Abstract:
:Despite the consensus that activation of TWIK-related spinal cord K+ (TRESK) might contribute to the pathogenesis of chronic pain, the specific mechanisms underlying the transfer and development of pain signals still remain obscure. In the present study, we validated that TRESK was expressed in neurons instead of glial cells. Furthermore, in the SNI model of neuropathic pain (NP), downregulation of TRESK in spinal cord neurons resulted in upregulation of connexin 36 (Cx36) and connexin 43 (Cx43), both being subtypes of gap junctions in the spinal cord, with gliocytes in the spinal cord activated ultimately. Compared with SNI rats, intrathecal injection of TRESK gene recombinant adenovirus significantly downregulated the expression levels of Cx36 and Cx43 and suppressed the activation of gliocytes in the spinal cord, with hyperalgesia significantly reduced. In conclusion, TRESK contributes to the pathogenesis of NP by upregulation of synaptic transmission and activation of gliocytes.
journal_name
Neurochem Resjournal_title
Neurochemical researchauthors
Zhou J,Chen H,Yang C,Zhong J,He W,Xiong Qdoi
10.1007/s11064-016-2170-zsubject
Has Abstractpub_date
2017-05-01 00:00:00pages
1288-1298issue
5eissn
0364-3190issn
1573-6903pii
10.1007/s11064-016-2170-zjournal_volume
42pub_type
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