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. 2018 Aug 13;9:3230. doi: 10.1038/s41467-018-05709-0

Fig. 6.

Fig. 6

Antipruritic actions of TPA023B. a Antipruritic actions of TPA023B (p.o.) in mouse models of acute itch. Circles are total number of scratching bouts observed in individual mice within 30 min after intracutaneuos pruritogen injection. ANOVA, followed Dunnett’s post hoc test with vehicle as control. *P < 0.05, **P < 0.01, ***P < 0.001. Chloroquine (100 µg). F(5,29) = 6.44, n = 6, 7, 6, 6, 6, 5 for vehicle, and 0.01, 0.03, 0.1, 1.0, and 3.0 mg kg−1. α-Me5HT-evoked itch (20 µg). n = 8, 6, 7, 7, 6, 6 for vehicle, and 0.01, 0.03, 0.1, 1.0, and 3.0 mg kg−1. Histamine-evoked itch (100 µg). F(5,41) = 5.20, n = 9, 8, 11, 7, 6, 6 for vehicle, and 0.01, 0.03, 0.1, 1.0, and 3.0 mg kg−1. b The antipruritic action of TPA023B occurs via the benzodiazepine bind site of GABAARs. α-methyl 5-HT (20 µg) was injected intracutaneously into the right cheek. TPA023B (1 mg kg−1, p.o.) exerted strong antipruritic actions in wild-type mice. In HRRR mice, in which all TPA023B sensitive GABAARs subtypes had been rendered benzodiazepine-insensitive, TPA023B had completely lost its antipruritic action. Two-way ANOVA F(2,22) = 6.45. P = 0.019 for genotype × treatment. P = 0.005 (**) and 0.60 (ns) for treatment effect in wild-type and HRRR mice, respectively (n = 7, 6 (wild-type, vehicle and TPA023B); n = 6, 7 (HRRR mice, vehicle and TPA023B)). ++P < 0.01 relative to TPA023B-treated wild-type mice. c–e TPA023B (3 mg kg−1, p.o.) did not interfere with responses to somatosensory or acute noxious stimulation. c light mechanical stimulation with a paint brush, d punctate mechanical stimulation with von Frey filaments, e noxious heat stimulation with a radiant heat source. Five mice per group. Error bars indicate s.e.m.