Changes of excitatory and inhibitory neurotransmitters in the colon of rats underwent to the wrap partial restraint stress

Abstract

Background

Animal models proposed to reproduce some of the human irritable bowel syndrome (IBS) symptoms are based on the hypothesis that psychosocial stressors play a pivotal role in the IBS etio-pathology.

We investigated the wrap restraint stress (WRS) model with the aim to analyze the morphological changes of the entire colonic wall of these animals that showed some of the human IBS symptoms such as visceral hypersensitivity.

Methods

Male Wistar rats were used and WRS was maintained for 2 h. Abdominal contractions (AC) were recorded in the colon-rectum by balloon distension. Fecal pellets were quantitated. Colonic specimens were examined by routine histology, immunohistochemistry and western blot.

Key Results

WRS animals were characterized by: (i) increase in AC number and fecal pellets mean weight; (ii) clusters of mononucleated cells, increase in eosinophilic granulocytes and mast cells in the mucosa; (iii) increase in CGRP-immunoreactive (IR) nerve fibers in the lamina propria; (iv) decrease in myenteric NK1r-IR and nNOS-IR neurons and in submucous nNOS-IR neurons; (v) decrease in SP-IR nerve fibers in the muscle wall; (vi) reduction in S100β-IR glia in the entire colonic wall; (vii) increase in CRF1r-IR myenteric neurons; (viii) no change in ChAT-IR neurons, smooth muscle cells and interstitial cells of Cajal.

Conclusions and Inferences

The present results support the consistency of the WRS as a potential model where part of the human IBS signs and symptoms are reproduced. The changes in glial cells and in excitatory and inhibitory neurotransmitters might represent the substrate for the dysmotility and hypersensitivity.

This study aims to investigate possible morphological changes in the colonic wall of wrap restraint stress (WRS) rats and correlates the results with functional data to improve our understanding of irritable bowel syndrome (IBS) pathogenesis. WRS was maintained for 2 h. At the end, fecal pellets were quantitated and abdominal contractions were recorded in the colon-rectum. Colonic specimens were examined by histology, immunohistochemistry, and western blot. The functional data showed a significant increase in fecal pellet production and the presence of a visceral hypersensitivity. The morphological findings showed the presence of a mucosal inflammation and important changes in nerve structures. The present results support the consistency of the WRS as a potential model for understanding IBS pathogenesis. The changes in nerve structures might represent the main substrates for dysmotility and visceral hypersensitivity. This is the first report of an increase in CRF1r expressing neurons. This datum fits well with the role of the receptor in mediating the stress responses and supports our hypothesis that changes in neurotransmission are mainly involved in the genesis of colonic dysmotility.

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