scholarly journals Satellite Glial Cells in Pain Research: A Targeted Viewpoint of Potential and Future Directions

2021 ◽  
Vol 2 ◽  
Author(s):  
Parisa Gazerani
Keyword(s):  
Chronic Pain ◽  
Nervous System ◽  
Glial Cells ◽  
Time Course ◽  
Normal Function ◽  
Spontaneous Pain ◽  
Future Directions ◽  
Satellite Glial Cells ◽  
Pain Research

Chronic pain is known to be caused by sensitization within the pain circuits. An imbalance occurs between excitatory and inhibitory transmission that enables this sensitization to form. In addition to neurons, the contribution of central glia, especially astrocytes and microglia, to the pathogenesis of pain induction and maintenance has been identified. This has led to the targeting of astrogliosis and microgliosis to restore the normal functions of astrocytes and microglia to help reverse chronic pain. Gliosis is broadly defined as a reactive response of glial cells in response to insults to the central nervous system (CNS). The role of glia in the peripheral nervous system (PNS) has been less investigated. Accumulating evidence, however, points to the contribution of satellite glial cells (SGCs) to chronic pain. Hence, understanding the potential role of these cells and their interaction with sensory neurons has become important for identifying the mechanisms underlying pain signaling. This would, in turn, provide future therapeutic options to target pain. Here, a viewpoint will be presented regarding potential future directions in pain research, with a focus on SGCs to trigger further research. Promising avenues and new directions include the potential use of cell lines, cell live imaging, computational analysis, 3D tissue prints and new markers, investigation of glia–glia and macrophage–glia interactions, the time course of glial activation under acute and chronic pathological pain compared with spontaneous pain, pharmacological and non-pharmacological responses of glia, and potential restoration of normal function of glia considering sex-related differences.

Glial Cells and Pro-inflammatory Cytokines as Shared Neurobiological Bases for Chronic Pain and Psychiatric Disorders

2020 ◽  
pp. 27-49
Author(s):  
Judith A. Strong ◽  
Sang Won Jeon ◽  
Jun-Ming Zhang ◽  
Yong-Ku Kim
Keyword(s):  
Chronic Pain ◽  
Nervous System ◽  
Psychiatric Disorders ◽  
Inflammatory Cytokines ◽  
Glial Cells ◽  
Neuronal Excitability ◽  
Pro Inflammatory Cytokines

This chapter reviews the roles of cytokines and glial cells in chronic pain and in psychiatric disorders, especially depression. One important role of cytokines is in communicating between activated glia and neurons, at all levels of the nervous system. This process of neuroinflammation plays important roles in pain and depression. Cytokines may also directly regulate neuronal excitability. Many cytokines have been implicated in both pain and psychiatric disorders, including interleukin-1β‎ (IL-1β‎), tumor necrosis factor-α‎, and IL-6. More generally, an imbalance between type 1, pro-inflammatory cytokines and type 2, anti-inflammatory cytokines has been implicated in both pain and psychiatric disorders. Activation of the sympathetic nervous system can contribute to both pain and psychiatric disorders, in part through its actions on inflammation and the cytokine profile.

What is the role of fear and escape/avoidance in chronic pain? Models, structural analysis and future directions

2012 ◽  
Vol 2 (3) ◽  
pp. 295-303 ◽  
Author(s):  
Gordon JG Asmundson ◽  
Holly A Parkerson ◽  
Mark Petter ◽  
Melanie Noel
Keyword(s):  
Chronic Pain ◽  
Structural Analysis ◽  
Future Directions ◽  
Pain Models

scholarly journals On the Role of Glial Cells in the Mammalian Nervous System

1974 ◽  
Vol 249 (6) ◽  
pp. 1769-1780
Author(s):  
Bruce K. Schrier ◽  
Edward J. Thompson
Keyword(s):  
Nervous System ◽  
Glial Cells

scholarly journals Optogenetics and photopharmacology in pain research and therapeutics

