Extended Data Fig. 2: Different to the spinal cord, pain stimuli do not promote major glycogen accumulation in DRGs and higher brain centers processing pain signals (related to Fig. 2).

(a) Glycogen content of ipsilateral dorsal spinal cord tissue compared to that of the contralateral side 2 or 8 weeks after Spared Nerve Injury- (SNI-)induced pain and with or without intraplantar capsaicin injection 6 h prior to tissue preparation; expressed as percent glycogen content of the ipsilateral dorsal spinal cord of sham/untreated mice. Note that SNI or capsaicin alone only slightly elevate glycogen levels while the combination of the two synergistically increases glycogen accumulation. (N = 3 mice); one-way ANOVA with Tukey’s post hoc test. (b) qPCR-determined relative expression level of Ptg mRNA transcripts in L2-L5 DRGs 2 hours after formalin stimulation compared to naïve DRGs (N = 4 mice). Unpaired two-tailed t-test. (c) Glycogen content of ipsilateral L2-L5 DRGs 1 day after formalin injection compared to that of naïve mice (N = 4 independent samples of 4 mice). (d-g) Glycogen content in the amygdala (d), insula cortex (e), prefrontal cortex (f) and hindlimb region of the somatosensory cortex (g) isolated from naïve or 6 h CFA-treated mice. Glycogen content of these bilateral brain regions is expressed as percent of the average of the left and right side of the naïve mice. Two-way ANOVA with Bonferroni post hoc test; data shown as mean ±s.e.m. N = 4 mice for naïve animals and N = 6 animals for CFA-treated animals.