We are analyzing https://link.springer.com/article/10.1007/s10571-009-9390-6.

Title:
Spinal Astrogliosis in Pain Models: Cause and Effects | Cellular and Molecular Neurobiology
Description:
Pathological pain has been subjected to intense research to shed light on the underlying mechanisms of key symptoms, such as allodynia and hyperalgesia. The main focus has by and large concerned plasticity of spinal cord neurons and the primary afferent nerves relaying peripheral information to the spinal cord. Animal pain models display an increased presence of reactive astrocytes in the spinal cord, but in contrast to neurons, little is known about how they contribute to abnormal pain sensation. However, astrocytes are now beginning to receive greater attention, and as new information is emerging, it appears that astrocytes undertake critical roles in manifesting pathological pain. Through the secretion of diffusible transmitters, such as interleukins, ATP, and NO, astrocytes may augment primary afferent neuronal signaling or sensitize second order neurons in the spinal cord. In addition, astrocytes might lead to altered pain perception by a direct modulation of synaptic transmission between neurons in the nociceptive pathway or through the creation of astrocytic networks capable of transducing signals for extended distances across and along the spinal cord. Future research in astrocyte activation and signaling may therefore reveal novel drug targets for managing pathological pain.
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Keywords {🔍}

article, google, scholar, pubmed, cas, pain, spinal, astrocytes, rat, cord, neurosci, neurons, nerve, glial, calcium, dorsal, activation, expression, astrocyte, neuropathic, doi, injury, res, primary, atp, dois, waves, nature, root, liu, release, brain, interleukin, sensory, induces, signaling, neuronal, glutamate, receptors, horn, wang, cell, necrosis, doijpain, content, models, hald, afferent, peripheral, neurochem,

Topics {✒️}

c-jun n-terminal kinase month download article/chapter glial-cytokine-neuronal interactions underlying calcitonin gene-related peptide tumor necrosis factor-alpha glutamate-mediated astrocyte-neuron signalling tumour necrosis factor-alpha c-fos gene expression long-range glial signaling afferent a-fiber neurons mitogen-activated protein kinases suppressed injury-induced rise extracellular signal-regulated kinase phosphoinositide-linked peptide response cholecystokinin-immunoreactive ganglion cells pma-induced interleukin-1 production long-term potentiation 125i-bolton hunter substance opioid-resistant bone pain spinal il-1beta expression interleukin-1beta induces substance p2x receptor-mediated modulation calcium channel subunit glutamate-stimulated atp release atp-induced atp release full article pdf spinal cord microglia substance p-induced activation related glial proteins spinal glial activation peripheral nerve injury primary afferent neurons primary afferent fibers lumbar spinal cord spinal nerve-injured rats long-term plasticity spinal dorsal horn peripheral nerve lesions calcium waves mediated dorsal root ganglion dorsal root ganglia privacy choices/manage cookies spinal nerve ligation spinal cord neurons interleukin-6 gene expression neuronal synchrony mediated primary sensory neurons dorsal root injury postoperative mechanical hypersensitivity lumbar root injury

Questions {❓}

Fyffe RE, Perl ER (1984) Is ATP a central synaptic mediator for certain primary afferent fibers from mammalian skin?
Hald A, Lotharius J (2005) Oxidative stress and inflammation in Parkinson’s disease: is there a causal link?
Ji RR, Kohno T, Moore KA, Woolf CJ (2003) Central sensitization and LTP: do pain and memory share similar mechanisms?
Kennedy C (2005) P2X receptors: targets for novel analgesics?
Tracey DJ, Walker JS (1995) Pain due to nerve damage: are inflammatory mediators involved?

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