Acute spinal cord injury (SCI) transforms how GABA affects nociceptive sensitization
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- 作者：Yung-Jen Huanga ; redkie@gmail.com" class="auth_mail" title="E-mail the corresponding author ; Kuan H. Leeb ; Lauren Murphya ; Sandra M. Garrawayc ; James W. Graua
- 关键词：Bic ; Bicuculline ; Cap ; Capsaicin ; CNS ; Central nervous system ; DIOA ; Dihydro-indenyl-oxy alkanoic acid ; EMR ; Enhanced mechanical reactivity ; ERK ; Extracellular signal-regulated kinases ; GABA ; Gamma-aminobutyric acid ; GBZ ; GABAzine ; 8-OH-DPAT ; 8-Hydroxy-2-dipropylaminotetralin hydrobromide ; i.t. ; Intrathecal ; KCC2 ; K+-Cl&minus ; cotransporter 2 ; LPS ; Lipopolysaccharides ; LTP ; Long-term potentiation ; Mus ; Muscimol ; N-CAD ; N-cadherin ; NKCC1 ; Na+-K+-Cl&minus ; cotransporter 1 ; NMDAR ; N-methyl-d-aspart
- 刊名：Experimental Neurology
- 出版年：2016
- 出版时间：November 2016
- 年：2016
- 卷：285
- 期：part_PA
- 页码：82-95
- 全文大小：2072 K
文摘
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Acute spinal cord injury induces a qualitative shift in how GABA affects nociceptive transmission.
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GABAA receptor antagonism blocks the development of central sensitization after spinal cord injury.
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Disrupting KCC2 function transforms how GABA impacts the development of nociceptive sensitization.