Spinal NK-1 receptor expressing neurons mediate opioid-induced hyperalgesia and antinociceptive tolerance via activation of descending pathways.
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From mouse to man: the 5-HT3 receptor modulates physical dependence on opioid narcoticsInduction of synaptic long-term potentiation after opioid withdrawalDescending facilitation maintains long-term spontaneous neuropathic painDescending facilitatory pathways from the rostroventromedial medulla mediate naloxone-precipitated withdrawal in morphine-dependent ratsThe puerperium alters spinal cord plasticity following peripheral nerve injury.Spinal mediators that may contribute selectively to antinociceptive tolerance but not other effects of morphine as revealed by deletion of GluR5Spinal NADPH oxidase is a source of superoxide in the development of morphine-induced hyperalgesia and antinociceptive toleranceLack of analgesic efficacy of spinal ondansetron on thermal and mechanical hypersensitivity following spinal nerve ligation in the rat.Exogenous and endogenous opioid-induced pain hypersensitivity in different rat strains.NADPH-oxidase 2 activation promotes opioid-induced antinociceptive tolerance in mice.Spinal or systemic TY005, a peptidic opioid agonist/neurokinin 1 antagonist, attenuates pain with reduced tolerance.Counter-regulation of opioid analgesia by glial-derived bioactive sphingolipids.Long-term potentiation in spinal nociceptive pathways as a novel target for pain therapy.5-hydroxytryptamine type 3 receptor modulates opioid-induced hyperalgesia and tolerance in mice.Neural correlates of an injury-free model of central sensitization induced by opioid withdrawal in humans.Analysis of opioid efficacy, tolerance, addiction and dependence from cell culture to humanActivation of descending pain-facilitatory pathways from the rostral ventromedial medulla by cholecystokinin elicits release of prostaglandin-E₂ in the spinal cord.Carrageenan induced phosphorylation of Akt is dependent on neurokinin-1 expressing neurons in the superficial dorsal hornContribution of afferent pathways to nerve injury-induced spontaneous pain and evoked hypersensitivity.Pregabalin suppresses spinal neuronal hyperexcitability and visceral hypersensitivity in the absence of peripheral pathophysiologyIncreased spinal dynorphin contributes to chronic nicotine-induced mechanical hypersensitivity in the rat.Tachykinin NK₁ receptor antagonist co-administration attenuates opioid withdrawal-mediated spinal microglia and astrocyte activationPain after discontinuation of morphine treatment is associated with synaptic increase of GluA4-containing AMPAR in the dorsal horn of the spinal cord.Continuous opioid therapy (COT) is rarely advisable for refractory chronic daily headache: limited efficacy, risks, and proposed guidelines.Building a better analgesic: multifunctional compounds that address injury-induced pathology to enhance analgesic efficacy while eliminating unwanted side effects.Preclinical and early clinical investigations related to monoaminergic pain modulation.Alterations in the endometrium of rats, rabbits, and Macaca mulatta that received an implantation of copper/low-density polyethylene nanocomposite.Roles of reactive oxygen and nitrogen species in painOpioid-induced hyperalgesia and burn pain.Calcium-permeable ion channels in pain signaling.Novel Molecular Strategies and Targets for Opioid Drug Discovery for the Treatment of Chronic Pain.Parabrachial complex links pain transmission to descending pain modulation.The Effect of Ondansetron on Acute Opioid Tolerance in Patients Receiving Intrathecal Opioids Prior to Cesarean Delivery.Preprotachykinin-A gene disruption attenuates nociceptive sensitivity after opioid administration and incision by peripheral and spinal mechanisms in mice.GluN2B N-methyl-D-aspartate receptor and excitatory amino acid transporter 3 are upregulated in primary sensory neurons after 7 days of morphine administration in rats: implication for opiate-induced hyperalgesia.Epigenetic regulation of spinal cord gene expression contributes to enhanced postoperative pain and analgesic tolerance subsequent to continuous opioid exposure.Discovery of Novel Multifunctional Ligands with μ/δ Opioid Agonist/Neurokinin-1 (NK1) Antagonist Activities for the Treatment of Pain.Tropisetron alleviate early post-operative pain after gynecological laparoscopy in sevoflurane based general anaesthesia: a randomized, parallel-group, factorial study.Effects of surgery and/or remifentanil administration on the expression of pERK1/2, c-Fos and dynorphin in the dorsal root ganglia in mice.Hyperalgesia and sensitization of dorsal horn neurons following activation of NK-1 receptors in the rostral ventromedial medulla.
P2860
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P2860
Spinal NK-1 receptor expressing neurons mediate opioid-induced hyperalgesia and antinociceptive tolerance via activation of descending pathways.
description
2006 nî lūn-bûn
@nan
2006 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած
@hyw
2006 թվականի նոյեմբերին հրատարակված գիտական հոդված
@hy
2006年の論文
@ja
2006年論文
@yue
2006年論文
@zh-hant
2006年論文
@zh-hk
2006年論文
@zh-mo
2006年論文
@zh-tw
2006年论文
@wuu
name
Spinal NK-1 receptor expressin ...... vation of descending pathways.
@ast
Spinal NK-1 receptor expressin ...... vation of descending pathways.
@en
type
label
Spinal NK-1 receptor expressin ...... vation of descending pathways.
@ast
Spinal NK-1 receptor expressin ...... vation of descending pathways.
@en
prefLabel
Spinal NK-1 receptor expressin ...... vation of descending pathways.
@ast
Spinal NK-1 receptor expressin ...... vation of descending pathways.
@en
P2093
P2860
P1433
P1476
Spinal NK-1 receptor expressin ...... vation of descending pathways.
@en
P2093
En-Tan Zhang
Frank Porreca
Josephine Lai
Louis P Vera-Portocarrero
Michael H Ossipov
Tamara King
Todd W Vanderah
P2860
P356
10.1016/J.PAIN.2006.09.033
P407
P577
2006-11-22T00:00:00Z