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Molecular Mechanisms of Chronic Pain and New Therapeutic Strategies Volume...
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Molecular Mechanisms of Chronic Pain and New Therapeutic Strategies Volume II

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (31 August 2023) | Viewed by 4331

Special Issue Editor

Dr. Elena Lucarini

E-Mail Website
Guest Editor
Department of Neuroscience, Psychology, Drug Research and Child Health, Neurofarba, Pharmacology and Toxicology Section, University of Florence, 50139 Florence, Italy
Interests: pain pharmacology; chronic pain; neuropathic pain, visceral pain; peripheral nervous system; central nervous system; glia; neuroimmune interactions; gut microbiota
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Chronic pain, which is predicted to affect up to 30% of adults worldwide, is one of the most frequent reasons for patients to seek medical care. Although pain itself is not immediately life-threatening, its persistence strongly impacts people’s quality of life. Different types of chronic pain can be identified based on their nature (somatic or visceral) and their etiopathogenesis (inflammatory pain, cancer pain, and neuropathic pain). It is generally acknowledged that chronic pain results from neuronal plasticity, involving both peripheral primary sensory neurons as well as central nociceptive neurons, leading to an altered perception of pain. The maladaptive response of the complex cellular network involved in the transmission and perception of pain dramatically upsets the nociceptive system as well as the physiological substrate of classical painkiller drugs. Despite recent advances in the identification of pain-generating mechanisms and the implementation of treatment guidelines, the management of chronic pain still represents a therapeutic problem. Thus, the identification of novel molecular and cellular targets for the development of effective and safe therapeutic strategies requires particular attention from the medical community. In recent years, the investigation has been shifted from neurons to non-neuronal cells able to modulate neuronal function and pain, like glial cells, immune cells, and gut microbiota. This Special Issue aims to collect original papers and reviews about pain mechanisms and suitable approaches to prevent and treat chronic pain in different pathologic conditions as a single therapy or as an adjuvant to other pain medications.

Dr. Elena Lucarini
Guest Editor

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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. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

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Keywords

  • chronic pain
  • neuropathic pain
  • visceral pain
  • musculoskeletal pain
  • pain biology
  • glial cells
  • neuroimmune interactions
  • gut microbiota
  • pain medicine
  • drug tolerance

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Related Special Issue

Published Papers (4 papers)