STEMedicine ◽  
2020 ◽  
Vol 1 (3) ◽  
pp. e43 ◽  
Author(s):  
Federico Iseppon ◽  
Manuel Arcangeletti
Keyword(s):  
Chronic Pain ◽  
Pain Treatment ◽  
Molecular Switches ◽  
Genetic Profiling ◽  
Pain Research ◽  
Recent Advances ◽  
Cellular Components ◽  
The Brain

Pain afflicts billions of people worldwide, who suffer especially from long-term chronic pain. This gruelling condition affects the nervous system at all levels: from the brain to the spinal cord, the Dorsal Root Ganglia (DRG) and the peripheral fibres innervating the skin. The nature of the different molecular and cellular components of the somatosensory modalities, as well as the complexity of the peripheral and central circuitry are yet poorly understood. Light-based techniques such as optogenetics, in concert with the recent advances in single-cell genetic profiling, can help to elucidate the role of diverse neuronal sub-populations in the encoding of different sensory and painful stimuli by switching these neurons on and off via optically active proteins, namely opsins.  Recently, photopharmacology has emerged from the efforts made to advance optogenetics. The introduction of azo-benzene-based light-sensitive molecular switches has been applied to a wide variety of molecular targets, from ion channels and receptors to transporters, enzymes and many more, some of which are paramount for pain research and therapy. In this Review, we summarise the recent advances in the fields of optogenetics and photopharmacology and we discuss the use of light-based techniques for the study of acute and chronic pain physiology, as well as their potential for future therapeutic use to improve pain treatment.

scholarly journals sli is required for proper morphology and migration of sensory neurons in the Drosophila PNS

2019 ◽  
Vol 14 (1) ◽  
Author(s):  
Madison Gonsior ◽  
Afshan Ismat
Keyword(s):  
Nervous System ◽  
Sensory Neurons ◽  
Glial Cells ◽  
System Development ◽  
Nervous System Development ◽  
Final Position ◽  
Neuron Development ◽  
Guidance Cues ◽  
And Migration

Abstract Neurons and glial cells coordinate with each other in many different aspects of nervous system development. Both types of cells are receiving multiple guidance cues to guide the neurons and glial cells to their proper final position. The lateral chordotonal organs (lch5) of the Drosophila peripheral nervous system (PNS) are composed of five sensory neurons surrounded by four different glial cells, scolopale cells, cap cells, attachment cells and ligament cells. During embryogenesis, the lch5 neurons go through a rotation and ventral migration to reach their final position in the lateral region of the abdomen. We show here that the extracellular ligand sli is required for the proper ventral migration and morphology of the lch5 neurons. We further show that mutations in the Sli receptors Robo and Robo2 also display similar defects as loss of sli, suggesting a role for Slit-Robo signaling in lch5 migration and positioning. Additionally, we demonstrate that the scolopale, cap and attachment cells follow the mis-migrated lch5 neurons in sli mutants, while the ventral stretching of the ligament cells seems to be independent of the lch5 neurons. This study sheds light on the role of Slit-Robo signaling in sensory neuron development.

The Ferrier Lecture - Neuroglial cells: physiological properties and a potassium mediated effect of neuronal activity on the glial membrane potential

1967 ◽  
Vol 168 (1010) ◽  
pp. 1-21 ◽  
Keyword(s):  
Nervous System ◽  
Glial Cells ◽  
Original Description ◽  
Large Mass ◽  
Electron Microscopic ◽  
Physiological Properties ◽  
Chemical Studies ◽  
Glial Membrane ◽  
Separate Class

