Table 1.
Time (min) | 0 | 15 | 30 | 45 | 60 | 90 | 120 | 180 |
---|---|---|---|---|---|---|---|---|
Normal | 0.5 ± 0.1 | 0.7 ± 0.1 | 0.6 ± 0.1 | 0.6 ± 0.1 | 0.5 ± 0.1 | 0.7 ± 0.1 | 0.6 ± 0.1 | 0.5 ± 0.1 |
V + S + S | 13.2 ± 0.4* | 13.4 ± 0.4* | 12.9 ± 0.4* | 12.9 ± 0.3* | 13.4 ± 0.4* | 12.9 ± 0.4* | 13.2 ± 0.4* | 13.0 ± 0.4* |
V + S + R-PIA 0.3 | 12.6 ± 0.3* | 11.7 ± 0.6* | 11.5 ± 0.4* | 11.8 ± 0.5* | 12.5 ± 0.3* | 11.6 ± 0.4* | 12.2 ± 0.4* | 12.7 ± 0.3* |
V + DPCPX + R-PIA 0.3 | 12.7 ± 0.4* | 12.6 ± 0.6* | 12.3 ± 0.5* | 12.1 ± 0.5* | 11.8 ± 0.4* | 12.4 ± 0.4* | 12.2 ± 0.4* | 12.7 ± 0.3* |
V + S + R-PIA 1.0 | 13.2 ± 0.4* | 4.2 ± 0.7*,† | 4.9 ± 0.9*,† | 6.8 ± 0.7*,† | 6.6 ± 0.4*,† | 7.7 ± 0.6*,† | 10.0 ± 0.3*,† | 11.0 ± 0.3*,† |
V + DPCPX + R-PIA 1.0 | 13.1 ± 0.3* | 11.4 ± 0.4*,‡ | 11.7 ± 0.4*,‡ | 12.2 ± 0.6*,‡ | 12.9 ± 0.2*,‡ | 12.4 ± 0.5*,‡ | 13.0 ± 0.2*,‡ | 13.3 ± 0.4* |
V + S + R-PIA 3.0 | 13.4 ± 0.4* | 0.7 ± 0.3† | 1.3 ± 0.6† | 2.0 ± 0.8† | 3.2 ± 0.8*,† | 3.7 ± 0.7*,† | 5.6 ± 0.6*,† | 6.7 ± 0.4*,† |
V + DPCPX + R-PIA 3.0 | 13.0 ± 0.4* | 11.1 ± 0.3*,§ | 10.6 ± 0.3*,§ | 11.2 ± 0.5*,§ | 11.2 ± 0.4*,§ | 11.7 ± 0.3*,§ | 12.7 ± 0.4*,§ | 12.9 ± 0.3*,§ |
Peripheral neuropathy was induced by the administration of vincristine (100 μg/kg, i.p.) for 10 days. On the 28th day, saline or DPCPX (10 μg/10 μl) was intrathecally administered 15 min before intrathecal R-PIA administration (1.0 μg/10 μl or 3.0 μg/10 μl). Cold allodynia was then assessed using the acetone drop test (seconds). Results are expressed as mean ± standard error of mean, n = 6 rats per group. One-way ANOVA followed by Tukey’s post hoc test.
P < 0.05 vs. normal control group,
P < 0.05 vs. vincristine control group,
P < 0.05 vs. R-PIA 1.0 μg/10 μl group,
P < 0.05 vs. R-PIA 3.0 μg/10 μl group. V: vincristine, S: saline, DPCPX: 1,3-dipropyl-8-cyclopentylxanthine = adenosine A1 receptor antagonist, R-PIA: N6-(2-phenylisopropyl)-adenosine R-(-)isomer = adenosine A1 receptor agonist.