ライフサイエンスコーパス: ritanserin

1 s blocked by the 5-HT(2) receptor antagonist ritanserin.

2 This effect was blocked by ritanserin.

3 with haloperidol (0.5 mg/kg) or haloperidol+ritanserin (0.5 mg/kg and 1.0 mg/kg, respectively) showe

4 The administration of ritanserin (1 mg/kg intraperitoneally) to older obese ra

5 ers at CT 6 with the serotonergic antagonist ritanserin (1-5 mg/kg, which acts at both 5-HT2 and the

6 oline (10 nmol) or GR55526 (10 nmol) but not ritanserin (10 nmol) into the PVN attenuated the anorect

7 ) which was blocked by the 5-HT2 antagonist, ritanserin (2.40 +/- 2.7 vs. 7.04 +/- 4.6 mV).

8 Ritanserin (2mg/kg) replicated the inhibitory effects se

9 nal ketanserin (1-100mug/50mul) and systemic ritanserin (2mg/kg), at these doses, have similar antino

10 her with WAY-100635, a 5-HT1A antagonist, or ritanserin, a 5-HT2A/2C antagonist, prior to d-fenfluram

11 ed the effects of systemic administration of ritanserin, a 5-HT2A/2C receptor antagonist and spinal a

12 ed the effects of systemic administration of ritanserin, a serotonin (5-HT) 2A and 2C receptor antago

13 Ritanserin also had no effect on ventilatory responses t

14 pretreatment with the 5-HT(2,7) antagonist, ritanserin, also significantly inhibited DRN-electricall

15 Ritanserin, an inhibitor of diacylglycerol kinase alpha

16 hibited by the 5-HT(2,7) receptor antagonist ritanserin and by the more selective 5-HT(7) receptor an

17 ngs demonstrate that the 5-HT(2) antagonists ritanserin and ketanserin, as well as the 5-HT(3) antago

18 2aR antibodies and by the 5HT2aR antagonists ritanserin and ketanserin.

19 ely related non-antipsychotic drugs, such as ritanserin and methysergide, also block 2AR function, bu

20 investigated by competitive inhibition with ritanserin and pindolol, respectively.

21 -methyl-5HT, N-omega-methyl-5HT, ketanserin, ritanserin, and spiperone and had no effect on the bindi

22 The 5-HT(2) receptor antagonist, ritanserin, and the 5-HT(2B) receptor antagonist, SB2047

23 ist methysergide, the pan-5-HT(2) antagonist ritanserin, and the 5-HT(2B/2C)-selective antagonist SB2

24 asis in mTORC1-hyperactive cells and suggest ritanserin as a novel therapeutic strategy for use in mT

25 In addition, ritanserin blocked the enhancement of type I response pr

26 Ritanserin decreased macropinocytic uptake of albumin, l

27 effect was less apparent in the haloperidol+ritanserin group.

28 loned human 5-HT7 receptor was: methiothepin>ritanserin>mesulergine=clozapine> or =metergoline=5-HT>S

29 In contrast, the 5-HT2 antagonist, ritanserin, had no effect on the amplitude of these EPSC

30 ine (5-MeOT, K(i)=111 nM)>5-HT (K(i)=150 nM)>ritanserin (K(i)=207 nM)>5-carboxamidotryptamine (5-CT,

31 ) MEFs, and treatment of Tsc2(-/-) MEFs with ritanserin led to depletion of phosphatidic acid as well

32 Targeting macropinocytosis with ritanserin may represent a novel therapeutic approach fo

33 onist (alpha-methyl-5-HT), or an antagonist (ritanserin) of 5-HT(2A) receptors to the primary auditor

34 as the long-term BF shifts; (5) in contrast, ritanserin reduced the auditory responses and reversed t

35 While ritanserin reduced the tolerance-like effects of haloper

36 (non-specific receptor subtypes 1 and 2), or ritanserin (selective 2C), or GR55562 (selective l B) wa

37 dol (low 5-HT(2A/2C)/high D(2)), haloperidol+ritanserin (selective 5-HT(2A/2C)), or vehicle.

38 The administration of ritanserin significantly increased Pcrit in older obese

39 In a mouse model of TSC, ritanserin treatment decreased cyst frequency and volume