Neuroglial cells constitute a separate class of cells in the nervous system; they have been studied intensively since their original description by Virchow in 1846. As a rule anatomists find no difficulty in recognizing them by their staining properties, their shape and configuration as well as by their characteristic location between and around neurons. Electron microscopy has in recent years added much important subcellular detail and has shown how intermingled neurons and glial cells are, being separated from each other by narrow clefts 100 to 200 Å wide (figures 1 A, B and 5, plates 1, 2 and 4). These studies have not changed the well-established grouping of mammalian glial cells into two main classes, the oligodendrocytes and the astrocytes . It is customary to state that glial cells outnumber neurons by 10 to 1 in the vertebrate nervous sytem. They are, however, smaller and according to some rough estimates they make up as much as 50% of the volume of mammalian brains. That glial cells differ significantly from neurons was clear from the beginning because they do not possess axons and, unlike mammalian neurons, they retain their ability to divide throughout life. The possible role of the large mass of glial cells in our nervous system has been of continued interest. During the past decade this interest in the physiology of neuroglia has been reinforced, largely under the stimulus of electron-microscopic and chemical studies of the nervous system. Among the numerous recent reviews and symposia only a few will be mentioned (Windle 1958; Nakai 1963; Mugnaini & Walberg 1964). The recent studies of the physiology of neuroglial cells have been reviewed by Kufller & Nicholls (1966) and a biblio­graphy on neuroglia has been compiled by Little & Morris (1965).

Perspectives in Pain Research 2014: Neuroinflammation and glial cell activation: The cause of transition from acute to chronic pain?

2015 ◽  
Vol 6 (1) ◽  
pp. 3-6 ◽  
Author(s):  
Brian E. Cairns ◽  
Lars Arendt-Nielsen ◽  
Paola Sacerdote
Keyword(s):  
Spinal Cord ◽  
Chronic Pain ◽  
Dorsal Root Ganglion ◽  
Glial Cell ◽  
Schwann Cells ◽  
Glial Cells ◽  
Proinflammatory Cytokines ◽  
Immune Cells ◽  
Dorsal Root ◽  
Satellite Glial Cells

AbstractBackgroundIt is unknown why an acute pain condition under various circumstances can transition into a chronic pain condition.There has been a shift towards neuroinflammation and hence glial cell activations specifically in the dorsal root ganglion and spinal cord as a mechanism possibly driving the transition to chronic pain. This has led to a focus on non-neuronal cells in the peripheral and central nervous system. Besides infiltrating macrophages, Schwann cells and satellite glial cells release cytokines and therefore important mechanisms in the maintenance of pain. Activated Schwann cells, satellite glial cells, microglia, and astrocytes may contribute to pain sensitivity by releasing cytokines leading to altered neuronal function in the direction of sensitisation.Aims of this perspective paper1) Highlight the complex but important recent achievement in the area of neuroinflammation and pain at spinal cord level and in the dorsal root ganglion.2) Encourage further research which hopefully may provide better understanding of new key elements driving the transition from acute to chronic pain.Recent results in the area of neuroinflammation and painFollowing a sciatic nerve injury, local macrophages, and Schwann cells trigger an immune response immediately followed by recruitment of blood-derived immune cells. Schwann cells, active resident, and infiltrating macrophages release proinflammatory cytokines. Proinflammatory cytokines contribute to axonal damage and also stimulate spontaneous nociceptor activity. This results in activation of satellite glial cells leading to an immune response in the dorsal root ganglia driven by macrophages, lymphocytes and satellite cells. The anterograde signalling progresses centrally to activate spinal microglia with possible up regulation of glial-derived proinflammatory/pronociceptive mediators.An important aspect is extrasegmental spreading sensitisation where bilateral elevations in TNF-α, IL-6, and IL-10 are found in dorsal root ganglion in neuropathic models. Similarly in inflammatory pain models, bilateral up regulation occurs for TNF-α, IL-1 β, and p38 MAPK. Bilateral alterations in cytokine levels in the DRG and spinal cord may underlie the spread of pain to the uninjured side.An important aspect is how the opioids may interact with immune cells as opioid receptors are expressed by peripheral immune cells and thus can induce immune signaling changes. Furthermore, opioids may stimulate microglia cells to produce proinflammatory cytokines such as IL-1.ConclusionsThe present perspective paper indicates that neuroinflammation and the associated release of pro-inflammatory cytokines in dorsal root ganglion and at the spinal cord contribute to the transition from acute to chronic pain. Neuroinflammatory changes have not only been identified in the spinal cord and brainstem, but more recently, in the sensory ganglia and in the nerves as well. The glial cell activation may be responsible for contralateral spreading and possible widespread sensitisation.ImplicationsCommunication between glia and neurons is proposed to be a critical component of neuroinflammatory changes that may lead to chronic pain. Sensory ganglia neurons are surrounded by satellite glial cells but how communication between the cells contributes to altered pain sensitivity is still unknown. Better understanding may lead to new possibilities for (1) preventing development of chronic pain and (2) better pain management.

