Exploring Neuroinflammation in Central and Peripheral Neuropathic Pain and Related Disorders

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: 31 December 2025 | Viewed by 366

Special Issue Editor


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Guest Editor
Department of Entomology and Nematology, and Comprehensive Cancer Center, University of California, Davis, CA, USA
Interests: neuroscience; neuroinflammation; neuropsychological disorders; pathway analysis
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Special Issue Information

Dear Colleagues,

Neuropathic pain, driven by central and peripheral nervous system dysfunction, is intricately linked to neuroinflammation and often accompanied by affective (e.g., anxiety and depression) and cognitive (e.g., memory deficits and executive dysfunction) disorders. This Special Issue of Biomedicines invites preclinical research and review articles utilizing in silico, in vitro, and in vivo approaches to elucidate neuroinflammatory mechanisms in neuropathic pain and its comorbidities. We welcome studies employing computational modeling (in silico), cell-based assays (in vitro), and animal models (in vivo) to explore molecular pathways, cytokine signaling, and neuroimmune interactions. Submissions should focus on identifying novel biomarkers, therapeutic targets, or signaling cascades, emphasising medical, chemical, and non-pharmacological (e.g., neuromodulation and lifestyle interventions) treatment strategies. Clinical trial data will be excluded. We encourage contributions leveraging advanced techniques, such as omics-based pathway analyses, neural circuit modeling, or neuroimmune modulation, to address the interplay between neuropathic pain and affective–cognitive impairments. This issue aims to advance preclinical neuroscience, fostering innovative therapeutic strategies for debilitating conditions.

Dr. Tahmineh Mokhtari
Guest Editor

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Keywords

  • neuroinflammation
  • neuropathic pain
  • central nervous system
  • peripheral nervous system
  • affective disorders
  • cognitive disorders
  • in silico modeling
  • in vitro assays
  • in vivo models
  • medical and non-pharmacological interventions

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Published Papers (1 paper)

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Research

28 pages, 8304 KB  
Article
Monocyte-Derived Macrophages Expressing Dopamine D2-Subtype Receptors Drive Alcohol Effects on Mesolimbic Neurons and Microglia
by Christina A. Nelson, J. Daniel Obray, Travis J. Clarke, James N. Brundage, Ryan J. Folsom, Carlos M. Moreno, Pacen E. Williams, Lauren H. Ford, Sandra Hope, K. Scott Weber, Kyle B. Bills, Jordan T. Yorgason and Scott C. Steffensen
Biomedicines 2025, 13(10), 2327; https://doi.org/10.3390/biomedicines13102327 - 23 Sep 2025
Viewed by 39
Abstract
Background/Objectives: Microglia are the primary immune cells in the central nervous system (CNS) and are known as “resident” macrophages. The aim of this study was to determine the effect of acute ethanol (EtOH) on the microglia state and monocyte infiltration into the [...] Read more.
Background/Objectives: Microglia are the primary immune cells in the central nervous system (CNS) and are known as “resident” macrophages. The aim of this study was to determine the effect of acute ethanol (EtOH) on the microglia state and monocyte infiltration into the CNS, with particular attention to the role of peripheral and central dopamine (DA) D2 receptors (D2Rs) in mediating EtOH effects on peripheral and central substrates. We hypothesize that EtOH interacts with peripheral immune mediators via D2Rs including monocyte-derived macrophages (MDMs) to modulate midbrain neurons, DA transmission in the mesolimbic pathway from the ventral tegmental area (VTA) to nucleus accumbens (NAc), and the intoxicating effects of acute EtOH. Methods: Using the Macrophage FAS-Induced Apoptosis (MaFIA) mouse model (GFP+ on Csf1r promoter), we assessed the effects of three intraperitoneal (IP) doses of EtOH (1, 2, and 4 g/kg) at three time points (0.5, 1, and 2 h after injection) on D2R expression in blood leukocytes and microglia, as well as midbrain neuronal activity, DA release, and behavior. Results: Acute EtOH significantly enhanced lymphocyte and monocyte D2R expression at 1.0 g/kg by 2 h after injection in vivo but decreased D2R expression in vitro. Ethanol enhanced microglia D2R expression in the NAc, while not altering D2R expression in the VTA, but altered the microglia state in these areas, shifting them toward an inflammatory phenotype. Acute EtOH induced prolonged and progressive hypersensitivity of D2R activation of VTA GABA neurons. Intravenous injection of the macrophage depleter liposomal clodronate significantly reduced blood macrophages by 55.3% and blocked the typical inhibition of VTA GABA neurons by EtOH, as well as the enhancement of DA levels in the NAc, and the locomotor indices of intoxication produced by acute EtOH, but not choice place preference. Conclusions: These findings strongly suggest a neuroimmune peripheral connection for acute low-dose EtOH use and challenge the dogma that central actions of EtOH exclusively mediate its effect on DA neuronal activity and release. Full article
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