Chen Pengfei, Yang Lei, Tong Yu, Meng Li, Zhou Renyuan
Department of Urology, Jing'an District Central Hospital, Fudan University, Shanghai, China.
Neurourol Urodyn. 2022 Apr;41(4):894-904. doi: 10.1002/nau.24890. Epub 2022 Feb 27.
We aimed to explore if the intracerebroventricular (i.c.v.) injection of lipopolysaccharide (LPS) was able to evoke the cognitive and locomotive impairment and detrusor overactivity (DO) symptoms in mice.
This study compared the bladder function of mice that received the i.c.v. injection of LPS or saline. Specifically, basal pressure (BP), threshold pressure (TP), micturition pressure (MP), bladder capacity (BC), micturition volume (MV), bladder compliance (COM), frequency of micturition (MF), detrusor overactive index (DOI), frequency of non-voiding contractions (FNVCs), and amplitude of non-voiding contractions (ANVCs) were assessed by cystometry. The spontaneous voiding spot assay (VSA) was exerted to further assess the micturition patterns of mice. The Morris water maze (MWM) and the open field test (OFT) were used to detect the cognition and locomotive behaviors, respectively. Hematoxylin and eosin staining was conducted to evaluate the changes in morphology and histology of mice. The extent of injury in the prefrontal cortex was tested by using Nissl staining.
The LPS-treated mice exhibited evidently DO characterized by the increase of MF, FNVCs, ANVCs, and DOI and the decrease of BC. The VSA further suggested that LPS induced urinary frequency and urinary incontinence in mice. Furthermore, neither signs of bladder inflammation nor the damage of bladder smooth muscle and urothelium in LPS-exposed mice was observed. LPS induced deficits in spatial learning, memory, and locomotor activity in mice. Neuronal cells in the prefrontal cortex were obviously lost in the LPS-treated mice.
Acute neuroinflammation induced the cognitive and locomotive impairment and the neurogenic overactive bladder (NOAB) symptoms in mice. This novel animal model may contribute to further study the mechanisms of NOAB in neurodegenerative patients and assess the novel therapeutic strategies in the future.
我们旨在探究脑室内（i.c.v.）注射脂多糖（LPS）是否能够诱发小鼠的认知和运动障碍以及逼尿肌过度活动（DO）症状。
本研究比较了接受i.c.v.注射LPS或生理盐水的小鼠的膀胱功能。具体而言，通过膀胱测压评估基础压力（BP）、阈值压力（TP）、排尿压力（MP）、膀胱容量（BC）、排尿量（MV）、膀胱顺应性（COM）、排尿频率（MF）、逼尿肌过度活动指数（DOI）、非排尿收缩频率（FNVCs）和非排尿收缩幅度（ANVCs）。采用自发排尿点试验（VSA）进一步评估小鼠的排尿模式。分别使用莫里斯水迷宫（MWM）和旷场试验（OFT）检测认知和运动行为。进行苏木精-伊红染色以评估小鼠的形态和组织学变化。使用尼氏染色检测前额叶皮质的损伤程度。
LPS处理的小鼠表现出明显的DO，其特征为MF、FNVCs、ANVCs和DOI增加以及BC降低。VSA进一步表明LPS诱导小鼠尿频和尿失禁。此外，未观察到LPS暴露小鼠的膀胱炎症迹象以及膀胱平滑肌和尿路上皮的损伤。LPS诱导小鼠出现空间学习、记忆和运动活动缺陷。LPS处理的小鼠前额叶皮质中的神经元细胞明显丢失。
急性神经炎症诱发小鼠的认知和运动障碍以及神经源性膀胱过度活动（NOAB）症状。这种新型动物模型可能有助于进一步研究神经退行性疾病患者中NOAB的机制，并在未来评估新型治疗策略。
