# Neuromolecular Mechanisms of Chronic Pelvic Pain in Neonatally-induced Cystitis

> **NIH NIH R01** · MEDICAL COLLEGE OF WISCONSIN · 2020 · $560,466

## Abstract

SUMMARY
There is a growing interest to understand how painful events in the neonatal period affect the development of
nociceptive neural circuitry and alters pain perception in adulthood. Accumulating evidence from clinical studies
indicates that the pain experience as a child has a significant impact on the pain responses at adulthood. Pre-
clinical studies also clearly demonstrated that the exposure to noxious stimuli early in life causes long-term
alterations in sensory processing. However, the etiology of chronic pelvic pain (CPP) is complex and poorly
defined. The NIDDK has estimated that CPP is responsible for 4,137,000 outpatient or clinic visits/year and
about 90% of them are female. Recent study also indicates that estimated medical cost for treating CPP exceeds
$2 billion/year. The focus of our ongoing NIH application (R01 DK099201-01A1) is to study how the pain
signaling pathway from the bladder to the spinal cord alters following neonatal bladder inflammation in rats.
During this funding period, we have established for the first time the involvement of miRNAs (noncoding small
RNAs) in post-transcriptional suppression of the developing spinal GABAergic system and long-term visceral
hypersensitivity in a model of neonatal zymosan-induced cystitis. However, little is known regarding the
involvement of supraspinal descending pain modulatory systems in spinal hyperexcitability following this early-
life induced cystitis in rats.
In this competitive renewal application, we would like to extend our study to investigate further the contribution
of higher brain regions including midbrain PAG-RVM axis in the development of CPP in neonatal-cystitis rats.
We will test the hypothesis that the long-lasting spinal sensitization following intense painful visceral stimulus in
early-life is due to i) altered functional connectivity between PAG and higher brain regions ii) altered functional
characteristics of RVM neurons projecting to spinal cord, and (iii) miRNA-mediated post-transcriptional
dysregulation of pain modulatory neurons in the RVM. The proposed experiments will be systematic
investigation to explore the intrinsic neuromolecular mechanisms and functional changes of descending pain
modulation in neonatal cystitis-induced CPP. The identification of differentially expressed RVM miRNAs and
molecular characterization of neuronal plasticity in the RVM neuron are of significance in designing receptor
and/or miRNA-based pharmacological manipulation for better detection and therapeutic targeting of CPP.

## Key facts

- **NIH application ID:** 9968320
- **Project number:** 5R01DK099201-07
- **Recipient organization:** MEDICAL COLLEGE OF WISCONSIN
- **Principal Investigator:** BANANI B BANERJEE
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $560,466
- **Award type:** 5
- **Project period:** 2014-08-05 → 2022-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9968320

## Citation

> US National Institutes of Health, RePORTER application 9968320, Neuromolecular Mechanisms of Chronic Pelvic Pain in Neonatally-induced Cystitis (5R01DK099201-07). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/9968320. Licensed CC0.

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