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Research

11 pages, 1519 KiB  
Article
Role of Spinal Cholecystokinin Octapeptide, Nociceptin/Orphanin FQ, and Hemokinin-1 in Diabetic Allodynia
by Takafumi Hayashi, Syu-ichi Kanno, Chizuko Watanabe, Damiana Scuteri, Yasuyuki Agatsuma, Akiyoshi Hara, Giacinto Bagetta, Tsukasa Sakurada and Shinobu Sakurada
Biomedicines 2024, 12(6), 1332; https://doi.org/10.3390/biomedicines12061332 - 15 Jun 2024
Viewed by 832
Abstract
A complication of diabetes is neuropathic pain, which is difficult to control with medication. We have confirmed that neuropathic pain due to mechanical allodynia in diabetic mice is mediated by a characteristic neuropeptide in the spinal cord. We evaluated the strength of mechanical [...] Read more.
A complication of diabetes is neuropathic pain, which is difficult to control with medication. We have confirmed that neuropathic pain due to mechanical allodynia in diabetic mice is mediated by a characteristic neuropeptide in the spinal cord. We evaluated the strength of mechanical allodynia in mice using von Frey filaments. When mice were intravenously injected with streptozotocin, mechanical allodynia appeared 3 days later. Antibodies of representative neuropeptides were intrathecally (i.t.) administered to allodynia-induced mice 7 days after the intravenous administration of streptozotocin, and allodynia was reduced by anti-cholecystokinin octapeptide antibodies, anti-nociceptin/orphanin FQ antibodies, and anti-hemokinin-1 antibodies. In contrast, i.t.-administered anti-substance P antibodies, anti-somatostatin antibodies, and anti-angiotensin II antibodies did not affect streptozotocin-induced diabetic allodynia mice. Mechanical allodynia was attenuated by the i.t. administration of CCK-B receptor antagonists and ORL-1 receptor antagonists. The mRNA level of CCK-B receptors in streptozotocin-induced diabetic allodynia mice increased in the spinal cord, but not in the dorsal root ganglion. These results indicate that diabetic allodynia is caused by cholecystokinin octapeptide, nociceptin/orphanin FQ, and hemokinin-1 released from primary afferent neurons in the spinal cord that transmit pain to the brain via the spinal dorsal horn. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Chronic Pain and New Therapeutic Strategies Volume II)
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11 pages, 448 KiB  
Article
Perceived Stress and Life Stressors in Adults with and without Fibromyalgia
by Ha M. Nguyen, Barbara J. Cherry and Laura Zettel-Watson
Biomedicines 2024, 12(6), 1233; https://doi.org/10.3390/biomedicines12061233 - 1 Jun 2024
Viewed by 783
Abstract
Chronic medical conditions (i.e., chronic widespread pain) may contribute to accelerated/accentuated aging, such that middle-aged individuals with comorbidities may actually show increased declines in physical, cognitive, and mental health compared to normal aging adults. We examined perceived stress, life stressors, and depression in [...] Read more.
Chronic medical conditions (i.e., chronic widespread pain) may contribute to accelerated/accentuated aging, such that middle-aged individuals with comorbidities may actually show increased declines in physical, cognitive, and mental health compared to normal aging adults. We examined perceived stress, life stressors, and depression in adults with and without fibromyalgia, a chronic pain condition. Ninety-four participants (52% with fibromyalgia, 78% female) aged 50 to 93 were administered the Perceived Stress Scale, Social Readjustment Rating Scale, and Beck Depression Inventory. Hierarchical regression analyses were conducted: the predictor variables were age, gender, fibromyalgia status, depression, and fibromyalgia–depression interaction. The interaction term significantly predicted perceived stress, but not life stressors. Depression significantly predicted stress for Social Readjustment Rating Scale measures after controlling for covariates. Significant associations were found between perceived stress and life stressors in all participants. In addition, those with fibromyalgia were significantly more likely to report higher levels of stress above standardized scores on both the Perceived Stress Scale and the Social Readjustment Rating Scale. Finally, depressive symptoms played a more significant role than fibromyalgia status in predicting life stressors. Conclusions: These findings emphasize the importance of assessing different types of stress and stressors in individuals with chronic widespread pain and/or depression in mid-life and beyond to better treat individuals with these conditions. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Chronic Pain and New Therapeutic Strategies Volume II)
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14 pages, 2563 KiB  
Article
Differential Regulation of Intracisternally Injected Angiotensin II-Induced Mechanical Allodynia and Thermal Hyperalgesia in Rats
by Ki-Don Park, Jo-Young Son, Hak-Kyun Kim, Yu-Mi Kim, Jin-Sook Ju, Min-Jeong Jo, Min-Kyoung Park, Min-Kyung Lee and Dong-Kuk Ahn
Biomedicines 2023, 11(12), 3279; https://doi.org/10.3390/biomedicines11123279 - 12 Dec 2023
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Abstract
The present study examined the underlying mechanisms of mechanical allodynia and thermal hyperalgesia induced by the intracisternal injection of angiotensin (Ang) II. Intracisternal Ang II injection decreased the air puff threshold and head withdrawal latency. To determine the operative receptors for each distinct [...] Read more.
The present study examined the underlying mechanisms of mechanical allodynia and thermal hyperalgesia induced by the intracisternal injection of angiotensin (Ang) II. Intracisternal Ang II injection decreased the air puff threshold and head withdrawal latency. To determine the operative receptors for each distinct type of pain behavior, we intracisternally injected Ang II receptor antagonists 2 h after Ang II injection. Losartan, an Ang II type 1 receptor (AT1R) antagonist, alleviated mechanical allodynia. Conversely, PD123319, an Ang II type 1 receptor (AT2R) antagonist, blocked only thermal hyperalgesia. Immunofluorescence analyses revealed the co-localization of AT1R with the astrocyte marker GFAP in the trigeminal subnucleus caudalis and co-localization of AT2R with CGRP-positive neurons in the trigeminal ganglion. Intracisternal pretreatment with minocycline, a microglial inhibitor, did not affect Ang II-induced mechanical allodynia, whereas L-α-aminoadipate, an astrocyte inhibitor, significantly inhibited Ang II-induced mechanical allodynia. Furthermore, subcutaneous pretreatment with botulinum toxin type A significantly alleviated Ang II-induced thermal hyperalgesia, but not Ang II-induced mechanical allodynia. These results indicate that central Ang II-induced nociception is differentially regulated by AT1R and AT2R. Thus, distinct therapeutic targets must be regulated to overcome pain symptoms caused by multiple underlying mechanisms. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Chronic Pain and New Therapeutic Strategies Volume II)
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11 pages, 1537 KiB  
Article
Antinociceptive Effect of the Combination of a Novel α4β2* Agonist with Donepezil in a Chronic Pain Model
by Fernanda B. de M. Monte, Tadeu L. Montagnoli, Bruno E. Dematté, Fernanda Gubert, Vitória S. Ventura, Jaqueline S. da Silva, Margarete M. Trachez, Rosalia Mendez-Otero and Gisele Zapata-Sudo
Biomedicines 2023, 11(12), 3249; https://doi.org/10.3390/biomedicines11123249 - 8 Dec 2023
Viewed by 1072
Abstract
Chronic pain presents a major challenge in contemporary medicine, given the limited effectiveness and numerous adverse effects linked to available treatments. Recognizing the potential of the cholinergic pathway as a therapeutic target, the present work evaluates the antinociceptive activity of a combination of [...] Read more.
Chronic pain presents a major challenge in contemporary medicine, given the limited effectiveness and numerous adverse effects linked to available treatments. Recognizing the potential of the cholinergic pathway as a therapeutic target, the present work evaluates the antinociceptive activity of a combination of Cris-104, a novel α4β2* receptor agonist, and donepezil, a central anticholinesterase agent. Isobolographic analysis revealed that equimolar combination was approximately 10 times more potent than theoretically calculated equipotent additive dose. Administration of Cris-104 and donepezil combination (3 μmol/kg) successfully reversed hyperalgesia and mechanical allodynia observed in rats subjected to spinal nerve ligation (SNL). The combination also modulated neuroinflammation by reducing astrocyte activation, evident in the decreased expression of glial fibrillary acidic protein (GFAP) in the spinal cord. The observed synergism in combining a nicotinic receptor agonist with an anticholinesterase agent underscores its potential for treating chronic pain. This alternative therapeutic distinct advantage, including dose reduction and high selectivity for the receptor, contribute to a more favorable profile with minimized adverse effects. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Chronic Pain and New Therapeutic Strategies Volume II)
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