Diminished enteric neuromuscular transmission in the distal colon following experimental spinal cord injury

White, Amanda R; Werner, Caryn; Holmes, Gregory M.

doi:10.1016/j.expneurol.2020.113377

Cited by 12 publications

(17 citation statements)

References 63 publications

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“…Furthermore, only the responsiveness to a cholinergic agonist was explored and cell counts for cholinergic excitatory and nitrergic inhibitory enteric neurons were not performed nor were evoked responses in the form of smooth muscle junction potentials. Our previous report of reduced cholinergic and nitrergic myenteric neuron populations in SCI rats would be consistent with a loss‐of‐function, despite the increase in ICC networks 16 . Electrophysiological recording of smooth muscle membrane potential in response to pharmacologically targeted ICC activation would begin to clarify our understanding of how these increased ICC‐MP networks effect colonic function.…”

Section: Discussionsupporting

confidence: 55%

“…Our study explored the hypothesis that NB following T3‐SCI is accompanied by extensive depletion and/or remodeling of the distal colon ICC networks, reminiscent of the loss of enteric neurons we previously reported 15,16 . The net depletion of ICC is widely recognized to occur in GI motility disorders and has received considerable attention 20–23 .…”

Section: Discussionmentioning

confidence: 89%

“…Immediately following euthanasia, an incision was made along the linea alba to expose the abdominopelvic cavity. A segment of the distal colon (~1 cm long) was extracted and placed in ice cold oxygenated Krebs solution as previously described 16 . The extracted colon was placed in a Sylgard lined petri dish and fresh Krebs solution was replaced every 15 min.…”

Section: Methodsmentioning

confidence: 99%

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Plasticity of colonic enteric nervous system following spinal cord injury in male and female rats

Werner

Willing

Goudsward

et al. 2023

Neurogastroenterology Motil

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BackgroundNeurogenic bowel is a dysmotility disorder following spinal cord injury (SCI) that negatively impacts quality of life, social integration, and physical health. Colonic transit is directly modulated by the enteric nervous system. Interstitial Cells of Cajal (ICC) distributed throughout the small intestine and colon serve as specialized pacemaker cells, generating rhythmic electrical slow waves within intestinal smooth muscle, or serve as an interface between smooth muscle cells and enteric motor neurons of the myenteric plexus. Interstitial Cells of Cajal loss has been reported for other preclinical models of dysmotility, and our previous experimental SCI study provided evidence of reduced excitatory and inhibitory enteric neuronal count and smooth muscle neural control.MethodsImmunohistochemistry for the ICC‐specific marker c‐Kit was utilized to examine neuromuscular remodeling of the distal colon in male and female rats with experimental SCI.Key ResultsMyenteric plexus ICC (ICC‐MP) exhibited increased cell counts 3 days following SCI in male rats, but did not significantly increase in females until 3 weeks after SCI. On average, ICC‐MP total primary arborization length increased significantly in male rats at 3‐day, 3‐week, and 6‐week time points, whereas in females, this increase occurred most frequently at 6 weeks post‐SCI. Conversely, circular muscle ICC (ICC‐CM) did not demonstrate post‐SCI changes.Conclusions and InferencesThese data demonstrate resiliency of the ICC‐MP in neurogenic bowel following SCI, unlike seen in other related disease states. This plasticity underscores the need to further understand neuromuscular changes driving colonic dysmotility after SCI in order to advance therapeutic targets for neurogenic bowel treatment.

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Section: Discussionsupporting

confidence: 55%

Section: Discussionmentioning

confidence: 89%

Section: Methodsmentioning

confidence: 99%

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Plasticity of colonic enteric nervous system following spinal cord injury in male and female rats

Werner

Willing

Goudsward

et al. 2023

Neurogastroenterology Motil

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“…It has been studied to exclude the influence of sympathetic and parasympathetic on intestinal tract by injuring the high level thoracic spinal cord, in the mice with T8 SCI, it found that the number of nitroergic nerve cells decreased, and the number of acetylcholine decreased although the proportion of acetylcholinergic nerve did not change significantly ( Lefèvre et al, 2020 ). Another study found that nitroergic and cholinergic neurons decreased in the mice with T3 SCI ( White et al, 2020 ). These results suggest that the ENS is damaged after SCI, which lead to the destruction of colonic content secretion, propulsion and local reflex regulation related to colonic segmentation ( Furness et al, 2014 ).…”

Section: Spinal Cord Injury and Intestinal Microbiotamentioning

confidence: 99%

Intestinal microbiota and melatonin in the treatment of secondary injury and complications after spinal cord injury

Zhang

Lang²,

Guo³

et al. 2022

Front. Neurosci.

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Spinal cord injury (SCI) is a central nervous system (CNS) disease that can cause sensory and motor impairment below the level of injury. Currently, the treatment scheme for SCI mainly focuses on secondary injury and complications. Recent studies have shown that SCI leads to an imbalance of intestinal microbiota and the imbalance is also associated with complications after SCI, possibly through the microbial-brain-gut axis. Melatonin is secreted in many parts of the body including pineal gland and gut, effectively protecting the spinal cord from secondary damage. The secretion of melatonin is affected by circadian rhythms, known as the dark light cycle, and SCI would also cause dysregulation of melatonin secretion. In addition, melatonin is closely related to the intestinal microbiota, which protects the barrier function of the gut through its antioxidant and anti-inflammatory effects, and increases the abundance of intestinal microbiota by influencing the metabolism of the intestinal microbiota. Furthermore, the intestinal microbiota can influence melatonin formation by regulating tryptophan and serotonin metabolism. This paper summarizes and reviews the knowledge on the relationship among intestinal microbiota, melatonin, and SCI in recent years, to provide new theories and ideas for clinical research related to SCI treatment.

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“…Transmission refers to the time it takes for food or other substances to pass through a specific area of the intestine, reflecting the overall result of the interaction of a variety of intricate parameters (contraction activity, tension, compliance, etc.) [ 20 ]. In addition to the realization of propulsive movement, the motor function of the colon also includes receptivity or storage and rapid emptying during defecation.…”

Section: Introductionmentioning

confidence: 99%

Interaction between the Gut Microbiota and Intestinal Motility

Liu

Luo

2022

Evidence-Based Complementary and Alternative Medicine

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The gut microbiota is the largest symbiotic ecosystem with the host and has been proven to play an important role in maintaining the stability of the intestinal environment. The imbalance of the gut microbiota is caused by the imbalance between the symbiotic microbiota and the pathogenic microbiota. The commensal microbiome regulates intestinal motility, while the pathogenic microbiome causes intestinal motility disorder, resulting in disease development. Intestinal motility is a relatively general term, and its meaning may include intestinal muscle contraction, intestinal wall biomechanics, intestinal compliance, and transmission. The role of intestinal microecology and intestinal motility are interrelated, intestinal flora disorder mediates intestinal motility, and abnormal intestinal motility affects colonization of the intestinal flora. In this review, we briefly outlined the interaction between gut microbiota and intestinal motility and provided a reference for future studies.

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Diminished enteric neuromuscular transmission in the distal colon following experimental spinal cord injury

Cited by 12 publications

References 63 publications

Plasticity of colonic enteric nervous system following spinal cord injury in male and female rats

Plasticity of colonic enteric nervous system following spinal cord injury in male and female rats

Intestinal microbiota and melatonin in the treatment of secondary injury and complications after spinal cord injury

Interaction between the Gut Microbiota and Intestinal Motility

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