Title : Activation of JNK pathway in spinal astrocytes contributes to acute ultra-low-dose morphine thermal hyperalgesia.

Pub. Date : 2015 Jul

PMID : 25806604






8 Functional Relationships(s)
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1 Activation of JNK pathway in spinal astrocytes contributes to acute ultra-low-dose morphine thermal hyperalgesia. Morphine mitogen-activated protein kinase 8 Homo sapiens
2 Morphine elevated spinal JNK1, JNK2, and c-Jun phosphorylation. Morphine mitogen-activated protein kinase 8 Homo sapiens
3 Pretreatment with a PKC inhibitor prevented morphine hyperalgesia and JNK and c-Jun overphosphorylation, indicating PKC is a JNK upstream modulator and illustrating the presence of a pathway involving PKC, NMDA, and JNK activated by morphine. Morphine mitogen-activated protein kinase 8 Homo sapiens
4 Pretreatment with a PKC inhibitor prevented morphine hyperalgesia and JNK and c-Jun overphosphorylation, indicating PKC is a JNK upstream modulator and illustrating the presence of a pathway involving PKC, NMDA, and JNK activated by morphine. Morphine mitogen-activated protein kinase 8 Homo sapiens
5 Pretreatment with a PKC inhibitor prevented morphine hyperalgesia and JNK and c-Jun overphosphorylation, indicating PKC is a JNK upstream modulator and illustrating the presence of a pathway involving PKC, NMDA, and JNK activated by morphine. Morphine mitogen-activated protein kinase 8 Homo sapiens
6 Pretreatment with a PKC inhibitor prevented morphine hyperalgesia and JNK and c-Jun overphosphorylation, indicating PKC is a JNK upstream modulator and illustrating the presence of a pathway involving PKC, NMDA, and JNK activated by morphine. Morphine mitogen-activated protein kinase 8 Homo sapiens
7 Pretreatment with a PKC inhibitor prevented morphine hyperalgesia and JNK and c-Jun overphosphorylation, indicating PKC is a JNK upstream modulator and illustrating the presence of a pathway involving PKC, NMDA, and JNK activated by morphine. Morphine mitogen-activated protein kinase 8 Homo sapiens
8 These results illustrate the selective activation of an astrocyte JNK pathway after the stimulation of neuronal MOR, which contributes to ultra-low-dose morphine hyperalgesia. Morphine mitogen-activated protein kinase 8 Homo sapiens