Intercellular communication and ion channels in neuropathic pain chronicization
- 1 September 2020
- journal article
- review article
- Published by Springer Science and Business Media LLC in Inflammation Research
- Vol. 69 (9), 841-850
- https://doi.org/10.1007/s00011-020-01363-9
Abstract
Background Neuropathic pain is caused by primary lesion or dysfunction of either peripheral or central nervous system. Due to its complex pathogenesis, often related to a number of comorbidities, such as cancer, neurodegenerative and neurovascular diseases, neuropathic pain still represents an unmet clinical need, lacking long-term effective treatment and complex case-by-case approach. Aim and methods We analyzed the recent literature on the role of selective voltage-sensitive sodium, calcium and potassium permeable channels and non-selective gap junctions (GJs) and hemichannels (HCs) in establishing and maintaining chronic neuropathic conditions. We finally focussed our review on the role of extracellular microenvironment modifications induced by resident glial cells and on the recent advances in cell-to-cell and cell-to-extracellular environment communication in chronic neuropathies. Conclusion In this review, we provide an update on the current knowledge of neuropathy chronicization processes with a focus on both neuronal and glial ion channels, as well as on channel-mediated intercellular communication.This publication has 105 references indexed in Scilit:
- T‐type voltage‐gated calcium channels as targets for the development of novel pain therapiesBritish Journal of Pharmacology, 2011
- GABA and central neuropathic pain following spinal cord injuryNeuropharmacology, 2011
- Mechanisms Underlying Inflammation in NeurodegenerationCell, 2010
- Voltage-gated potassium channels as therapeutic targetsNature Reviews Drug Discovery, 2009
- Central Sensitization: A Generator of Pain Hypersensitivity by Central Neural PlasticityThe Journal of Pain, 2009
- Hypoxia in high glucose followed by reoxygenation in normal glucose reduces the viability of cortical astrocytes through increased permeability of connexin 43 hemichannelsGlia, 2009
- Neuropathic Pain: A Maladaptive Response of the Nervous System to DamageAnnual Review of Neuroscience, 2009
- Physiological and pathological functions of P2X7 receptor in the spinal cordPurinergic Signalling, 2009
- Modulation of Brain Hemichannels and Gap Junction Channels by Pro-Inflammatory Agents and Their Possible Role in NeurodegenerationAntioxidants and Redox Signaling, 2009
- Gliopathy ensures persistent inflammation and chronic pain after spinal cord injuryExperimental Neurology, 2008