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7 edition of Immune and glial regulation of pain found in the catalog.

Immune and glial regulation of pain

Immune and glial regulation of pain

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Published by IASP Press in Seattle .
Written in English

    Subjects:
  • Pain -- Pathophysiology,
  • Neuroimmunology,
  • Inflammation -- Mediators,
  • Neuroglia,
  • Pain -- metabolism,
  • Analgesics -- therapeutic use,
  • Chronic Disease -- drug therapy,
  • Glial Cell Line-Derived Neurotrophic Factors -- physiology,
  • Pain -- drug therapy,
  • Peripheral Nerves -- metabolism

  • Edition Notes

    Includes bibliographical references and index.

    Statementeditors, Joyce A. De Leo, Linda S. Sorkin, Linda R. Watkins.
    ContributionsDe Leo, Joyce A., 1960-, Sorkin, Linda S., 1953-, Watkins, Linda R., 1954-, International Association for the Study of Pain.
    Classifications
    LC ClassificationsRB127 .I46 2007
    The Physical Object
    Paginationp. ;
    ID Numbers
    Open LibraryOL17884820M
    ISBN 109780931092671
    LC Control Number2007013915

    Pain regulation by non-neuronal cells and inflammation Ru-Rong Ji,1,2* Alexander Chamessian,1 Yu-Qiu Zhang3 Acute pain is protective and a cardinal feature of inflammation. Chronic pain after arthritis, nerve injury, cancer, and chemotherapy is associated with chronic neuroinflammation, a local inflammation in the peripheral or central nervous. Cytokines have an important role in modulating the pain experience including linking the immune and nervous system through an interplay with glial cells (Sommer and Kress, , McMahon et al.

    The glial modulatory drug AV attenuates mechanical allodynia in rat models of neuropathic pain, Neuron-Glia Biology Special issue on immune & glial regulation of pain, 2() Psychoneuroimmunology is the study of interactions among behavioral, neural and endocrine, and immunologic processes of adaptation. These two volumes provide a clearly written, extensively referenced summary of some of the behavioral, neural and endocrine regulators of immune responses and immunologically mediated disease processes and of the behavioral and neuroendocrine effects of immune.

    Mammalian microglia, which migrate into the brain from peripheral tissues, are known to be important for immune surveillance in the nervous system, but they are also required for the refinement of neuronal connectivity and the regulation of behavioral plasticity (Salter & Beggs, ).Cited by: [Special Issue Review] Pain regulation by non-neuronal cells and inflammation Acute pain is protective and a cardinal feature of inflammation. Chronic pain after arthritis, nerve injury, cancer, and chemotherapy is associated with chronic neuroinflammation, a local inflammation in the peripheral or central nervous system.


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Immune and glial regulation of pain Download PDF EPUB FB2

- Immune and Glial Regulation of Pain describes immune and glial factors Immune and glial regulation of pain book the peripheral and central nervous systems that relate to chronic pain states.

This authoritative volume describes immune-pain interactions in the peripheral tissues, nerves, dorsal root ganglia, and the spinal cord and brain and identifies novel immune and glial targets for clinical pain control that may yield new analgesic Cited by: Immune and Glial Regulation of Pain.

Edited by Joyce A. DeLeo, PhD; Linda S. Sorkin, PhD; Linda R. Watkins, PhD IASP Press, Seattle,pages, $Author: Alice A. Larson. Get this from a library.

Immune and glial regulation of pain. [Joyce A De Leo; Linda S Sorkin; Linda R Watkins; International Association for the Study of Pain.;] -- "Review of immune and glial factors within the peripheral and central nervous systems that relate to chronic pain states.

Discussion of novel immune and glial targets for clinical pain control that. Hematogenous immune cells may migrate/infiltrate to the brain and circulating inflammatory mediators may penetrate the blood brain barrier to participate in central glial responses to injury.

Inflammatory cytokines such as IL-1β released from glia may facilitate pain transmission through its coupling to neuronal glutamate by: [14] [15][16] Recent research suggests opioids are able to activate innate immune toll-like receptor 4 (TLR4) on glial cells.

17 While at the neuron opioids facilitate pain relief, activated glial Author: Linda Watkins. Accumulating evidence suggests that non-neuronal cells such as immune cells, glial cells, keratinocytes, cancer cells, and stem cells play active roles in the pathogenesis and resolution of pain.

