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Table 1 Loss of nerve injury- and LPA-induced spinal SP-mediated functional reduction in LPA1 -/- mice and mice with BoNT/C3 treatment.

From: Loss of spinal substance P pain transmission under the condition of LPA1 receptor-mediated neuropathic pain

 

SP (0.01 pmol, i.pl.)

SP (0.1 pmol, i.pl.)

SP (1 pmol, i.pl.)

WT (Sham)

19.2 ± 2.4

36.0 ± 1.9

52.8 ± 2.4

WT (Injury)

5.7 ± 3.6 *

10.9 ± 3.9 *

8.6 ± 6.6 *

KO (Injury)

20.0 ± 4.5 #

34.9 ± 4.6 #

52.2 ± 2.1 #

Sham (Veh)

13.0 ± 2.3

23.8 ± 3.1

66.2 ± 6.6

Injury (Veh)

3.8 ± 0.5 *

6.1 ± 3.7 *

14.6 ± 7.7 *

Injury (BoNT/C3)

11.1 ± 6.8 #

21.2 ± 5.6 #

65.1 ± 8.8 #

WT (Veh)

10.1 ± 3.6

23.9 ± 4.6

53.2 ± 3.2

WT (LPA)

0 *

6.3 ± 0.8 *

11.1 ± 4.0 *

KO (LPA)

13.3 ± 2.6 #

28.2 ± 2.0 #

52.9 ± 1.7 #

Veh (Veh)

9.2 ± 1.2

21.6 ± 3.2

64.8 ± 6.0

LPA (Veh)

1.2 ± 0.2 *

4.8 ± 0.1 *

12.0 ± 4.8 *

LPA (BoNT/C3)

10.1 ± 1.9 #

19.2 ± 4.8 #

62.4 ± 6.0 #

  1. Nociceptive flexor responses induced by injection (2 μl) of SP at each dose were normalized to the 'maximal reflex' defined as the biggest response among the responses occurring immediately after cannulation. Significance was set to *, #p < 0.05. Data are presented as means ± S.E.M. from experiments using at least 6 mice.
  2. WT (Sham), WT (Injury) and KO (Injury) represent LPA1 +/+ mice with sham-operation, LPA1 +/+ mice with injury, and LPA1 -/- mice with injury, respectively.
  3. Sham (Veh), Injury (Veh) and Injury (BoNT/C3) represent sham-operated mice with vehicle treatment, injured mice with vehicle treatment, and injured mice with BoNT/C3 (10 ng, 1 hr before injury), respectively.
  4. WT (Veh), WT (LPA) and KO (LPA) represent LPA1 +/+ mice with vehicle-treatment, LPA1 +/+ mice with LPA-treatment injury, and LPA1 -/- mice with LPA-treatment, respectively.
  5. Veh (Veh), LPA (Veh) and LPA (BoNT/C3) represent vehicle-treated mice with vehicle treatment, LPA-treated mice with vehicle treatment, and LPA-treated mice with BoNTC3 (10 ng, 1 hr before LPA treatment), respectively.