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Pharmacology of Chronic Pain Transmission and Its Modulation
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Pharmacology of Chronic Pain Transmission and Its Modulation

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pharmacology".

Deadline for manuscript submissions: closed (20 July 2021) | Viewed by 7036

Special Issue Editor

Dr. Romina Nassini

E-Mail Website
Guest Editor
Department of Health Sciences, Clinical Pharmacology Unit, University of Florence, 50139 Florence, Italy
Interests: neuroscience; pharmacology; ion channel; pain
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Pain that resolves quickly (acute) is a commonly experienced and evolutionarily conserved mechanism of survival. Chronic pain, which may persist for years, is associated with inflammatory diseases, peripheral and central neuropathies, and idiopathic conditions, and is a distinct and debilitating condition affecting approximatively 30–50% of the population worldwide. Thus, the burden of chronic pain is enormous in terms of suffering, disability, healthcare, and social and economic cost. Furthermore, due to the increase in the aging population, chronic pain is foreseen to increase remarkably in the near future. Currently available medicines for treating neuropathic pain are often unsatisfactory. Those for treating inflammatory pain have gastrointestinal (non-steroidal anti-inflammatory drugs, NSAIDs), or cardiovascular [cyclooxygenase-2, (COX2) inhibitors, Coxibs)] liability, thus remarkably increasing morbidity and mortality in the elderly. The opioid epidemic in the US further highlights the inadequacy of current therapies for chronic pain. There is thus an urgent need to understand the fundamental mechanisms of chronic pain and to develop more effective therapies. The identification of such pathways is essential to discover better and safer pain medicines.

This Special Issue will focus on basic science and translational research to obtain a complete comprehension of both peripheral and central nervous system components of chronic pain. The identification of such pathways is essential to discover better and safer pain medicines.

Dr. Romina Nassini
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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
  • ion channels
  • peripheral nervous system
  • central nervous system
  • animal models
  • primary sensory neurons
  • non-neuronal cells
  • inflammatory cells

Published Papers (3 papers)

