Contribution of afferent pathways to nerve injury-induced spontaneous pain and evoked hypersensitivity. - Wikidata - awgldk - TriplyDB

Contribution of afferent pathways to nerve injury-induced spontaneous pain and evoked hypersensitivity.

Contribution of afferent pathways to nerve injury-induced spontaneous pain and evoked hypersensitivity.

http://www.wikidata.org/entity/Q35837446

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Inhibition of mechanical allodynia in neuropathic pain by TLR5-mediated A-fiber blockade.Use of Capsaicin to Treat Pain: Mechanistic and Therapeutic Considerations Brain Circuits Encoding Reward from Pain Relief Descending facilitation maintains long-term spontaneous neuropathic pain Engagement of descending inhibition from the rostral ventromedial medulla protects against chronic neuropathic pain.Afferent drive elicits ongoing pain in a model of advanced osteoarthritis.Contribution of PKMζ-dependent and independent amplification to components of experimental neuropathic pain Negative reinforcement reveals non-evoked ongoing pain in mice with tissue or nerve injury.Spontaneous Chronic Pain After Experimental Thoracotomy Revealed by Conditioned Place Preference: Morphine Differentiates Tactile Evoked Pain From Spontaneous Pain Pain processing by spinal microcircuits: afferent combinatorics Behavioral and neurochemical analysis of ongoing bone cancer pain in rats.Partial nerve injury induces electrophysiological changes in conducting (uninjured) nociceptive and nonnociceptive DRG neurons: Possible relationships to aspects of peripheral neuropathic pain and paresthesias.Unravelling the mystery of capsaicin: a tool to understand and treat pain Pain relief produces negative reinforcement through activation of mesolimbic reward-valuation circuitry.Nociceptor Sensitization Depends on Age and Pain Chronicity(1,2,3).Activation of Peripheral μ-opioid Receptors by Dermorphin [D-Arg2, Lys4] (1-4) Amide Leads to Modality-preferred Inhibition of Neuropathic Pain Low Frequency Electroacupuncture Alleviated Spinal Nerve Ligation Induced Mechanical Allodynia by Inhibiting TRPV1 Upregulation in Ipsilateral Undamaged Dorsal Root Ganglia in Rats.Targeting Pain-evoking Transient Receptor Potential Channels for the Treatment of Pain.Criticality and degeneracy in injury-induced changes in primary afferent excitability and the implications for neuropathic pain.Systems biology approaches to finding novel pain mediators.Evaluation of reward from pain relief.Calcium-permeable ion channels in pain signaling.Studying ongoing and spontaneous pain in rodents--challenges and opportunities.ThermoTRPs and Pain.Mediation of Movement-Induced Breakthrough Cancer Pain by IB4-Binding Nociceptors in Rats.Electrically evoked compound action potentials recorded from the sheep spinal cord.Nerve injury induced activation of fast-conducting high threshold mechanoreceptors predicts non-reflexive pain related behavior.Conditioned place preference and spontaneous dorsal horn neuron activity in chronic constriction injury model in rats.Persistent hyperalgesia in the cisplatin-treated mouse as defined by threshold measures, the conditioned place preference paradigm, and changes in dorsal root ganglia activated transcription factor 3: the effects of gabapentin, ketorolac, and etaner The effect of gabapentin and ketorolac on allodynia and conditioned place preference in antibody-induced inflammation.Co-application of lidocaine and QX-572 induces divergent pain behaviours in mice.Voltage-gated sodium channel function and expression in injured and uninjured rat dorsal root ganglia neurons.5-Hydroxymethylcytosine (5hmC) and Ten-eleven translocation 1-3 (TET1-3) proteins in the dorsal root ganglia of mouse: Expression and dynamic regulation in neuropathic pain.Understanding chronic inflammatory and neuropathic pain.Peripherally Acting μ-Opioid Receptor Agonists Attenuate Ongoing Pain-associated Behavior and Spontaneous Neuronal Activity after Nerve Injury in Rats.Reducing CXCR4-mediated nociceptor hyperexcitability reverses painful diabetic neuropathy.Spontaneous and Bite-Evoked Muscle Pain Are Mediated by a Common Nociceptive Pathway With Differential Contribution by TRPV1.NALCN channels enhance the intrinsic excitability of spinal projection neurons.

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Contribution of afferent pathways to nerve injury-induced spontaneous pain and evoked hypersensitivity.

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Contribution of afferent pathw ...... n and evoked hypersensitivity.

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Contribution of afferent pathw ...... n and evoked hypersensitivity.

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Contribution of afferent pathw ...... n and evoked hypersensitivity.

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Chaoling Qu

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Frank Porreca

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Jiyang Ren

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Josephine Lai

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Triza Brion

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P2860

Ectopic discharge in Abeta afferents as a source of neuropathic pain

Central changes in processing of mechanoreceptive input in capsaicin-induced secondary hyperalgesia in humans

Quantitative assessment of tactile allodynia in the rat paw

Nerve injury-induced tactile allodynia is present in the absence of FOS labeling in retrogradely labeled post-synaptic dorsal column neurons

Spinal NK-1 receptor expressing neurons mediate opioid-induced hyperalgesia and antinociceptive tolerance via activation of descending pathways.

Pain: an unpleasant topic.

Murine models of inflammatory, neuropathic and cancer pain each generates a unique set of neurochemical changes in the spinal cord and sensory neurons.

An experimental model for peripheral neuropathy produced by segmental spinal nerve ligation in the rat.

Postherpetic neuralgia: irritable nociceptors and deafferentation.

Bad news from the brain: descending 5-HT pathways that control spinal pain processing.

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