ライフサイエンスコーパス: citalopram

1 n drug metabolism of codeine, tamoxifen, and citalopram.

2 f the selective serotonin reuptake inhibitor citalopram.

3 omparison with the reference antidepressant, citalopram.

4 ne > fluoxetine > paroxetine > fluvoxamine > citalopram.

5 clozapine withdrawal with concomitant use of citalopram.

6 reductions in [(11)C]AZ10419369 binding than citalopram.

7 fter pre- and postnatal exposure to the SSRI citalopram.

8 the selective serotonin reuptake inhibitor, citalopram.

9 vidence include memantine, carbamazepine and citalopram.

10 previous suicide attempts or intolerance to citalopram.

11 TLPR is associated with treatment outcome to citalopram.

12 sociated with response to the antidepressant citalopram.

13 n treatment response to the initial trial of citalopram.

14 inadequate benefit from an initial trial of citalopram.

15 mptomatic remission from a 12-week course of citalopram.

16 lective serotonin reuptake inhibitor (SSRI), citalopram.

17 the selective serotonin reuptake inhibitor, citalopram.

18 ffinity binding of many SSRIs, including (S)-citalopram.

19 n [(11)C]CUMI-101 BP(ND) (placebo 1.3 (0.2); citalopram 1.4 (0.2); paired t-test P=0.003).

20 ons to the N, 4, 5, and 4' positions of (+/-)citalopram (1) are reported.

21 ive serotonin reuptake inhibitor (SSRI), (S)-citalopram (1).

22 (+/-)-Citalopram (1, 1-(3-(dimethylamino)propyl)-1-(4-fluoroph

23 1 after receiving an intravenous infusion of citalopram 10 mg or placebo in a double-blind, crossover

24 elective serotonin reuptake inhibitor (SSRI) citalopram (10 mg) intravenously in a double-blind cross

25 Twelve weeks of treatment with citalopram (10 mg/5 mL) or placebo.

26 ys) or subchronically (9 days) with the SSRI citalopram (10 mg/kg/day) before extinction training.

27 e the selective serotonin reuptake inhibitor citalopram (20 mg) or placebo for 7 days.

28 Impairment scale (N=1,928) were treated with citalopram (20-40 mg/day) in the Sequenced Treatment Alt

29 d NPI scores at week 9 in patients receiving citalopram (30 mg/day) or placebo with regard to both th

30 a saline placebo infusion (Day 1) and after citalopram (40 mg, IV, Day 2).

31 be specific to the SERT as displacement with citalopram (a potent SERT ligand) reduced radioactivity

32 nhanced serotonin in healthy volunteers with citalopram (a selective serotonin reuptake inhibitor) an

33 ts were induced by subchronic treatment with citalopram, a prototypical selective serotonin reuptake

34 ping levels of the in vivo-administered drug citalopram, a selective serotonin reuptake inhibitor, in

35 We identified citalopram, a selective serotonin reuptake inhibitor, in

36 Treatment with citalopram abolished the abnormal amygdala responses to

37 -101 availability identified following acute citalopram administration could be attributable to a dec

38 ce are insensitive to chronic fluoxetine and citalopram administration in the novelty induced hypopha

39 The effect of in vivo citalopram administration on the serotonin neurotransmit

40 ainstem TD signal was not increased by acute citalopram administration.

41 The HTTLPR polymorphism is associated with citalopram adverse effects.

42 er as solvent for the analysis of verapamil, citalopram, amitriptyline, lidocaine, and sunitinib in d

43 unknown compounds against colorectal cancer: citalopram (an antidepressant), troglitazone (an antidia

44 ERT), a series of (+/-)-4- and 5-substituted citalopram analogues were designed, synthesized, and eva

45 ant to an initial prospective treatment with citalopram and a second switch or augmentation trial wer

46 Citalopram and BI-11A7 both significantly reduced immobi

47 dministration of the 5-HT reuptake inhibitor citalopram and by low doses of the DA reuptake inhibitor

48 tibule reduces the allosteric potency of (S)-citalopram and clomipramine.

49 Citalopram and decynium-22 attenuated the removal of 5-H

50 e noradrenaline transporter (NET) inhibitors citalopram and desipramine (1 mg kg(-1) ).