scholarly journals A Review of the Complex Roles of Glial Cells in Alzheimer’s Disease and Potential Glial-Oriented Therapeutic Targets

2018 ◽  
Author(s):  
Saif Shahriar Rahman Nirzhor ◽  
Rubayat Islam Khan ◽  
Sharmind Neelotpol
Keyword(s):  
Quality Of Life ◽  
Central Nervous System ◽  
Nervous System ◽  
Glial Cells ◽  
Therapeutic Targets ◽  
Concentration Of Ions ◽  
The Central Nervous System

The pathogenesis of Alzheimer’s disease (AD) is very complicated and not well-understood. As more and more studies are performed with regards to this disease, new insights are coming to light. Much of the research in AD so far has been very neuron-oriented however, recent studies suggest that certain glial cells i.e. microglia, astrocytes, oligodendrocytes, and NG2 glia are linked to the pathogenesis of AD and may offer several potential therapeutic targets in the long-standing battle against AD. Glial cells are responsible for maintaining homeostasis (i.e. concentration of ions and neurotransmitters) within the neuronal environment of the central nervous system (CNS) and are crucial to the integrity of neurons. This review explores the (1) role of glial cells in AD pathogenesis, (2) complex functionalities of the components involved and (3) potential therapeutic targets that it could eventuate leading to a better quality of life for AD patients.

scholarly journals Modulation of Glia-Mediated Processes by Spinal Cord Stimulation in Animal Models of Neuropathic Pain

2021 ◽  
Vol 2 ◽  
Author(s):  
David L. Cedeño ◽  
Courtney A. Kelley ◽  
Krishnan Chakravarthy ◽  
Ricardo Vallejo
Keyword(s):  
Spinal Cord ◽  
Chronic Pain ◽  
Nervous System ◽  
Neuropathic Pain ◽  
Animal Models ◽  
Glial Cells ◽  
Mechanism Of Action ◽  
Spinal Cord Stimulation ◽  
Expression Levels ◽  
Gate Control Theory

Glial cells play an essential role in maintaining the proper functioning of the nervous system. They are more abundant than neurons in most neural tissues and provide metabolic and catabolic regulation, maintaining the homeostatic balance at the synapse. Chronic pain is generated and sustained by the disruption of glia-mediated processes in the central nervous system resulting in unbalanced neuron–glial interactions. Animal models of neuropathic pain have been used to demonstrate that changes in immune and neuroinflammatory processes occur in the course of pain chronification. Spinal cord stimulation (SCS) is an electrical neuromodulation therapy proven safe and effective for treating intractable chronic pain. Traditional SCS therapies were developed based on the gate control theory of pain and rely on stimulating large Aβ neurons to induce paresthesia in the painful dermatome intended to mask nociceptive input carried out by small sensory neurons. A paradigm shift was introduced with SCS treatments that do not require paresthesia to provide effective pain relief. Efforts to understand the mechanism of action of SCS have considered the role of glial cells and the effect of electrical parameters on neuron–glial interactions. Recent work has provided evidence that SCS affects expression levels of glia-related genes and proteins. This inspired the development of a differential target multiplexed programming (DTMP) approach using electrical signals that can rebalance neuroglial interactions by targeting neurons and glial cells differentially. Our group pioneered the utilization of transcriptomic and proteomic analyses to identify the mechanism of action by which SCS works, emphasizing the DTMP approach. This is an account of evidence demonstrating the effect of SCS on glia-mediated processes using neuropathic pain models, emphasizing studies that rely on the evaluation of large sets of genes and proteins. We show that SCS using a DTMP approach strongly affects the expression of neuron and glia-specific transcriptomes while modulating them toward expression levels of healthy animals. The ability of DTMP to modulate key genes and proteins involved in glia-mediated processes affected by pain toward levels found in uninjured animals demonstrates a shift in the neuron–glial environment promoting analgesia.

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