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Cells
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Molecular and Cellular Mechanisms of Chronic Pain
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Molecular and Cellular Mechanisms of Chronic Pain

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 15 July 2024 | Viewed by 2817

Special Issue Editor

Dr. Enza Palazzo

E-Mail Website
Guest Editor
Department of Experimental Medicine, Pharmacology Division, University of Campania “L. Vanvitelli”, 80138 Naples, Italy
Interests: identification of the anatomical and molecular substrate where the reciprocal interactions between chronic pain and affective/cognitive disorders occur; novel pharmacological targets for the therapy of chronic pain and associated neuropsychiatric comorbidity; modulation of neurotransmissions involved in acute, persistent, inflammatory, and neuropathic pain in the pain descending system or closely associated brain areas; metabotropic and ionotropic glutamate, cannabinoid CB1 and CB2, vanilloid TRPV1, serotonin, adenosine and prostaglandin receptor role on pain transmission; animal models of chronic pain, anxiety, depression, social behavior, chronic stress, obsessive/compulsive and cognitive disorders; pharmacological modulation of the neuron electric activity and aminoacidergic/monoaminergic neurotransmitter levels involved in pain transmission and affective and cognitive disorders

Special Issue Information

Dear Colleagues,

Chronic pain, with a prevalence in the general population that according to some estimates reaches 18% of diagnoses each year, represents an unresolved medical emergency. Currently available analgesics are not satisfactorily effective and are associated with severe side effects and tolerance and addiction potential. There are different types of chronic pain such as musculoskeletal, visceral, neuropathic and oncological, with different etiologies and underlying mechanisms not yet clearly understood. However, what unites all types of chronic pain is synaptic plasticity: mediators, neurotransmitters, mechanisms and circuits involved under intense and prolonged stimulation facilitate pain signals generating hypersensitivity. Synaptic plasticity, at the basis of peripheral and central sensitization, represents the conversion point of pain from useful to pathological. Therefore, all investigations aiming to identify these pathophysiological mechanisms are essential to identify and develop new, more effective and better-tolerated painkillers. All studies related to this field of interest will be collected for this Special Issue.

Dr. Enza Palazzo
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • chronic pain
  • nociceptors
  • ascending pain pathway
  • descending pain pathway
  • peripheral and central sensitization
  • neural plasticity
  • pain neurotransmitters
  • hyperalgesia
  • allodynia
  • analgesics

Published Papers (3 papers)