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Research

17 pages, 2680 KiB  
Article
Distinct Mechanisms Account for In Vitro Activation and Sensitization of TRPV1 by the Porphyrin Hemin
by Natalie E. Palmaers, Steffen B. Wiegand, Christine Herzog, Frank G. Echtermeyer, Mirjam J. Eberhardt and Andreas Leffler
Int. J. Mol. Sci. 2021, 22(19), 10856; https://doi.org/10.3390/ijms221910856 - 08 Oct 2021
Cited by 3 | Viewed by 2166
Abstract
TRPV1 mediates pain occurring during sickling episodes in sickle cell disease (SCD). We examined if hemin, a porphyrin released during intravascular hemolysis modulates TRPV1. Calcium imaging and patch clamp were employed to examine effects of hemin on mouse dorsal root ganglion (DRG) neurons [...] Read more.
TRPV1 mediates pain occurring during sickling episodes in sickle cell disease (SCD). We examined if hemin, a porphyrin released during intravascular hemolysis modulates TRPV1. Calcium imaging and patch clamp were employed to examine effects of hemin on mouse dorsal root ganglion (DRG) neurons and HEK293t cells expressing TRPV1 and TRPA1. Hemin induced a concentration-dependent calcium influx in DRG neurons which was abolished by the unspecific TRP-channel inhibitor ruthenium red. The selective TRPV1-inhibitor BCTC or genetic deletion of TRPV1 only marginally impaired hemin-induced calcium influx in DRG neurons. While hTRPV1 expressed in HEK293 cells mediated a hemin-induced calcium influx which was blocked by BCTC, patch clamp recordings only showed potentiated proton- and heat-evoked currents. This effect was abolished by the PKC-inhibitor chelerythrine chloride and in protein kinase C (PKC)-insensitive TRPV1-mutants. Hemin-induced calcium influx through TRPV1 was only partly PKC-sensitive, but it was abolished by the reducing agent dithiothreitol (DTT). In contrast, hemin-induced potentiation of inward currents was not reduced by DTT. Hemin also induced a redox-dependent calcium influx, but not inward currents on hTRPA1. Our data suggest that hemin induces a PKC-mediated sensitization of TRPV1. However, it also acts as a photosensitizer when exposed to UVA-light used for calcium imaging. The resulting activation of redox-sensitive ion channels such as TRPV1 and TRPA1 may be an in vitro artifact with limited physiological relevance. Full article
(This article belongs to the Special Issue Pharmacology of Chronic Pain Transmission and Its Modulation)
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18 pages, 4557 KiB  
Article
Disulfiram Abrogates Morphine Tolerance—A Possible Role of µ-Opioid Receptor-Related G-Protein Activation in the Striatum
by Anna de Corde-Skurska, Pawel Krzascik, Anna Lesniak, Mariusz Sacharczuk, Lukasz Nagraba and Magdalena Bujalska-Zadrozny
Int. J. Mol. Sci. 2021, 22(8), 4057; https://doi.org/10.3390/ijms22084057 - 14 Apr 2021
Cited by 3 | Viewed by 2412
Abstract
One of the key strategies for effective pain management involves delaying analgesic tolerance. Early clinical reports indicate an extraordinary effectiveness of off-label disulfiram—an agent designed for alcohol use disorder—in potentiating opioid analgesia and abrogation of tolerance. Our study aimed to determine whether sustained [...] Read more.
One of the key strategies for effective pain management involves delaying analgesic tolerance. Early clinical reports indicate an extraordinary effectiveness of off-label disulfiram—an agent designed for alcohol use disorder—in potentiating opioid analgesia and abrogation of tolerance. Our study aimed to determine whether sustained µ-opioid signaling upon disulfiram exposure contributes to these phenomena. Wistar rats were exposed to acute and chronic disulfiram and morphine cotreatment. Nociceptive thresholds were assessed with the mechanical Randal-Selitto and thermal tail-flick tests. µ-opioid receptor activation in brain structures important for pain processing was carried out with the [35S]GTPγS assay. The results suggest that disulfiram (12.5–50 mg/kg i.g.) augmented morphine antinociception and diminished morphine (25 mg/kg, i.g.) tolerance in a supraspinal, opioid-dependent manner. Disulfiram (25 mg/kg, i.g.) induced a transient enhancement of µ-opioid receptor activation in the periaqueductal gray matter (PAG), rostral ventromedial medulla (RVM), hypothalamus, prefrontal cortex and the dorsal striatum at day 1 of morphine treatment. Disulfiram rescued µ-opioid receptor signaling in the nucleus accumbens and caudate-putamen 14 days following morphine and disulfiram cotreatment. The results of this study suggest that striatal µ-opioid receptors may contribute to the abolition of morphine tolerance following concomitant treatment with disulfiram. Full article
(This article belongs to the Special Issue Pharmacology of Chronic Pain Transmission and Its Modulation)
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15 pages, 4337 KiB  
Article
Novel 1,3,4-Oxadiazole Derivatives of Pyrrolo[3,4-d]pyridazinone Exert Antinociceptive Activity in the Tail-Flick and Formalin Test in Rodents and Reveal Reduced Gastrotoxicity
by Marta Szandruk-Bender, Benita Wiatrak, Łukasz Szczukowski, Piotr Świątek, Maria Rutkowska, Stanisław Dzimira, Anna Merwid-Ląd, Maciej Danielewski and Adam Szeląg
Int. J. Mol. Sci. 2020, 21(24), 9685; https://doi.org/10.3390/ijms21249685 - 18 Dec 2020
Cited by 7 | Viewed by 1924
Abstract
Despite the availability of the current drug arsenal for pain management, there is still a clinical need to identify new, more effective, and safer analgesics. Based on our earlier study, newly synthesized 1,3,4-oxadiazole derivatives of pyrrolo[3,4-d]pyridazinone, especially 10b and 13b, [...] Read more.
Despite the availability of the current drug arsenal for pain management, there is still a clinical need to identify new, more effective, and safer analgesics. Based on our earlier study, newly synthesized 1,3,4-oxadiazole derivatives of pyrrolo[3,4-d]pyridazinone, especially 10b and 13b, seem to be promising as potential analgesics. The current study was designed to investigate whether novel derivatives attenuate nociceptive response in animals subjected to thermal or chemical noxious stimulus, and to compare this effect to reference drugs. The antinociceptive effect of novel compounds was studied using the tail-flick and formalin test. Pretreatment with novel compounds at all studied doses increased the latency time in the tail-flick test and decreased the licking time during the early phase of the formalin test. New derivatives given at the medium and high doses also reduced the late phase of the formalin test. The achieved results indicate that new derivatives dose-dependently attenuate nociceptive response in both models of pain and exert a lack of gastrotoxicity. Both studied compounds act more efficiently than indomethacin, but not morphine. Compound 13b at the high dose exerts the greatest antinociceptive effect. It may be due to the reduction of nociceptor sensitization via prostaglandin E2 and myeloperoxidase levels decrease. Full article
(This article belongs to the Special Issue Pharmacology of Chronic Pain Transmission and Its Modulation)
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