The Signaling and Cellular Mechanisms of Pain—Second Edition

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

Deadline for manuscript submissions: closed (31 May 2024) | Viewed by 962

Special Issue Editor


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Guest Editor
Department of Experimental and Clinical Medicine (DMSC), Anatomy Section, School of Human Health Sciences, University of Florence, Florence, Italy
Interests: neuropathic pain; blood–brain barrier; cadmium toxicity; neuroprotection
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Special Issue Information

Dear Colleagues,

The physiological perception of pain is essential for the brain to engage appropriate responses against noxious stimuli. In pathological conditions, such as chronicity, pain lacks the positive characteristic of alarm evolving to disease. Based on three major characteristics, namely symptoms, mechanisms and syndromes, pain may be classified into three classes: nociceptive, neuropathic, and inflammatory pain. The events that follow one another leading to the onset of pain can originate from various sources and consist of three events: the transduction, transmission and modulation of noxious stimuli.

The cell type most involved in the various phases of pain projection are the sensory neurons whose sensitivity can be modulated by various mediators. The latter trigger the activation of many different signaling cascades, which, in turn, determine the response to painful stimuli.

Although many studies have shed light on some components of the intracellular signal transduction cascades, the signaling pathways downstream of receptor–ligand interactions are still largely unknown.

Another very important aspect to consider is the plethora of plastic changes that take place in the peripheral and the central nervous systems to contribute to pain perception. In addition, the molecular mechanism responsible for neuronal and glial plasticity is widely accepted as the mechanism underpinning the transition from acute/physiological pain to chronic/pathological pain.

Thus, understanding the molecular and cellular mechanisms of pain is essential for the advance of pain physiopathology knowledge for the identification of new therapeutic targets and, finally, to improve its management.

Dr. Alessandra Pacini
Guest Editor

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Keywords

  • nociception
  • neuropathic pain
  • visceral pain
  • pain pathophysiological pathways
  • glia
  • analgesia

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16 pages, 1364 KiB  
Article
The Role of the Insular Cortex and Serotonergic System in the Modulation of Long-Lasting Nociception
by Ulises Coffeen, Gerardo B. Ramírez-Rodríguez, Karina Simón-Arceo, Francisco Mercado, Angélica Almanza, Orlando Jaimes, Doris Parra-Vitela, Mareli Vázquez-Barreto and Francisco Pellicer
Cells 2024, 13(20), 1718; https://doi.org/10.3390/cells13201718 - 17 Oct 2024
Viewed by 669
Abstract
The insular cortex (IC) is a brain region that both receives relevant sensory information and is responsible for emotional and cognitive processes, allowing the perception of sensory information. The IC has connections with multiple sites of the pain matrix, including cortico-cortical interactions with [...] Read more.
The insular cortex (IC) is a brain region that both receives relevant sensory information and is responsible for emotional and cognitive processes, allowing the perception of sensory information. The IC has connections with multiple sites of the pain matrix, including cortico-cortical interactions with the anterior cingulate cortex (ACC) and top-down connections with sites of descending pain inhibition. We explored the changes in the extracellular release of serotonin (5HT) and its major metabolite, 5-hydroxyindoleacetic acid (5HIAA), after inflammation was induced by carrageenan injection. Additionally, we explored the role of 5HT receptors (the 5HT1A, 5HT2A, and 5HT3 receptors) in the IC after inflammatory insult. The results showed an increase in the extracellular levels of 5HT and 5-HIAA during the inflammatory process compared to physiological levels. Additionally, the 5HT1A receptor was overexpressed. Finally, the 5HT1A, 5HT2A, and 5HT3 receptor blockade in the IC had antinociceptive effects. Our results highlight the role of serotonergic neurotransmission in long-lasting inflammatory nociception within the IC. Full article
(This article belongs to the Special Issue The Signaling and Cellular Mechanisms of Pain—Second Edition)
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