When Good Pain Turns Bad
Research findings suggest a novel approach to human pain control that targets glia, and it is likely that such glial-neuronal interactions are not unique to pain, but rather reflect a general rule of sensory processing.
Role of Astrocytes in Pain
- BiologyNeurochemical Research
The interactions between astrocytes, microglia and neurons are now recognized as fundamental mechanisms underlying acute and chronic pain states.
Spinal glial activation contributes to pathological pain states
- BiologyNeuroscience & Biobehavioral Reviews
P2 receptors, microglial cytokines and chemokines, and neuropathic pain
- BiologyJournal of neuroscience research
This review highlights recent advances in understanding of the mechanisms that underlie neuropathic pain caused by peripheral nerve injury, with a specific focus on purinergic signaling in spinal cord microglia and P2 receptors.
Glia as a Link between Neuroinflammation and Neuropathic Pain
- BiologyImmune network
This review will briefly discuss the recent findings that have shed light on the molecular and cellular mechanisms of glia as a connecting link between neuropathic pain and neuroinflammation.
Immune responses of microglia in the spinal cord: Contribution to pain states
- BiologyExperimental Neurology
Beyond neurons: evidence that immune and glial cells contribute to pathological pain states.
- BiologyPhysiological reviews
All nerves and neurons regardless of modality or function are likely affected by immune and glial activation in the ways described for pain, and proinflammatory cytokines appear to be of special importance in the creation of peripheral nerve and neuronal hyperexcitability.
Do glial cells control pain?
- BiologyNeuron glia biology
Accumulating evidence that supports an important role for microglial cells in the spinal cord for pain control under injury conditions is reviewed and possible signaling mechanisms, in particular mitogen-activated protein kinase pathways that are crucial for glial-mediated control of pain are discussed.
SHOWING 1-10 OF 76 REFERENCES
Glial proinflammatory cytokines mediate exaggerated pain states: implications for clinical pain.
- BiologyAdvances in experimental medicine and biology
The present review argues that neurons in fact are not the only cell type involved in pain and that spinal cord cells called "glia" are also critically important, and that drugs that target glia and the chemical substances that these glia release are predicted to be powerful remedies for pain problems in people.
The pain of being sick: implications of immune-to-brain communication for understanding pain.
- Biology, MedicineAnnual review of psychology
Evidence is reviewed supporting the idea that proinflammatory cytokines exert powerful pain facilitatory effects following their release in the body, in the brain, and in the spinal cord.
Transgenic expression of TNF by astrocytes increases mechanical allodynia in a mouse neuropathy model
- Biology, PsychologyNeuroreport
Transgenic mice were used in which expression of murine TNF was targeted to astrocytes using a glial fibrillary acidic protein (GFAP–TNF fusion gene) to support a central role of glial expression of TNF in the generation of neuropathic pain.
Proinflammatory cytokines and glial cells: Their role in neuropathic pain
- Medicine, Psychology
The laboratory has focused on understanding mechanisms that lead to neuropathic pain, and this knowledge may then translate into development of new, effective approaches for treatment and even prevention of chronic pain syndromes.
Neuronal plasticity: increasing the gain in pain.
Here, a conceptual framework for the contribution of plasticity in primary sensory and dorsal horn neurons to the pathogenesis of pain is developed, identifying distinct forms of Plasticity, which are term activation, modulation, and modification, that by increasing gain, elicit pain hypersensitivity.
- BiologyJournal of neurochemistry
The evidence strongly suggests that these cytokines perform neural functions in normal brain, and it is proposed that they should be thought of as neuromodulators in addition to inflammatory mediators.
IMMUNOLOGICALLY INDUCED ELECTROPHYSIOLOGICAL DYSFUNCTION: IMPLICATIONS FOR INFLAMMATORY DISEASES OF THE CNS AND PNS
- Biology, MedicineProgress in Neurobiology
Spinal nerve lesion-induced mechanoallodynia and adrenergic sprouting in sensory ganglia are attenuated in interleukin-6 knockout mice