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Transient inhibition of LIMKs significantly attenuated central sensitization and delayed the development of chronic pain.

Abstract：

:Central sensitization represents a key mechanism mediating chronic pain, a major clinical problem lacking effective treatment options. LIM-domain kinases (LIMKs) selectively regulate several substrates, e.g. cofilin and cAMP response element-binding protein (CREB), that profoundly affect neural activities, such as synaptogenesis and gene expression, thus critical in the consolidation of long-term synaptic potentiation and memory in the brain. In this study, we demonstrate that LIMK deficiency significantly impaired the development of multiple forms of chronic pain. Mechanistic studies focusing on spared nerve injury (SNI) model reveal a pivotal role of LIMKs in the up-regulation of spontaneous excitatory synaptic transmission and synaptogenesis after pain induction. Depending on the pain induction methods, LIMKs can be transiently activated with distinct time courses. Accordingly, pharmacological inhibition of LIMKs targeting this critical period remarkably attenuated central sensitization in the spinal cord and alleviated pain behaviors. We propose selectively targeting LIMKs during their activation phase as a potential therapeutic strategy for clinical management of chronic pain, especially for chronic pain with predictable onset and development time courses, such as chronic post-surgical pain (PSP).

journal_name

Neuropharmacology

journal_title

Neuropharmacology

authors

Yang X,He G,Zhang X,Chen L,Kong Y,Xie W,Jia Z,Liu WT,Zhou Z

doi

10.1016/j.neuropharm.2017.06.031

subject

Has Abstract

pub_date

2017-10-01 00:00:00

pages

284-294

eissn

0028-3908

issn

1873-7064

pii

S0028-3908(17)30304-0

journal_volume

125

pub_type

杂志文章

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