Nunzio Vicario1, Rita Turnaturi2, Federica Maria Spitale1, Filippo Torrisi1, Agata Zappalà1, Rosario Gulino1, Lorella Pasquinucci2, Santina Chiechio3,4, Carmela Parenti5, Rosalba Parenti6. 1. Section of Physiology, Department of Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy. 2. Section of Medicinal Chemistry, Department of Drug Sciences, University of Catania, Catania, Italy. 3. Section of Pharmacology, Department of Drug Sciences, University of Catania, Catania, Italy. 4. Oasi Research Institute IRCCS, Troina, Italy. 5. Section of Pharmacology, Department of Drug Sciences, University of Catania, Catania, Italy. cparenti@unict.it. 6. Section of Physiology, Department of Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy. parenti@unict.it.
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.
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.
Entities:
Keywords:
Connexin; Gap junction; Glia; Neurodegeneration; Neuropathic pain
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