Fig. 6.
Selective adenosine monophosphate–activated protein kinase α1 genetic deletion (AMPKα1 KO) induced thermal hyperalgesia and mechanical allodynia, which is associated with decreased glial glutamate transporter-1 (GLT-1) expression and increased glial fibrillary acidic protein promoter (GFAP) and interleukin-1β (IL-1β) protein expression and glycogen synthase kinase 3β (GSK3β) activity. (A) Bar graphs show summaries (+ SEM) of the withdrawal latency to heat stimuli in the AMPKα1 KO and littermate mice. (B) Bar graphs show summaries (+ SEM) of the 50% mechanical withdrawal threshold in the AMPKα1 KO and littermate mice. (C) Bar graphs show the mean (+ SEM) relative density of GLT-1, GFAP, and IL-1β to β-actin and phosphorylated GSK3β (pGSK3β) to total GSK3β (tGSK3β) in the spinal cord of AMPKα1 knockout mice and littermates. Samples of each molecule protein expression in each group are shown. *P < 0.05, **P < 0.01. KO = knockout.

Selective adenosine monophosphate–activated protein kinase α1 genetic deletion (AMPKα1 KO) induced thermal hyperalgesia and mechanical allodynia, which is associated with decreased glial glutamate transporter-1 (GLT-1) expression and increased glial fibrillary acidic protein promoter (GFAP) and interleukin-1β (IL-1β) protein expression and glycogen synthase kinase 3β (GSK3β) activity. (A) Bar graphs show summaries (+ SEM) of the withdrawal latency to heat stimuli in the AMPKα1 KO and littermate mice. (B) Bar graphs show summaries (+ SEM) of the 50% mechanical withdrawal threshold in the AMPKα1 KO and littermate mice. (C) Bar graphs show the mean (+ SEM) relative density of GLT-1, GFAP, and IL-1β to β-actin and phosphorylated GSK3β (pGSK3β) to total GSK3β (tGSK3β) in the spinal cord of AMPKα1 knockout mice and littermates. Samples of each molecule protein expression in each group are shown. *P < 0.05, **P < 0.01. KO = knockout.

Close Modal
This Feature Is Available To Subscribers Only

or Create an Account

Close Modal
Close Modal