Abstract:
:Extracellular signal-regulated kinase (ERK), a mitogen-activated protein kinases (MAPK), transduces a broad range of extracellular stimuli into diverse intracellular responses. Recent studies have showed that ERK activation in the supraspinal level involved in the development of drug dependence, especially in psychological dependence. In this study, we reported that the spinal ERK signaling pathway was activated by chronic morphine injection. There was a further increase in ERK activation after naloxone-precipitated withdrawal. Furthermore, attenuation of the spinal ERK phosphorylation by intrathecal a MAPK kinase (MEK) inhibitor U0126 or knockdown of the spinal ERK by antisense oligonucleotides not only decreased the scores of morphine withdrawal, but also attenuated withdrawal-induced allodynia, which were accompanied by decreased ERK phosphorylation in the spinal cord. The spinal ERK inhibition or knockdown also reduced morphine withdrawal-induced phosphorylation of cAMP response element binding protein (CREB), which is one of the important downstream substrates of ERK pathway, and Fos expression. The involvement of the spinal ERK in morphine withdrawal was supported by our finding that intrathecal N-methyl-D-aspartate receptor antagonist MK-801 or protein kinase C inhibitor chelerythrine chloride suppressed withdrawal-induced ERK activation in the spinal cord and attenuated morphine withdrawal symptoms. These findings suggest activation of the spinal ERK signaling pathway contributes naloxone-precipitated withdrawal in morphine-dependent rats.
journal_name
Painjournal_title
Painauthors
Cao JL,He JH,Ding HL,Zeng YMdoi
10.1016/j.pain.2005.09.006keywords:
subject
Has Abstractpub_date
2005-12-05 00:00:00pages
336-349issue
3eissn
0304-3959issn
1872-6623pii
00006396-200512050-00007journal_volume
118pub_type
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