Acute inhibition of Ca2+/calmodulin-dependent protein kinase II reverses experimental neuropathic pain in mice.
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Ca2+/calmodulin-dependent protein kinase II alpha is required for the initiation and maintenance of opioid-induced hyperalgesiaPLGA-Curcumin Attenuates Opioid-Induced Hyperalgesia and Inhibits Spinal CaMKIIαCaMKIIα may modulate fentanyl-induced hyperalgesia via a CeLC-PAG-RVM-spinal cord descending facilitative pain pathway in ratsSpontaneous itch in the absence of hyperalgesia in a mouse hindpaw dry skin modelLamotrigine increases intracellular Ca(2+) levels and Ca(2+)/calmodulin-dependent kinase II activation in mouse dorsal root ganglion neurones.Haloperidol disrupts opioid-antinociceptive tolerance and physical dependenceCurcumin attenuates opioid tolerance and dependence by inhibiting Ca2+/calmodulin-dependent protein kinase II α activityCalcium/calmodulin kinase II in the pedunculopontine tegmental nucleus modulates the initiation and maintenance of wakefulnessDifferential expression of CaMKII isoforms and overall kinase activity in rat dorsal root ganglia after injury.Early insights into the neurobiology of pain in sickle cell disease: A systematic review of the literature.Negative reinforcement reveals non-evoked ongoing pain in mice with tissue or nerve injury.Inhibition of Ca2+/calmodulin-dependent protein kinase II reverses oxaliplatin-induced mechanical allodynia in rats.Ca(2+)/calmodulin-dependent protein kinase II is associated with pelvic pain of neurogenic cystitis.Post-translational modifications of voltage-gated sodium channels in chronic pain syndromesNeurobiological mechanisms of pain in sickle cell disease.Mechanism-driven phase I translational study of trifluoperazine in adults with sickle cell disease.Roles of reactive oxygen and nitrogen species in painInhibition of CaMKIIα in the Central Nucleus of Amygdala Attenuates Fentanyl-Induced Hyperalgesia in Rats.Genetic inactivation of calpain-1 attenuates pain sensitivity in a humanized mouse model of sickle cell disease.CaMKIIα underlies spontaneous and evoked pain behaviors in Berkeley sickle cell transgenic mice.Ca2+ /calmodulin-dependent protein kinase II in spinal dorsal horn contributes to the pain hypersensitivity induced by γ-aminobutyric acid type a receptor inhibition.CaMKIIα Mediates the Effect of IL-17 To Promote Ongoing Spontaneous and Evoked Pain in Multiple Sclerosis.Electroacupuncture alleviates chemotherapy-induced pain through inhibiting phosphorylation of spinal CaMKII in rats.
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Acute inhibition of Ca2+/calmodulin-dependent protein kinase II reverses experimental neuropathic pain in mice.
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article científic
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article scientifique
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articolo scientifico
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artigo científico
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bilimsel makale
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scientific article published on 28 May 2009
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
Acute inhibition of Ca2+/calmo ...... ntal neuropathic pain in mice.
@en
Acute inhibition of Ca2+/calmo ...... ntal neuropathic pain in mice.
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type
label
Acute inhibition of Ca2+/calmo ...... ntal neuropathic pain in mice.
@en
Acute inhibition of Ca2+/calmo ...... ntal neuropathic pain in mice.
@nl
prefLabel
Acute inhibition of Ca2+/calmo ...... ntal neuropathic pain in mice.
@en
Acute inhibition of Ca2+/calmo ...... ntal neuropathic pain in mice.
@nl
P2093
P2860
P356
P1476
Acute inhibition of Ca2+/calmo ...... ntal neuropathic pain in mice.
@en
P2093
Chelsea M Kirkmire
Cheng Yang
Zaijie Jim Wang
P2860
P304
P356
10.1124/JPET.109.152165
P407
P577
2009-05-28T00:00:00Z