The Underlying Mechanism Of Chronic Pain And Chronic Itch Inducing Synaptic Plasticity In Anterior Cingulate Cortex

Objective We aimed to study the changes of synaptic plasticity of anterior cingulate cortex(ACC)in rats with chronic pain or chronic itch.Methods SD rats were divided into sham group,CCI group,veh group and meflo group.Other rats were divided into control group and DCP group.And each group was treated accordingly.Behavioral tests for each group were performed accordingly.mEPSC was recorded in the ACC layer II/III pyramidal cells in sham,CCI,control,and DCP groups by whole-cell patch-clamp recording.Next,the expression of Cx36,membrane GluR1,GluR2 and p-GluR1 in the anterior cingulate cortex of rats were detected by Western blotting.Results In chronic pain experiments,we found that(1)the frequency and amplitude of mEPSC were significantly increased in CCI group(P < 0.05),and(2)the time courses were also significantly shortened(P < 0.05).Protein expression assays showed that(3)the expression level of Cx36 was significantly increased in CCI group(P < 0.05).Compared with sham group,(4)membrane GluR1 of CCI group was significantly increased(P < 0.05).And the level of p-GluR1 was also significantly increased(P < 0.05).In chronic itch research,protein expression assays showed that(5)there was no significant difference in the expression level of Cx36 compared with veh group(P > 0.05),(6)membrane GluR1 and p-GluR1 were significantly decreased(P < 0.05).(7)The frequency and amplitude of mEPSC were significantly increased in model group(P < 0.05).However,time courses of mEPSC were no difference between the two groups(P > 0.05).Western blotting analysis showed that(8)there was no significant difference in the expression of membrane GluR1 or GluR2 between the two groups(P > 0.05).Conclusions 1.Chronic pain led to increased expression of Cx36,membrane GluR1 and increased GluR1 phosphorylation.2.The amplitude and frequency of mEPSC increased,and the time course was shortened in chronic pain rats.3.Normal distribution and phosphorylation of GluR1 was dependent on the function of Cx36.4.Chronic itch enhanced excitatory synaptic transmission in ACC 5.Chronic itch did not influence membrane trafficking of GluR1.