We review how non-neuronal cells interact with nociceptive neurons by secreting neuroactive signaling molecules that modulate by:   The “Missing Link” in the Physiology of Pain: Glial Cells – Practical Pain Management – May glial cells and their interactions have become recognized as having a critically important role in the generation and maintenance of acute and chronic pain and may now be a “missing link” in our understanding of the conversion of acute to chronic pain and the development of chronic.

TNF-α is upregulated in pain pathways after injury and secreted by immune and glial ce TNFα induces the phosphorylation of JNK1 and activates NF-κB in astrocytes, leading to CCL2 releaseCCL2 then acts on CCR2 receptors on neurons and interacts positively with neuronal NMDA and AMPA receptors (Fig.

3b).Cited by:   Here, the authors describe the immune mechanisms that are involved in pain, one of the key features of inflammation.

They explain how the immune and Cited by:   Neuropathic pain refers to a variety of chronic pain conditions with differing underlying pathophysiologic mechanisms and origins. Recent studies indicate a communication between the immune system and the nervous system. A common underlying mechanism of neuropathic pain is the presence of inflammation at the site of the damaged or affected Cited by: Changes in immune and glial markers in the CSF of patients with Complex Regional Pain Syndrome Guillermo M.

Alexander, Marielle J. Perreault, Erin R. Reichenberger, Robert J. Regulation of pain induction via macrophage-nociceptor interactions.

(a) In macrophages, activation of TLRs (e.g. TLR4 and TLR9) by PAMPs and DAMPs increases the synthesis and release of inflammatory cytokines and chemokines (e.g. TNF, IL-1β, CCL2, CXCL1) and Author: Ouyang Chen, Christopher R Donnelly, Ru-Rong Ji. Pain is defined as an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.

1 Pain is a subjective experience, which involves not only nociception, but also emotional, cognitive, and social components.

1 Acute pain serves as an alarm system to protect us from tissue damage. 2 Patients with congenital insensitivity Cited by: 3. of glia and the immune system in the development and maintenance of neuropathic pain. Key Words: neuropathic pain, hyperalgesia, adhesion and migration,30 and up-regulation of MHC I aptic transmission but also activating glial Role of Glia in Neuropathic Pain † File Size: KB.

Acute pain is protective and a cardinal feature of inflammation. Chronic pain after arthritis, nerve injury, cancer, and chemotherapy is associated with chronic neuroinflammation, a local inflammation in the peripheral or central nervous system.

Accumulating evidence suggests that non-neuronal cells such as immune cells, glial cells, keratinocytes, cancer cells, and stem cells, play Cited by: Glial Cells and Chronic Pain.

suggest that glia may be involved in the regulation of the affective. Cafferty WB, Marchand F. Immune and glial cell factors as pain mediators and. modulators. DeLeo, J. A., Sorkin, L.

& Watkins, L. (eds) Immune and Glial Regulation of Pain (IASP, Seattle, ). A book dedicated to understanding the current evidence and Cited by: transmitters from glia themselves, and (2) glial transmitters cause feedback regulation of neuronal activity and synaptic strength.

Table 1 Distinct reaction of microglia, astrocytes, and satellite glial cells (SGCs) in different pain conditions, as examined by upregulation of the glial markers IBA1, CD11b, and glial fibrillary acidic protein Cited by: Ninety percent of the cells in the CNS are glia – microglia, astrocytes, oligodendroglia, perivascular glia.

Glia outnumber neurons by almost 10 to 1. Microglia and astrocytes are immune cells that can release inflammatory responses with harmful effects on nerve cells such as. The more recent findings of the possible activation of 3 types of glial cells in the development and maintenance of chronic pain activation via a number of synergistic neuro-glial interactions.

A decade later glial cell activation in the spinal cord had been implicated in a wide array of animal pain models including trauma, inflammation, chemotherapy, multiple sclerosis, migraine, back pain, and others. Glial cells are now also known to play critical roles in immune surveillance in the brain and in cleansing the brain of unwanted.Recent studies have also pointed to non-neuronal mechanisms such as immune and glial regulation for neuropathic pain [].

Nerve injury induces a profound activation of glial cells including microglia and astrocytes in the spinal cord, and both microglia and astrocytes contribute to neuropathic pain sensitization via glial-neural interaction [ 23, 24 ].Cited by: Accumulating evidence suggests that non-neuronal cells such as immune cells, glial cells, keratinocytes, cancer cells, and stem cells play active roles in the pathogenesis and resolution of pain.