Abdominal pain frequently accompanies inflammatory disorders of the gastrointestinal tract (GIT), and animal models of GIT inflammation have been developed to explore the role of the central nervous system (CNS) in this process. Here, we summarize the evidence from animal studies for CNS plasticity following GIT inflammation.
A systematic review was conducted to identify studies that: (1) used inflammation of GIT organs, (2) assessed pain or visceral hypersensitivity, and (3) presented evidence of CNS involvement. Two hundred and eight articles were identified, and 79 were eligible for analysis.
Rats were most widely used (76%). Most studies used adult animals (42%) with a bias toward males (74%). Colitis was the most frequently used model (78%) and 2,4,6-trinitrobenzenesulfonic acid the preferred inflammatory agent (33%). Behavioral (58%), anatomical/molecular (44%), and physiological (24%) approaches were used alone or in combination to assess CNS involvement during or after GIT inflammation. Measurement times varied widely (<1 h–> 2 wk after inflammation). Blinded outcomes were used in 42% studies, randomization in 10%, and evidence of visceral inflammation in 54%. Only 3 studies fulfilled our criteria for high methodological quality, and no study reported sample size calculations.
The included studies provide strong evidence for CNS plasticity following GIT inflammation, specifically in the spinal cord dorsal horn. This evidence includes altered visceromotor responses and indices of referred pain, elevated neural activation and peptide content, and increased neuronal excitability. This evidence supports continued use of this approach for preclinical studies; however, there is substantial scope to improve study design.