Upper gastrointestinal dysmotility after spinal cord injury

Is diminished vagal sensory processing one culprit?

Research output: Contribution to journalReview article

15 Citations (Scopus)

Abstract

Despite the widely recognized prevalence of gastric, colonic, and anorectal dysfunction after spinal cord injury (SCI), significant knowledge gaps persist regarding the mechanisms leading to post-SCI gastrointestinal (GI) impairments. Briefly, the regulation of GI function is governed by a mix of parasympathetic, sympathetic, and enteric neurocircuitry. Unlike the intestines, the stomach is dominated by parasympathetic (vagal) control whereby gastric sensory information is transmitted via the afferent vagus nerve to neurons of the nucleus tractus solitarius (NTS). The NTS integrates this sensory information with signals from throughout the central nervous system. Glutamatergic and GABAergic NTS neurons project to other nuclei, including the preganglionic parasympathetic neurons of the dorsal motor nucleus of the vagus (DMV). Finally, axons from the DMV project to gastric myenteric neurons, again, through the efferent vagus nerve. SCI interrupts descending input to the lumbosacral spinal cord neurons that modulate colonic motility and evacuation reflexes. In contrast, vagal neurocircuitry remains anatomically intact after injury. This review presents evidence that unlike the post-SCI loss of supraspinal control which leads to colonic and anorectal dysfunction, gastric dysmotility occurs as an indirect or secondary pathology following SCI. Specifically, emerging data points toward diminished sensitivity of vagal afferents to GI neuroactive peptides, neurotransmitters and, possibly, macronutrients. The neurophysiological properties of rat vagal afferent neurons are highly plastic and can be altered by injury or energy balance. A reduction of vagal afferent signaling to NTS neurons may ultimately bias NTS output toward unregulated GABAergic transmission onto gastric-projecting DMV neurons. The resulting gastroinhibitory signal may be one mechanism leading to upper GI dysmotility following SCI.

Original languageEnglish (US)
Article numberArticle 277
JournalFrontiers in Physiology
Volume3 JUL
DOIs
StatePublished - Sep 25 2012

Fingerprint

Solitary Nucleus
Spinal Cord Injuries
Stomach
Neurons
Vagus Nerve
Afferent Neurons
Wounds and Injuries
Motor Neurons
Plastics
Intestines
Neurotransmitter Agents
Axons
Reflex
Spinal Cord
Central Nervous System
Pathology
Peptides

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)

Cite this

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title = "Upper gastrointestinal dysmotility after spinal cord injury: Is diminished vagal sensory processing one culprit?",
abstract = "Despite the widely recognized prevalence of gastric, colonic, and anorectal dysfunction after spinal cord injury (SCI), significant knowledge gaps persist regarding the mechanisms leading to post-SCI gastrointestinal (GI) impairments. Briefly, the regulation of GI function is governed by a mix of parasympathetic, sympathetic, and enteric neurocircuitry. Unlike the intestines, the stomach is dominated by parasympathetic (vagal) control whereby gastric sensory information is transmitted via the afferent vagus nerve to neurons of the nucleus tractus solitarius (NTS). The NTS integrates this sensory information with signals from throughout the central nervous system. Glutamatergic and GABAergic NTS neurons project to other nuclei, including the preganglionic parasympathetic neurons of the dorsal motor nucleus of the vagus (DMV). Finally, axons from the DMV project to gastric myenteric neurons, again, through the efferent vagus nerve. SCI interrupts descending input to the lumbosacral spinal cord neurons that modulate colonic motility and evacuation reflexes. In contrast, vagal neurocircuitry remains anatomically intact after injury. This review presents evidence that unlike the post-SCI loss of supraspinal control which leads to colonic and anorectal dysfunction, gastric dysmotility occurs as an indirect or secondary pathology following SCI. Specifically, emerging data points toward diminished sensitivity of vagal afferents to GI neuroactive peptides, neurotransmitters and, possibly, macronutrients. The neurophysiological properties of rat vagal afferent neurons are highly plastic and can be altered by injury or energy balance. A reduction of vagal afferent signaling to NTS neurons may ultimately bias NTS output toward unregulated GABAergic transmission onto gastric-projecting DMV neurons. The resulting gastroinhibitory signal may be one mechanism leading to upper GI dysmotility following SCI.",
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Upper gastrointestinal dysmotility after spinal cord injury : Is diminished vagal sensory processing one culprit? / Holmes, Gregory.