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Research

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19 pages, 2941 KiB  
Article
Chemogenetic Manipulation of Amygdala Kappa Opioid Receptor Neurons Modulates Amygdala Neuronal Activity and Neuropathic Pain Behaviors
by Guangchen Ji, Peyton Presto, Takaki Kiritoshi, Yong Chen, Edita Navratilova, Frank Porreca and Volker Neugebauer
Cells 2024, 13(8), 705; https://doi.org/10.3390/cells13080705 - 19 Apr 2024
Viewed by 516
Abstract
Neuroplasticity in the central nucleus of the amygdala (CeA) plays a key role in the modulation of pain and its aversive component. The dynorphin/kappa opioid receptor (KOR) system in the amygdala is critical for averse-affective behaviors in pain conditions, but its mechanisms are [...] Read more.
Neuroplasticity in the central nucleus of the amygdala (CeA) plays a key role in the modulation of pain and its aversive component. The dynorphin/kappa opioid receptor (KOR) system in the amygdala is critical for averse-affective behaviors in pain conditions, but its mechanisms are not well understood. Here, we used chemogenetic manipulations of amygdala KOR-expressing neurons to analyze the behavioral consequences in a chronic neuropathic pain model. For the chemogenetic inhibition or activation of KOR neurons in the CeA, a Cre-inducible viral vector encoding Gi-DREADD (hM4Di) or Gq-DREADD (hM3Dq) was injected stereotaxically into the right CeA of transgenic KOR-Cre mice. The chemogenetic inhibition of KOR neurons expressing hM4Di with a selective DREADD actuator (deschloroclozapine, DCZ) in sham control mice significantly decreased inhibitory transmission, resulting in a shift of inhibition/excitation balance to promote excitation and induced pain behaviors. The chemogenetic activation of KOR neurons expressing hM3Dq with DCZ in neuropathic mice significantly increased inhibitory transmission, decreased excitability, and decreased neuropathic pain behaviors. These data suggest that amygdala KOR neurons modulate pain behaviors by exerting an inhibitory tone on downstream CeA neurons. Therefore, activation of these interneurons or blockade of inhibitory KOR signaling in these neurons could restore control of amygdala output and mitigate pain. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Chronic Pain)
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24 pages, 3146 KiB  
Article
Prokineticin System Is a Pharmacological Target to Counteract Pain and Its Comorbid Mood Alterations in an Osteoarthritis Murine Model
by Giulia Galimberti, Giada Amodeo, Giulia Magni, Benedetta Riboldi, Gianfranco Balboni, Valentina Onnis, Stefania Ceruti, Paola Sacerdote and Silvia Franchi
Cells 2023, 12(18), 2255; https://doi.org/10.3390/cells12182255 - 12 Sep 2023
Cited by 2 | Viewed by 962
Abstract
Osteoarthritis (OA) is the most prevalent joint disease associated with chronic pain. OA pain is often accompanied by mood disorders. We addressed the role of the Prokineticin (PK) system in pain and mood alterations in a mice OA model induced with monosodium iodoacetate [...] Read more.
Osteoarthritis (OA) is the most prevalent joint disease associated with chronic pain. OA pain is often accompanied by mood disorders. We addressed the role of the Prokineticin (PK) system in pain and mood alterations in a mice OA model induced with monosodium iodoacetate (MIA). The effect of a PK antagonist (PC1) was compared to that of diclofenac. C57BL/6J male mice injected with MIA in the knee joint were characterized by allodynia, motor deficits, and fatigue. Twenty-eight days after MIA, in the knee joint, we measured high mRNA of PK2 and its receptor PKR1, pro-inflammatory cytokines, and MMP13. At the same time, in the sciatic nerve and spinal cord, we found increased levels of PK2, PKR1, IL-1β, and IL-6. These changes were in the presence of high GFAP and CD11b mRNA in the sciatic nerve and GFAP in the spinal cord. OA mice were also characterized by anxiety, depression, and neuroinflammation in the prefrontal cortex and hippocampus. In both stations, we found increased pro-inflammatory cytokines. In addition, PK upregulation and reactive astrogliosis in the hippocampus and microglia reactivity in the prefrontal cortex were detected. PC1 reduced joint inflammation and neuroinflammation in PNS and CNS and counteracted OA pain and emotional disturbances. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Chronic Pain)
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Review

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19 pages, 2005 KiB  
Review
Neural Circuitry Polarization in the Spinal Dorsal Horn (SDH): A Novel Form of Dysregulated Circuitry Plasticity during Pain Pathogenesis
by Xufeng Chen and Shao-Jun Tang
Cells 2024, 13(5), 398; https://doi.org/10.3390/cells13050398 - 25 Feb 2024
Viewed by 1024
Abstract
Pathological pain emerges from nociceptive system dysfunction, resulting in heightened pain circuit activity. Various forms of circuitry plasticity, such as central sensitization, synaptic plasticity, homeostatic plasticity, and excitation/inhibition balance, contribute to the malfunction of neural circuits during pain pathogenesis. Recently, a new form [...] Read more.
Pathological pain emerges from nociceptive system dysfunction, resulting in heightened pain circuit activity. Various forms of circuitry plasticity, such as central sensitization, synaptic plasticity, homeostatic plasticity, and excitation/inhibition balance, contribute to the malfunction of neural circuits during pain pathogenesis. Recently, a new form of plasticity in the spinal dorsal horn (SDH), named neural circuit polarization (NCP), was discovered in pain models induced by HIV-1 gp120 and chronic morphine administration. NCP manifests as an increase in excitatory postsynaptic currents (EPSCs) in excitatory neurons and a decrease in EPSCs in inhibitory neurons, presumably facilitating hyperactivation of pain circuits. The expression of NCP is associated with astrogliosis. Ablation of reactive astrocytes or suppression of astrogliosis blocks NCP and, concomitantly, the development of gp120- or morphine-induced pain. In this review, we aim to compare and integrate NCP with other forms of plasticity in pain circuits to improve the understanding of the pathogenic contribution of NCP and its cooperation with other forms of circuitry plasticity during the development of pathological pain. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Chronic Pain)
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