Cited by 77Gastrointestinal motility and disordersPain Mechanisms and TreatmentsNeuropeptides and Animal Physiology

Neural plasticity in the gastrointestinal tract: chronic inflammation, neurotrophic signals, and hypersensitivity

Demir, Ihsan Ekin, Schäfer, Karl-Herbert, Tieftrunk, Elke, Friess, Helmut, Ceyhan, Güralp O.·2013·Acta Neuropathologica

Abstract

Neural plasticity is not only the adaptive response of the central nervous system to learning, structural damage or sensory deprivation, but also an increasingly recognized common feature of the gastrointestinal (GI) nervous system during pathological states. Indeed, nearly all chronic GI disorders exhibit a disease-stage-dependent, structural and functional neuroplasticity. At structural level, GI neuroplasticity usually comprises local tissue hyperinnervation (neural sprouting, neural, and ganglionic hypertrophy) next to hypoinnervated areas, a switch in the neurochemical (neurotransmitter/neuropeptide) code toward preferential expression of neuropeptides which are frequently present in nociceptive neurons (e.g., substance P/SP, calcitonin-gene-related-peptide/CGRP) and of ion channels (TRPV1, TRPA1, PAR2), and concomitant activation of peripheral neural glia. The functional counterpart of these structural alterations is altered neuronal electric activity, leading to organ dysfunction (e.g., impaired motility and secretion), together with reduced sensory thresholds, resulting in hypersensitivity and pain. The present review underlines that neural plasticity in all GI organs, starting from esophagus, stomach, small and large intestine to liver, gallbladder, and pancreas, actually exhibits common phenotypes and mechanisms. Careful appraisal of these GI neuroplastic alterations reveals that--no matter which etiology, i.e., inflammatory, infectious, neoplastic/malignant, or deg…

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Crossref · 10.1007/s00401-013-1099-4

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  • The ENS maintains its capacity to adapt and reorganize its synapses throughout the host's lifetime, similar to synaptic plasticity in the CNS.

    “Much like the CNS, the ENS maintains its capacity to adapt and reorganize its synapses throughout the host's lifetime, similar to synaptic plasticity in the CNS (Demir et al., 2013;Lomax et al., 2005).”

    From The Microbiota-Gut-Brain Axis (2019) · cites this paper as Demir et al., 2013

  • Neuronal plastic changes also occur in the enteric nervous system.

    “recently it has become ever more apparent that neuronal plastic changes also occur in the ENS (Demir et al., 2013;Lomax et al., 2005).”

    From The Microbiota-Gut-Brain Axis (2019) · cites this paper as Demir et al., 2013

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Authors
Demir, I. E., Schäfer, K.-H., Tieftrunk, E., Friess, H., & Ceyhan, G. O.
Affiliations
  • University of Applied Sciences Kaiserslautern (DE)
  • TUM Klinikum (DE)
Venue
Acta Neuropathologica
Published
2013-02-17
Volume
125
Issue
4
Pages
491-509
ISSN
  • 0001-6322 (ISSN-L)
  • 1432-0533
OpenAlex
W1977884263
Cited by
77
References
121
Citations by year
2026: 3 · 2025: 3 · 2024: 2 · 2023: 6 · 2022: 7 · 2021: 5 · 2020: 7 · 2019: 9 · 2018: 1 · 2017: 7 · 2016: 5 · 2015: 14 · 2014: 4 · 2013: 4
FWCI
1.44
Type
journal article
Language
en
Open access
closed
Locations
  • Acta Neuropathologica (publishedVersion)
  • PubMed (publishedVersion)
  • mediaTUM (Technical University of Munich) (submittedVersion)
Topics
  • Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
  • Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
Keywords
neuroplasticity, chronic inflammation, hypersensitivity, visceral pain, hyperinnervation, neuropeptides, substance P, calcitonin gene-related peptide, ion channels, TRPV1, TRPA1, PAR2, peripheral glia, neuroimmune interactions, gastrointestinal motility, gastrointestinal secretion
MeSH terms
Humans, Inflammation, Neuronal Plasticity, Neurons, Nociceptors, Calcitonin Gene-Related Peptide, Gastrointestinal Tract, TRPV Cation Channels

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