In: Frontiers in Physiology, Vol. 3 JUL, Article 277, 25.09.2012.

Research output: Contribution to journalReview article

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T2 - Is diminished vagal sensory processing one culprit?

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PY - 2012/9/25

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N2 - Despite the widely recognized prevalence of gastric, colonic, and anorectal dysfunction after spinal cord injury (SCI), significant knowledge gaps persist regarding the mechanisms leading to post-SCI gastrointestinal (GI) impairments. Briefly, the regulation of GI function is governed by a mix of parasympathetic, sympathetic, and enteric neurocircuitry. Unlike the intestines, the stomach is dominated by parasympathetic (vagal) control whereby gastric sensory information is transmitted via the afferent vagus nerve to neurons of the nucleus tractus solitarius (NTS). The NTS integrates this sensory information with signals from throughout the central nervous system. Glutamatergic and GABAergic NTS neurons project to other nuclei, including the preganglionic parasympathetic neurons of the dorsal motor nucleus of the vagus (DMV). Finally, axons from the DMV project to gastric myenteric neurons, again, through the efferent vagus nerve. SCI interrupts descending input to the lumbosacral spinal cord neurons that modulate colonic motility and evacuation reflexes. In contrast, vagal neurocircuitry remains anatomically intact after injury. This review presents evidence that unlike the post-SCI loss of supraspinal control which leads to colonic and anorectal dysfunction, gastric dysmotility occurs as an indirect or secondary pathology following SCI. Specifically, emerging data points toward diminished sensitivity of vagal afferents to GI neuroactive peptides, neurotransmitters and, possibly, macronutrients. The neurophysiological properties of rat vagal afferent neurons are highly plastic and can be altered by injury or energy balance. A reduction of vagal afferent signaling to NTS neurons may ultimately bias NTS output toward unregulated GABAergic transmission onto gastric-projecting DMV neurons. The resulting gastroinhibitory signal may be one mechanism leading to upper GI dysmotility following SCI.

AB - Despite the widely recognized prevalence of gastric, colonic, and anorectal dysfunction after spinal cord injury (SCI), significant knowledge gaps persist regarding the mechanisms leading to post-SCI gastrointestinal (GI) impairments. Briefly, the regulation of GI function is governed by a mix of parasympathetic, sympathetic, and enteric neurocircuitry. Unlike the intestines, the stomach is dominated by parasympathetic (vagal) control whereby gastric sensory information is transmitted via the afferent vagus nerve to neurons of the nucleus tractus solitarius (NTS). The NTS integrates this sensory information with signals from throughout the central nervous system. Glutamatergic and GABAergic NTS neurons project to other nuclei, including the preganglionic parasympathetic neurons of the dorsal motor nucleus of the vagus (DMV). Finally, axons from the DMV project to gastric myenteric neurons, again, through the efferent vagus nerve. SCI interrupts descending input to the lumbosacral spinal cord neurons that modulate colonic motility and evacuation reflexes. In contrast, vagal neurocircuitry remains anatomically intact after injury. This review presents evidence that unlike the post-SCI loss of supraspinal control which leads to colonic and anorectal dysfunction, gastric dysmotility occurs as an indirect or secondary pathology following SCI. Specifically, emerging data points toward diminished sensitivity of vagal afferents to GI neuroactive peptides, neurotransmitters and, possibly, macronutrients. The neurophysiological properties of rat vagal afferent neurons are highly plastic and can be altered by injury or energy balance. A reduction of vagal afferent signaling to NTS neurons may ultimately bias NTS output toward unregulated GABAergic transmission onto gastric-projecting DMV neurons. The resulting gastroinhibitory signal may be one mechanism leading to upper GI dysmotility following SCI.

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U2 - 10.3389/fphys.2012.00277

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