51 For example, escitalopram/citalopram and diphenhydramine, taken orally, were detec

52 ctive serotonin reuptake inhibitors (SSRIs), citalopram and escitalopram prolong the QT interval to t

53 Depression (STAR*D) study were treated with citalopram and genotyped for 53 single nucleotide polymo

54 ity is modulated by antidepressants, e.g., S-citalopram and imipramine, to alleviate symptoms of depr

55 o test this theory, measuring the effects of citalopram and lorazepam on the defensive behavior of 30

56 Combined treatment with citalopram and methylphenidate demonstrated an enhanced

57 Sertraline, citalopram and mitrazapine have been shown to be safe an

58 se venlafaxine (N=250) or to continue taking citalopram and receive augmentation with sustained-relea

59 After 15 min of extraction, basic drugs (citalopram and sertraline) were exhaustively extracted,

60 effects of the serotonin reuptake inhibitor citalopram and the dopamine precursor levodopa on decisi

61 tive serotonin reuptake inhibitors (e.g. (S)-citalopram) and tricyclic antidepressants (e.g. clomipra

62 ibitory potency against [(3)H]WIN35,428, [3H]citalopram, and [3H]nisoxetine binding to the dopamine,

63 ance to citalopram or at least a response to citalopram, and no prior suicide attempts.

64 y evidence include memantine, carbamazepine, citalopram, and prazosin, but none of these agents have

65 serotonin transporter and cellular target of citalopram, and the serotonin receptors SER-1 and SER-4

66 impairment were more likely to benefit from citalopram, and those with more severe agitation and gre

67 elective serotonin reuptake inhibitor (SSRI, citalopram) are studied over longer timescales, learning

68 This study proposes citalopram as a potential therapeutic option for patient

69 oviding an explanation for the action of (S)-citalopram as an allosteric ligand.

70 nidate to improve antidepressant response to citalopram, as assessed by clinical and cognitive outcom

71 tive 5-HT reuptake inhibitors fluoxetine and citalopram, as well as to cocaine.

72 ation cohort of 63 MDD patients treated with citalopram at another institution.

73 he drug-protein binding interactions for (S)-citalopram at hSERT.

74 A randomized, double-blind trial evaluated citalopram at target doses of 10, 20, or 30 mg/d versus

75 it dose, the efficacy participants tolerated citalopram better.

76 SERT crystal structures reveal two S-citalopram binding pockets in the central binding (S1) s

77 serotonin transporter also rescues [(3)H](S)-citalopram binding, suggesting a conserved feature.

78 Chronic treatment with an SSRI, citalopram, caused a 50% reduction in brain plaque load

79 examined how 20-day treatment with the SSRI citalopram (CIT) alters marble-burying (MB), open field

80 We included trials of amitriptyline, citalopram, clomipramine, desipramine, duloxetine, escit

81 ed by quetiapine (QTP; 8.51 mug/capita/day), citalopram (CLP; 5.45 mug/capita/day), and venlafaxine (

82 g psychosocial intervention, the addition of citalopram compared with placebo significantly reduced a

83 s to the negative self-descriptors following citalopram compared with placebo, in the absence of any

84 treatment was evaluated by measuring plasma citalopram concentration.

85 Evans rats were injected subcutaneously with citalopram (CTM) in one of three doses (5, 10 or 20mg/kg

86 rotonin reuptake inhibitors (SSRIs), such as citalopram (CTM), have been widely prescribed for major

87 Citalopram daily doses >40 mg were associated with lower

88 Citalopram daily doses of 21-40 mg were associated with

89 In the patients, relative to the controls, citalopram decreased glucose metabolism to a greater ext

90 elective serotonin reuptake inhibitor (SSRI) citalopram decreases amyloid-beta generation and plaque

91 Contrary to prediction, citalopram did not affect either form of defensive react

92 cules lacking antidepressant activity (eg, R-citalopram) did not produce the effect.

93 ne, olanzapine, quetiapine, risperidone, and citalopram do not appear to be effective.

94 iac, or noncardiac mortality associated with citalopram dosages >40 mg/day.

95 Stipulating a safety limit for citalopram dosages before the benefits and risks of doin

96 Administration (FDA) warning cautioned that citalopram dosages exceeding 40 mg/day may cause abnorma

97 e Food and Drug Administration declared that citalopram dosages exceeding 40 mg/day were no longer co

98 Reduction of prescribed citalopram dosages to a new safety limit was associated

99 The mean exit citalopram dose was 41.8 mg/day.

100 All SSRIs (except citalopram) dose-dependently inhibited OC formation and

101 Pharmaceutical blockade (citalopram dosing) or genetic ablation (SERT(-/-)) of SE

102 elective serotonin reuptake inhibitor (SSRI) citalopram downregulates the expression of the human imm

103 polar major depression in adults: bupropion, citalopram, duloxetine, escitalopram, fluoxetine, fluvox

104 We found that 2 weeks of citalopram enhanced reward and effort learning signals i

105 Critically, citalopram enhanced the NoGo-P3 signal in patients, rela

106 dissociable effects on response times, with citalopram enhancing behavioral inhibition and levodopa

107 er potential for prolonging the QT interval (citalopram, escitalopram) versus the risk among those in

108 ective serotonin reuptake inhibitors (SSRIs; citalopram, escitalopram, fluoxetine, paroxetine, and se

109 e the least potential for hepatotoxicity are citalopram, escitalopram, paroxetine, and fluvoxamine.

