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Updated: Jun 13, 2026
Assessment of Perigenital Sensitivity and Prostatic Mast Cell Activation in a Mouse Model of Neonatal Maternal Separation
Published on: August 13, 2015
Neonatal maternal separation elevates thalamic corticotrophin releasing factor type 1 receptor expression response to
Yung Wui Tjong1, Siu Po Ip, Lixing Lao
1School of Chinese Medicine, The Chinese University of Hong Kong, Shatin, NT, China.
Insights
Neonatal maternal separation (NMS) in rats increases visceral pain sensitivity. This stress model shows elevated thalamic corticotrophin-releasing factor (CRF) and CRF type 1 receptor (CRF-R1) expression, linking early life stress to pain responses.
Area of Science:
- Neuroscience
- Gastroenterology
- Stress Research
Background:
- Early life psychological stress is a known contributor to irritable bowel syndrome (IBS).
- Corticotrophin-releasing factor (CRF) is implicated in the pathophysiology of IBS.
- Neonatal maternal separation (NMS) serves as a validated animal model for early life stress.
Purpose of the Study:
- To investigate the impact of NMS on brain CRF expression.
- To assess CRF levels in response to visceral pain stimuli (colorectal distension - CRD).
- To examine the role of CRF in the heightened pain response observed in NMS rats.
Main Methods:
- Male Sprague-Dawley rats underwent daily maternal separation from postnatal day 2-21 (NMS group) or were normally reared (control group).
- Visceral pain sensitivity was evaluated using colorectal distension (CRD) and measuring electromyogram (EMG) signals.
- CRF mRNA and protein levels in the hippocampus, cortex, and thalamus were quantified using real-time qPCR and Western blotting post-CRD.
Main Results:
- NMS rats exhibited increased pain response and EMG magnitudes to CRD compared to controls.
- Elevated mRNA and protein levels of CRF were found in the thalamus of NMS rats.
- A significant increase in CRF type 1 receptor (CRF-R1) expression was observed in the thalamus of NMS rats, while hippocampus and cortex showed no significant changes.
Conclusions:
- Neonatal maternal separation leads to visceral hyperalgesia in rats.
- Up-regulation of CRF and CRF-R1 in the thalamus is associated with stress-induced visceral hypersensitivity.
- These findings highlight the thalamus as a key brain region in the development of IBS-like symptoms following early life stress.
Objectives:
Early life psychological stress is an essential factor contributing to the development of irritable bowel syndrome (IBS), with corticotrophin releasing factor (CRF) having been implicated in this common gastrointestinal disorder. The aim of our study is to examine the effect of neonatal maternal separation (NMS), an early life stress model, on the brain CRF expression following visceral pain induced by colorectal distension (CRD) stimuli in male rats.
Methods:
Male neonatal Sprague-Dawley rats were subjected to 3-hr daily maternal separation on postnatal day 2-21, with unseparated normal (N) rats serving as controls. Electromyogram signals (EMG) in response to phasic CRD were measured. The results demonstrated an increased pain response and EMG magnitudes in NMS rats as compared to N rats in response to CRD stimulation. The mRNA and protein expressions of CRF in hippocampus, cortex and thalamus of NMS and N group following the CRD stress were determined by real-time quantitative PCR and western-blotting studies respectively.
Results:
There was an increased mRNA and protein level of CRF in thalamus of NMS rats but no apparent change in CRF expression in hippocampus and cortex of both groups. Furthermore, an increased expression of CRF type 1 receptor (CRF-R1) was observed in the thalamus of NMS rats.
Conclusion:
These results suggested an up-regulation of thalamus CRF-R1 is associated with visceral hyperalgesia in the rat model of NMS.
