Neurogastroenterology in Spinal Cord Dysfunction

Holmes, Gregory M.; Hudson, Timothy R; Filart, Rosemarie

doi:10.1007/978-3-319-46293-6_16

Cited by 2 publications

(2 citation statements)

References 220 publications

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“…Damage of the supraspinal regulation of somatic and autonomic circuitry of the spinal cord was long thought to explain bowel dysfunction in patients with SCI. 2,3,12 However, the involvement of the ENS in these dysfunctions has been largely overlooked. Indeed, the ENS is an integrative neuronal network comprising more than 100 million neurons and 400 million enteric glial cells, which are distributed along the digestive tract and organized into two major ganglionated plexi-the myenteric plexus (or Auerbach's plexus) and the submucosal plexus (or Meissner's plexus).…”

Section: Introductionmentioning

confidence: 99%

Enteric Nervous System Remodeling in a Rat Model of Spinal Cord Injury: A Pilot Study

Lefèvre

Bessard

Arnaúd

et al. 2020

Neurotrauma Reports

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The physiopathology of digestive disorders in patients with spinal cord injury (SCI) remains largely unknown, particularly the involvement of the enteric nervous system (ENS). We aimed in a rat model of chronic thoracic SCI to characterize (1) changes in the neurochemical coding of enteric neurons and their putative consequences upon neuromuscular response, and (2) the inflammatory response of the colon. Ex vivo motility of proximal and distal colon segments of SCI and control (CT) rats were studied in an organ chamber in response to electrical field stimulation (EFS) and bethanechol. Immunohistochemical analysis of proximal and distal segments was performed using antibodies again Hu, neuronal nitric oxide synthase, (nNOS), and choline acetyltransferase. Colonic content of acetylcholine and acetylcholinesterase was measured; messenger RNA (mRNA) expression of inflammatory cytokines was measured using reverse transcription quantitative polymerase chain reaction (RT-qPCR) approaches. Compared with the CT rats, the contractile response to bethanechol was significantly decreased in the proximal colon of SCI rats but not in the distal colon. The proportion of nNOS immunoreactive (IR) neurons was significantly reduced in the proximal but not distal colon of SCI rats. No change in proportion of choline acetyltransferase (ChAT)-IR was reported; the tissue concentration of acetylcholine was significantly decreased in the proximal colon of SCI rats. The expression of tumor necrosis factor alpha (TNF-a) and intercellular adhesion molecule-1 (ICAM-1) was significantly reduced in the proximal and distal colon of SCI rats. This study demonstrates that functional motor and enteric neuroplastic changes affect preferentially the proximal colon compared with the distal colon. The underlying mechanisms and factors responsible for these changes remain to be discovered.

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Section: Introductionmentioning

confidence: 99%

Enteric Nervous System Remodeling in a Rat Model of Spinal Cord Injury: A Pilot Study

Lefèvre

Bessard

Arnaúd

et al. 2020

Neurotrauma Reports

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“…Bowel dysfunction is a multi-factorial consequence of SCI. Focus is often directed at the result of damage to the supraspinal regulation of somatic 7,8 and autonomic circuitry of the spinal cord [9][10][11] and is frequently compartmentalized as post-SCI deficits in storage and evacuation. The gastrointestinal tract, including the colon, however, is unique in that it has its own extensive intrinsic nervous system known as the enteric nervous system (ENS).…”

Section: Introductionmentioning

confidence: 99%

Anatomical and Functional Changes to the Colonic Neuromuscular Compartment after Experimental Spinal Cord Injury

White

Holmes

2018

Journal of Neurotrauma

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A profound reduction in colorectal transit time accompanies spinal cord injury (SCI), yet the colonic alterations after SCI have yet to be understood fully. The loss of descending supraspinal input to lumbosacral neural circuits innervating the colon is recognized as one causal mechanism. Remodeling of the colonic enteric nervous system/smooth muscle junction in response to inflammation, however, is recognized as one factor leading to colonic dysmotility in other pathophysiological models. We investigated the alterations to the neuromuscular junction in rats with experimental high-thoracic (T3) SCI. One day to three weeks post-injury, both injured and age-matched controls underwent in vivo experimentation followed by tissue harvest for histological evaluation. Spontaneous colonic contractions were reduced significantly in the proximal and distal colon of T3-SCI rats. Histological evaluation of proximal and distal colon demonstrated significant reductions of colonic mucosal crypt depth and width. Markers of intestinal inflammation were assayed by qRT-PCR. Specifically, Icam1, Ccl2 (MCP-1), and Ccl3 (MIP-1α) mRNA was acutely elevated after T3-SCI. Smooth muscle thickness and collagen content of the colon were increased significantly in T3-SCI rats. Colonic cross sections immunohistochemically processed for the pan-neuronal marker HuC/D displayed a significant decrease in colonic enteric neuron density that became more pronounced at three weeks after injury. Our data suggest that post-SCI inflammation and remodeling of the enteric neuromuscular compartment accompanies SCI. These morphological changes may provoke the diminished colonic motility that occurs during this same period, possibly through the disruption of intrinsic neuromuscular control of the colon.

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Neurogastroenterology in Spinal Cord Dysfunction

Cited by 2 publications

References 220 publications

Enteric Nervous System Remodeling in a Rat Model of Spinal Cord Injury: A Pilot Study

Enteric Nervous System Remodeling in a Rat Model of Spinal Cord Injury: A Pilot Study

Anatomical and Functional Changes to the Colonic Neuromuscular Compartment after Experimental Spinal Cord Injury

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