110 Neonatal citalopram exposure also produced significant dose-depen

111 amined the dose-response effects of neonatal citalopram exposure on sexual behavior.

112 Neonatal citalopram exposure produced persistent reductions in ma

113 ension and forced swim tests, fluoxetine and citalopram fail to reduce immobility in SERT Met172 mice

114 No EFr was observed for citalopram, fluoxetine, and venlafaxine despite almost c

115 Open treatment with citalopram followed by up to 3 sequential next-step trea

116 ts were then treated with the antidepressant citalopram for 8 weeks.

117 atients were treated with the antidepressant citalopram for 8 weeks.

118 terogeneity of response to citalopram in the Citalopram for Agitation in Alzheimer Disease (CitAD) st

119 The Citalopram for Agitation in Alzheimer Disease Study (Cit

120 In this planned secondary analysis of the Citalopram for Agitation in Alzheimer's Disease study, t

121 ry objective was to evaluate the efficacy of citalopram for agitation in patients with Alzheimer dise

122 stand in contrast to findings in a trial of citalopram for childhood autism.

123 ek 9 showed significant differences favoring citalopram for hallucinations and favoring placebo for s

124 ults of this trial do not support the use of citalopram for the treatment of repetitive behavior in c

125 ive disorder were enrolled in treatment with citalopram for up to 14 weeks.

126 HTT inhibitors fluoxetine, clomipramine, and citalopram from postnatal day 4 (P4) to P21 produced abn

127 icantly less likely than participants in the citalopram group to respond at week 12 if they entered t

128 95% CI, 6.1-30.1; P = .01) were seen in the citalopram group.

129 therapy (either alone or in combination with citalopram) had similar response and remission rates to

130 Citalopram has been shown to improve agitation in patien

131 Sertraline and citalopram have demonstrated efficacy for treating depre

132 A chase study with (R,S)-citalopram.HBr displaced [18F]1 radioactivity from all S

133 Twelve weeks of citalopram hydrobromide (10 mg/5 mL) or placebo.

134 D PARTICIPANTS: Randomized clinical trial of citalopram hydrobromide for children and adolescents wit

135 t study entry were subsequently treated with citalopram hydrobromide for up to 12 weeks.

136 rerandomization to another antipsychotic or citalopram hydrobromide or open treatment over 9 months.

137 The mean (SD) maximum dosage of citalopram hydrobromide was 16.5 (6.5) mg/d by mouth (ma

138 clozapine withdrawal and concomitant use of citalopram hydrobromide, a phenomenon that has been rare

139 line hydrochloride, bupropion hydrochloride, citalopram hydrobromide, duloxetine hydrochloride, escit

140 ed with fluoxetine hydrochloride initiation: citalopram hydrobromide, hazard ratio = 1.00 (95% confid

141 Chronic but not subchronic administration of citalopram impaired the acquisition of extinction and do

142 r the selective serotonin reuptake inhibitor citalopram improves response inhibition, in terms of bot

143 ors of attrition during acute treatment with citalopram in a large, "real world" clinical trial.

144 in the hippocampus following treatment with citalopram in currently depressed patients.

145 Blocking the SERT with citalopram in intact mice did not increase 5-HT sensitiv

146 mary and 23 psychiatric care sites, received citalopram in Level 1 of STAR*D.

147 rs assessed the heterogeneity of response to citalopram in the Citalopram for Agitation in Alzheimer

148 s significantly decreased after 0.3 mg/kg of citalopram in the dorsal raphe nucleus (5%), as well as

149 ial disadvantage, and at least a response to citalopram in the first step.

150 hotic major depressive disorder who received citalopram in the first treatment step.

151 der who were treated with the antidepressant citalopram in the Sequenced Treatment Alternatives for D

152 e selective 5-HT re-uptake inhibitor (SSRI), citalopram, in healthy human participants.

