Spinal neuronal excitability and neuroinflammation in a model of chemotherapeutic neuropathic pain: targeting the resolution pathways

Table 1 Correlations between behavioural pain responses and changes in mRNA expression

Cluster	Genes	Correlation of Δ^CT to mechanical pain threshold
		Spearman r	p value
Pro-inflammatory cascades	Tlr4	−0.6398	0.0210
	Nlrp1a	−0.5966	0.0493
	Tnfrsf1a	−0.6621	0.0160
	Tnfrsf1b	−0.6989	0.0138
Anti-inflammatory cascades	Soc2	−0.6705	0.0143
Anti-inflammatory cascades	Pparg	−0.7541	0.0095
Central sensitisation	Grin2b	−0.6677	0.0149
Chemokine	Cxcl6	−0.5442	0.0704
Chemokine receptors	Cxcr1	−0.5671	0.0461
	Cxcr5	−0.4874	0.1021
	Ccr1	−0.7106	0.0170
	CX3cr1	−0.6174	0.0273
Resolvin synthetic enzyme	Alox5ap	−0.6989	0.0199
Resolvin synthetic enzyme	Cyp2j4	−0.8145	0.0019
Resolvin degradation enzyme	Ptgr1	−0.6981	0.0151

Fold change of mRNA expression is Δ^CT of each gene of the PCX group relative to Δ^CT of the control group. The mechanical pain behaviour is expressed as the number of von Frey filaments changed (ΔvF) at day 28 compared to baseline. Group sizes, n = 11-13 rats

ISSN: 1742-2094