Role of the spinal neural mechanism controlling the micturition in conjunction with descending pathways from Barrington's nucleus
Project/Area Number |
17591703
|
Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Urology
|
Research Institution | Tokyo Medical University |
Principal Investigator |
SASAKI Mitsuyoshi Tokyo Medical University, School of Medicine, Associate Professor (10170698)
|
Project Period (FY) |
2005 – 2007
|
Project Status |
Completed (Fiscal Year 2007)
|
Budget Amount *help |
¥3,710,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥210,000)
Fiscal Year 2007: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2006: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2005: ¥2,200,000 (Direct Cost: ¥2,200,000)
|
Keywords | micturition / bladder / external urethral sphincter / Barrington's nucleus / sacral / preganglionic neuron / motoneuron / Barrineton核 / 仙随 |
Research Abstract |
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
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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
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Report
(4 results)
Research Products
(2 results)