Inhibitory effects of aspirin-triggered resolvin D1 on spinal nociceptive processing in rat pain models

Table 3 Comparison of pain behaviour, joint pathology and characteristics of WDR neurones in the MIA model of OA pain

	Saline-treated (n = 9)	MIA-treated (n = 11)	% change vs saline-treated
Pain behaviour day 28
% weight bearing difference	2 ± 2	15 ± 2**	NA
PWT (g)	17 ± 2.7	6 ± 0.8**	NA
Knee joint pathology
Macroscopic score	0 ± 0.14	14 ± 1.5****	NA
Presence of osteophytes	0/9	10/11	NA
Number of analysed neurones	7	9
Depth (μm)	780 ± 48	720 ± 47
Threshold (mA)
Aβ	0.14 ± 0.01	0.14 ± 0.01	100
C	1.41 ± 0.12	1.54 ± 0.14	109
Latency (ms)
Aβ	7.4 ± 1.04	7.5 ± 0.73	101
C	187.6 ± 24	141.1 ± 15	75
Electrically evoked responses (number of APs)
Aβ^a	129 ± 14	121 ± 14	94
Aβ^b	151 ± 12	135 ± 12	89
Aδ^b	146 ± 16	118 ± 19	81
C^b	384 ± 52	419 ± 49	109
PD^b	394 ± 42	365 ± 67	93
Input^b	280 ± 52	362 ± 61	129
WU^b	502 ± 63	426 ± 56	85

Pain behaviour (weight bearing difference and hind paw withdrawal thresholds) was assessed at 28 days following intra-articular injection of MIA. Spinal WDR neurones were recorded at 28–32 days following intra-articular injection of MIA or saline. Knee joint pathology was assessed following electrophysiological recordings
APs action potentials, NA not applicable for behavioural data
**p < 0.01, ****p < 0.0001 Mann-Whitney U test
^aResponses electrically evoked by 3× Aβ-fibre threshold
^bResponses electrically evoked by 3× C-fibre threshold

ISSN: 1742-2094