153 Compared with citalopram, in models adjusted for sociodemographic and

154 thritic potential of 2 SSRIs, fluoxetine and citalopram, in murine collagen-induced arthritis (CIA) a

155 two widely prescribed SSRIs, fluoxetine and citalopram, in tests sensitive to acute and chronic acti

156 haloperidol, clotiapine, phenothiazines, and citalopram (including escitalopram) remained statistical

157 ole, clotiapine, phenothiazines, fluoxetine, citalopram (including escitalopram), and methadone were

158 In Study 2, citalopram increased gaze maintenance over the face stim

159 tional models of choice behavior showed that citalopram increased harm aversion for both self and oth

160 In contrast, during galantamine treatment, citalopram increased metabolism in the right middle fron

161 The behavioural effect correlated with the citalopram-induced enhancement of prefrontal activation

162 hy male subjects received either a saline or citalopram infusion intravenously (10 mg over 30 min) on

163 Relative to placebo, citalopram infusion significantly increased [(11)C]CUMI-

164 Citalopram infusion when compared with saline resulted i

165 Similarly, SSRIs (except citalopram) inhibited ALP and bone mineralization by OB

166 to hSERT by all ligands, but the reduced (S)-citalopram inhibition of labeling by [(125)I]15 compared

167 Using a recently developed 'citalopram insensitive' transgenic mouse line and in vit

168 Citalopram is an effective, well-tolerated agent in mana

169 oethylmethanethiosulfonate-biotin, 5-HT, and citalopram, is incapable of inward 5-HT transport.

170 hough there was no beneficial main effect of citalopram, it reduced Stop-Signal Reaction Time and NoG

171 Samples of 10 muL of whole blood containing citalopram, loperamide, methadone, and sertraline as mod

172 N = 10, was 1.2, 5.5, 2.0, and 5.3 ng/mL for citalopram, loperamide, methadone, and sertraline, respe

173 of individual pharmaceuticals (i.e., high = citalopram; low = metformin) contributed to complex mixt

174 er, cognitive and cardiac adverse effects of citalopram may limit its practical application at the do

175 Daily doses ranged from 20 mg to 60 mg for citalopram (mean=32 mg) and from 5 mg to 40 mg for methy

176 For those who continued on citalopram, medication augmentation resulted in signific

177 -A estimated treatment difference at week 9 (citalopram minus placebo) was -0.93 (95% CI, -1.80 to -0

178 6 academic centers were randomly assigned to citalopram (n = 73) or placebo (n = 76).

179 eive a psychosocial intervention plus either citalopram (n = 94) or placebo (n = 92) for 9 weeks.

180 sed patients who received a prescription for citalopram (N=618,450) or for sertraline (N=365,898), a

181 can mimic the effect of neonatal exposure to citalopram on adult sexual behavior.

182 Thus we investigated the effect of acute citalopram on emotional processing and the relationship

183 fluence of methylphenidate, atomoxetine, and citalopram on error awareness in 27 healthy participants

184 Key secondary objectives examined effects of citalopram on function, caregiver distress, safety, cogn

185 in trait empathy showed stronger effects of citalopram on moral judgment and behavior than individua

186 In conclusion, the behavioural effect of citalopram on response inhibition depends on individual

187 n between disease severity and the effect of citalopram on response inhibition may be due to the prog

188 e study, the authors evaluated the effect of citalopram on the 12 neuropsychiatric symptom domains as

189 ioxetine by comparing its effect to the SSRI citalopram on the binding of [(11)C]AZ10419369 to the 5-

190 tly positively correlated with the effect of citalopram on the left amygdala response to fearful face

191 orter (SERT) and the S- and R-enantiomers of citalopram on the single molecule level.

192 tely insured or who had prior intolerance to citalopram or at least a response to citalopram, and no

193 ifically, 306 MDD patients were treated with citalopram or escitalopram and blood was drawn at baseli

194 n silico analysis indicates that the bound S-citalopram or imipramine in S1 is allosterically coupled

195 resolution bound to the antidepressants (S)-citalopram or paroxetine.

196 n expectancy, participants were treated with citalopram or placebo for 8 weeks.

197 rticipants were randomly assigned to receive citalopram or placebo for 9 weeks, with the dosage titra

198 , Hoehn and Yahr stage 1.5-3) received 30 mg citalopram or placebo in addition to their usual dopamin

199 elective serotonin reuptake inhibitor (SSRI) citalopram or placebo.

200 ients received either a single 30 mg dose of citalopram or placebo.

201 fter 4 weeks exposure, treatment with either citalopram or vehicle was administered for 2 weeks while

202 tch to a second, different SSRI (paroxetine, citalopram, or fluoxetine, 20-40 mg); (2) switch to a di

203 significant improvement in hot flashes with citalopram over placebo, with no significant differences

204 ective serotonin reuptake inhibitors (SSRIs: citalopram, paroxetine, fluoxetine and sertraline) in a

205 ollutants observed were the antidepressants (citalopram, paroxetine, sertraline, venlafaxine, and bup

206 Results from the mADCS-CGIC showed 40% of citalopram participants having moderate or marked improv

207 After an unsatisfactory response to citalopram, patients who consented to random assignment

208 ence to treatment was evaluated by measuring citalopram plasma concentrations.

