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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
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
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
14 pretreatment with the 5-HT(2,7) antagonist, ritanserin, also significantly inhibited DRN-electricall
15 hibited by the 5-HT(2,7) receptor antagonist ritanserin and by the more selective 5-HT(7) receptor an
16 ngs demonstrate that the 5-HT(2) antagonists ritanserin and ketanserin, as well as the 5-HT(3) antago
18 ely related non-antipsychotic drugs, such as ritanserin and methysergide, also block 2AR function, bu
20 -methyl-5HT, N-omega-methyl-5HT, ketanserin, ritanserin, and spiperone and had no effect on the bindi
22 ist methysergide, the pan-5-HT(2) antagonist ritanserin, and the 5-HT(2B/2C)-selective antagonist SB2
25 loned human 5-HT7 receptor was: methiothepin>ritanserin>mesulergine=clozapine> or =metergoline=5-HT>S
27 ine (5-MeOT, K(i)=111 nM)>5-HT (K(i)=150 nM)>ritanserin (K(i)=207 nM)>5-carboxamidotryptamine (5-CT,
28 onist (alpha-methyl-5-HT), or an antagonist (ritanserin) of 5-HT(2A) receptors to the primary auditor
29 as the long-term BF shifts; (5) in contrast, ritanserin reduced the auditory responses and reversed t
31 (non-specific receptor subtypes 1 and 2), or ritanserin (selective 2C), or GR55562 (selective l B) wa
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