Effects of water avoidance stress on peripheral and central responses during bladder filling in the rat: A multidisciplinary approach to the study of urologic chronic pelvic pain syndrome (MAPP) research network study.
Effects of water avoidance stress on peripheral and central responses during bladder filling in the rat: A multidisciplinary approach to the study of urologic chronic pelvic pain syndrome (MAPP) research network study.
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DOI：
10.1371/journal.pone.0182976
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发表时间：
2017
期刊：
影响因子：
3.7
通讯作者：
Rodriguez LV
中科院分区：
文献类型：
--
作者：
Wang Z;Chang HH;Gao Y;Zhang R;Guo Y;Holschneider DP;Rodriguez LV
压力在功能性下尿路疾病的恶化和可能的发展中起作用。啮齿类动物慢性避水应激（WAS）是一种结构和表面效度均较高的模型，可用于研究以尿频、膀胱痛觉过敏和应激反应性增强为特征的间质性膀胱炎/膀胱疼痛综合征（IC/BPS）等膀胱过敏综合征。考虑到压力、焦虑和排尿所涉及的大脑回路的重叠，我们评估了慢性压力对膀胱功能的影响，以及其对膀胱充盈期间局部大脑激活的影响。将雌性Wistar-Kyoto大鼠暴露于WAS（10天）或假模型。一天后，在滴定膀胱扩张期间获得膀胱测压图，同时记录内脏反应（VMR）。在被动膀胱扩张（20厘米水柱）后，静脉注射[14 C]-碘安替比林脑灌注进行了评估。局部脑血流量通过放射自显影进行定量，并在三维重建的大脑中进行统计参数映射分析。与对照组相比，WAS动物表现出降低的压力阈值和内脏阈值触发排尿期。在20 cmH 2 O时，WAS动物的VMR显著高于对照组。WAS动物在中枢排尿回路的皮质区域中表现出更大的激活，包括后扣带回、前压后、体感、后扣带回、眶和前次级（“补充”）运动皮质，以及丘脑、下丘脑前部、臂旁核和巴林顿核和纹状体。种子分析显示，与对照组动物相比，WAS的后扣带皮层与脑桥臂旁核的功能连接性增加;巴林顿核与前背中线和腹基底丘脑以及体感和压后皮层的功能连接性增加;以及后扣带皮层与前次级运动皮层的功能连接性增加。我们的研究结果表明，内脏超敏反应在膀胱填充在WAS动物，以及增加参与的部分排尿电路响应紧迫性，内脏感觉知觉和其中继到运动区域协调即将膀胱收缩。结果与最近在间质性膀胱炎患者中的发现一致，表明WAS可作为动物模型来阐明导致IC/BPS患者内脏敏感性脑表型的机制。
Stress plays a role in the exacerbation and possibly the development of functional lower urinary tract disorders. Chronic water avoidance stress (WAS) in rodents is a model with high construct and face validity to bladder hypersensitive syndromes, such as interstitial cystitis/bladder pain syndrome (IC/BPS), characterized by urinary frequency and bladder hyperalgesia and heightened stress responsiveness. Given the overlap of the brain circuits involved in stress, anxiety, and micturition, we evaluated the effects chronic stress has on bladder function, as well as its effects on regional brain activation during bladder filling. Female Wistar-Kyoto rats were exposed to WAS (10 days) or sham paradigms. One day thereafter, cystometrograms were obtained during titrated bladder dilation, with visceromotor responses (VMR) recorded simultaneously. Cerebral perfusion was assessed during passive bladder distension (20-cmH2O) following intravenous administration of [14C]-iodoantipyrine. Regional cerebral blood flow was quantified by autoradiography and analyzed in 3-dimensionally reconstructed brains with statistical parametric mapping. WAS animals compared to controls demonstrated a decreased pressure threshold and visceromotor threshold triggering the voiding phase. At 20-cmH2O, VMR was significantly greater in WAS animals compared to controls. WAS animals showed greater activation in cortical regions of the central micturition circuit, including the posterior cingulate, anterior retrosplenial, somatosensory, posterior insula, orbital, and anterior secondary (“supplementary”) motor cortices, as well as in the thalamus, anterior hypothalamus, parabrachial and Barrington nuclei, and striatum. Seed analysis showed increased functional connectivity of WAS compared to control animals of the posterior cingulate cortex to the pontine parabrachial nucleus; of the Barrington nucleus to the anterior dorsal midline and ventrobasilar thalamus and somatosensory and retrosplenial cortices; and of the posterior insula to anterior secondary motor cortex. Our findings show a visceral hypersensitivity during bladder filling in WAS animals, as well as increased engagement of portions of the micturition circuit responsive to urgency, viscerosensory perception and its relay to motor regions coordinating imminent bladder contraction. Results are consistent with recent findings in patients with interstitial cystitis, suggesting that WAS may serve as an animal model to elucidate the mechanisms leading to viscerosensitive brain phenotypes in humans with IC/BPS.
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DOI：
10.1093/cercor/bhq186
发表时间：
2011-07
期刊：
Cerebral cortex (New York, N.Y. : 1991)
影响因子：
--
作者：
Deen B;Pitskel NB;Pelphrey KA
通讯作者：
Pelphrey KA
影响因子：
6.6
作者：
Clemens, JQ;Meenan, RT;Calhoun, EA
通讯作者：
Calhoun, EA
影响因子：
14.5
作者：
Blok, BFM;Sturms, LM;Holstege, G
通讯作者：
Holstege, G
影响因子：
5.3
作者：
Asavasopon, Skulpan;Rana, Manku;Kutch, Jason J.
通讯作者：
Kutch, Jason J.
影响因子：
--
作者：
Griffiths, Derek
通讯作者：
Griffiths, Derek