骶节前神经元。在麻醉猫中，我们用电生理技术研究了这个核是否与骶神经节前神经元直接相连。从骶神经节前神经元进行细胞内记录。当膀胱压力较低时，单次至三次电击Barrington核在节前神经元中未诱发或诱发微弱的EPSP。事实上，Barrington核需要30-50串脉冲的刺激才能引起膀胱收缩。另一方面，单一电击Barrington核后，在排尿期可诱发出清晰的EPSP。在节前神经元中均未发现EPSPs的固定，表明EPSPs是多突触诱发的。进一步研究了来自Barrington核的输入和膀胱传入的相互作用。电 关于我们 刺激盆腔传入神经诱发的IPSPs与骶神经节前神经元，支配膀胱短的laveling。这些IPSP是通过脊髓神经通路诱发的。电刺激Barrington核可抑制IPSPs。结果表明，Barrington核和骶神经节前神经元之间没有直接联系，并且在排尿期促进了从Barrington核到骶神经节前神经元的下行通路。这些结果也支持了先前的假设，即巴林顿神经元可能参与激活脊髓兴奋性通路或解除抑制一个强抑制性神经机制，防止节前神经元放电容易。并观察了尿道外括约肌运动神经元的排尿通路。电刺激盆神经可诱发短潜伏期的EPSP和长潜伏期的IPSP：前者通过脊髓神经回路诱发。刺激Barrington核诱发括约肌运动神经元的IPSPs，其潜伏期与盆神经诱发的IPSPs相当。背侧灰质连合中的神经元被发现与排尿收缩一致。刺激该部位可抑制尿道外括约肌的放电活动。结果支持Barrington核通过位于背侧灰质连合的抑制性中间神经元抑制尿道外括约肌运动神经元的观点。少

Barrington's nucleus, or pontine micturition center, has been shown to project directly to the sacral preganglionic neurons that innervate the bladder muscle, using neuron tracing technique. We examined whether this nucleus connects directly to sacral preganglionic neurons in anesthetized cats, using electrophysiological technique. Intracellular recordings were made from sacral preganglionic neurons. Single to three electrical shocks applied to Barrington's nucleus evoked no or weak EPSPs in preganglionic neurons when the bladder pressure was low. In fact, stimulation of 30-50 train pulses was needed for Barrington's nucleus to evoke bladder contraction. On the other hand, clear EPSPs were evoked during voiding phase after a single shock to Barrington's nucleus. Latencies of EPSPs were not fixed in any preganglionic neurons, indicating that EPSPs were evoked polysynaptically. Interaction of inputs from Barrington's nucleus and the bladder afferents were further investigated. Electrical … More stimulation of the pelvic afferents evoked IPSPs with short latencies on the sacral preganglionic neurons that innervate the bladder. These IPSPs were evoked via spinal neural pathways. Electrical stimulation of Barrington's nucleus suppressed the IPSPs. The observations suggested that there is no direct connection between Barrington's nucleus and sacral preganglionic neurons, and that the descending pathway from Barrington's nucleus to sacral preganglionic neurons is facilitated during the voiding phase. The results also support the previous hypothesis that Barrington's neurons may participate in either activating the spinal excitatory pathway or disinhibiting a strong inhibitory neural mechanism that prevents preganglionic neurons from discharging easily. The micturition pathway to the external urethral sphincter motoneurons was also investigated. Electrical stimulation of the pelvic nerve evoked EPSPs with short latencies and IPSPs with long latency on the external urethral sphincter motoneurons : the former were evoked via a spinal neural circuit. Stimulation of Barrington's nucleus evoked IPSPs in the sphincter motoneurons, the latency of which was comparable to those IPSPs that were evoked by the pelvic nerve. Neurons in the dorsal gray commissure were found to fire in concert with micturition contraction. Stimulation of this site depressed the firing activity of the external urethral sphincter. The results supported the idea that Barrington's nucleus inhibits the external urethral sphincter motoneuron via inhibitory intemeurons located in the dorsal gray commissure. Less