ライフサイエンスコーパス: flinch

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1 average MFF and the average total number of flinches.

2 r, capsaicin-treated rats exhibited 59% less flinching and 45% smaller heart rate responses.

3 ting ET(B) receptors on ET-1-induced hindpaw flinching and excitation of nociceptors in rats.

4 T-1 (200 microm) reduced the time-to-peak of flinching and significantly enhanced the average maximal

5 namely phase 2 response of formalin-induced flinching, and attenuated tactile allodynia in the spina

6 antly attenuates phase 2 lifting/licking and flinching behavior and this AIDA-induced effect is block

7 hough there was no significant difference in flinching behavior between the morphine-tolerant and con

8 ve, naloxone-reversible abolition of phase 2 flinching behavior compared to rats infected with a cont

9 r cardiovascular responses and slightly less flinching behavior during Phase 1.

10 5% formalin into the dorsum caused a defined flinching behavior in the afflicted paw, and the amount

11 d-swim test, and it is a potent inhibitor of flinching behavior in the inflammatory pain model induce

12 ction of S1P induced significant licking and flinching behavior in wild-type mice and a dose-dependen

13 duced lifting and licking behaviors, however flinching behavior was not effected.

14 Akt attenuated Formalin-induced second-phase flinching behavior, as well as carrageenan-induced therm

15 nociception was accompanied by a spontaneous flinching behavior.

16 significantly reduced the number of Phase 2 flinches by about 80%.

17 e resulted in significantly reduced hind paw flinching compared with morphine alone in the first and

18 Hindpaw flinching developed within minutes after ET-1 (8-16 nmol

19 ochemical challenge model (capsaicin-induced flinch, ED50 = 0.33 mg/kg p.o.) and was antihyperalgesic

20 urface of the hindpaw, counted the number of flinches for 2 h and then processed the lumbar cord for

21 d significantly enhanced the average maximal flinch frequency (MFF).

22 tive scoring method used (weighted scores or flinch-frequency method) and was not accompanied by a co

23 as efficacious in blocking capsaicin-induced flinch in rats in a dose-dependent manner.

24 TRPV1 receptors, restored capsaicin-induced flinching in CB(1)KO mice.

25 dose-related inhibition of capsaicin-induced flinching in ICR mice.

26 LY235959 can also reduce the flinching in Phase 2 by 30% when given subcutaneously (s

27 ed dose-dependent inhibition of AITC-induced flinching in rats, validating its utility as a tool for

28 ein and activity, along with exaggerated paw flinching in response to 0.5% paw formalin injection.

29 the early analogs, failed to reduce phase 2 flinching in the mouse formalin test even at a dose of 1

30 In Experiment 2, foot shock responses (flinch, jump, sonic vocalizations) to escalating shock l

31 ced marked attenuation of the characteristic flinching, licking, and lifting responses resulting from

32 0 = 1.9 mg/kg, p.o. in the capsaicin-induced flinch model in rats) and was also effective at reducing

33 Increased flinching of diabetic rats was attenuated by intrathecal

34 sly evaluated formalin-evoked pain behavior (flinching of the afflicted paw), cardiovascular response

35 ttenuated the formalin paw injection-induced flinching, preferentially at the 2nd phase, that is know

36 behaviors and demonstration of a nonclassic "flinch" response to air gun signals.

37 apsaicin produced dose- and time-related paw flinch responses in ICR and CB(1)WT mice and induced pla

38 ceptive behaviors (paw lifting, licking, and flinching) that reflect the intensity and localization o

39 vior in the afflicted paw, and the amount of flinching was significantly (P<0.05) greater in diabetic

40 t formalin-evoked edema, as well as hind paw flinching, was observed in striated muscle control-trans

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