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Functional MRI Analysis of Brain Activity in Rats With Diabetic Bladder Dysfunction
Mingzhuo Li1, Xun Chen1, JingJing Ye2
1Department of Urology, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
CNS Neuroscience & Therapeutics
|June 3, 2025
Summary
Diabetic bladder dysfunction in rats alters brain activity, showing reduced cortical function and increased thalamic and periaqueductal gray activation during micturition. The drug NLX-112 did not impact these brain changes.
Area of Science:
- Neuroscience
- Urology
- Medical Imaging
Background:
- Diabetic bladder dysfunction (DBD) is a common complication of diabetes mellitus.
- Altered brain activity patterns are increasingly recognized in various chronic conditions.
- Previous research suggests 5-HT1A receptor agonists may offer therapeutic benefits for DBD.
Purpose of the Study:
- To investigate brain activity alterations in rats with 12-week diabetic bladder dysfunction (DBD) using functional magnetic resonance imaging (fMRI).
- To explore the effects of NLX-112, a selective 5-HT1A receptor agonist, on brain activity in DBD rats.
Main Methods:
- Male Sprague-Dawley rats with 12-week DBD and normal controls underwent cystometry and 9.4-Tesla fMRI.
- Resting-state fMRI was used to compare baseline brain activity.
- fMRI assessed brain activation during micturition versus relaxation.
Main Results:
- Diabetic rats showed reduced amplitude of low-frequency fluctuation (ALFF) in the basal forebrain and cerebral cortex.
- During micturition, diabetic rats exhibited increased activation in the thalamus, primary motor cortex, and periaqueductal gray (PAG).
- NLX-112 administration did not significantly alter brain activity in diabetic rats.
Conclusions:
- Diabetic bladder dysfunction is associated with altered brain activity, including heightened thalamic and PAG activity during micturition.
- Cortical activity may act as a compensatory mechanism in response to bladder dysfunction.
- These findings identify potential neural targets for therapeutic interventions in DBD.