209 (N=48), citalopram plus placebo (N=48), and citalopram plus methylphenidate (N=47).

210 improvement score was more prominent in the citalopram plus methylphenidate group compared with the

211 Additionally, the rate of improvement in the citalopram plus methylphenidate group was significantly

212 groups: methylphenidate plus placebo (N=48), citalopram plus placebo (N=48), and citalopram plus meth

213 up was significantly higher than that in the citalopram plus placebo group in the first 4 weeks of th

214 controls at baseline and after 12 weeks (of citalopram plus psychotherapy treatment for the depresse

215 The patients received flexible doses of citalopram prescribed by clinicians for up to 14 weeks.

216 s (mean age, 58 years [SD=11]; 92% male) had citalopram prescriptions for 64 mg/day (SD=8.3), on aver

217 retrospective study of a population filling citalopram prescriptions for more than 40 mg/day when th

218 ephalography protocol on one session without citalopram, providing normative data for this task.

219 ng acute treatment with typical (fluoxetine, citalopram, reboxetine, venlafaxine, clomipramine) and a

220 nergic antagonists such as amitriptyline and citalopram recapitulate this effect.

221 The selective serotonin reuptake inhibitor citalopram reduced mortality of Lmx1b(f/f) but not of Lm

222 Furthermore, one compound, citalopram, reduced tumor size as well as the number of

223 Treatment with citalopram rescued behavior in the forced swim test in h

224 s (SERT) = 1.26, 0.29, and 0.31 nM (vs [(3)H]citalopram), respectively.

225 7 (55%) for placebo and 10, 20, and 30 mg of citalopram, respectively (P <or= .002).

226 ion with phenotypes for general and specific citalopram response as well as remission.

227 Association between one SNP and specific citalopram response was observed.

228 ontributions of race and genetic ancestry to citalopram response.

229 nctional variants and depression severity or citalopram response.

230 lective serotonin reuptake inhibitor (SSRI), citalopram, results in persistent changes in behavior in

231 the selective serotonin reuptake inhibitor, citalopram, revealed a genotype-dependent behavioral res

232 served that two high-affinity SSRIs, racemic citalopram ((RS)-CIT) and paroxetine, affect the outgrow

233 ge constraints must be considered because of citalopram's adverse effect profile, this agent's overal

234 AN paradigm as a depression model by showing citalopram selectively improves depressive-like behavior

235 cription rates for CSM-contraindicated SSRIs citalopram, sertraline and especially paroxetine dropped

236 everal of these drugs, including imipramine, citalopram, sertraline, and fluoxetine (Prozac), bound m

237 Participants who received citalopram showed significant improvement compared with

238 Participants who received citalopram showed significant improvement on the CMAI, t

239 er, chronic treatment of CMVMJD135 mice with citalopram significantly reduced ataxin 3 neuronal inclu

240 e of methylphenidate, but not atomoxetine or citalopram, significantly improved the ability of health

241 restricted to 1,354 individuals treated with citalopram (STAR*D) or escitalopram (GENDEP) identified

242 eived selective serotonin reuptake inhibitor citalopram starting 7 days after MCAo.

243 erebral metabolic effects of galantamine and citalopram suggest, consistent with preclinical data, a

244 elective serotonin reuptake inhibitor (SSRI) citalopram synergistically reduced operant responding.

245 treatment-emergent suicidal ideation during citalopram therapy.

246 Among those who discontinued citalopram, there were no significant differences in out

247 creases in cerebral glucose metabolism after citalopram to a greater extent in the Alzheimer's diseas

248 posed hamsters to 5 lux LAN and treated with citalopram to determine effects on depressive-like behav

249 n of symptoms or could not tolerate the SSRI citalopram to receive one of the following drugs for up

250 tions of characteristic binding strengths of citalopram to SERT were revealed in Na(+)-containing buf

251 mpressions, Improvement subscale between the citalopram-treated group (32.9%) and the placebo group (

252 seline (mean [SD], -2.0 [3.4] points for the citalopram-treated group and -1.9 [2.5] points for the p

253 ed that platelets isolated from SERT(-/-) or citalopram-treated mice have reduced activation of G-pro

254 nteraction, indicating that HAM-D scores for citalopram-treated participants declined at a faster rat

255 Fluoxetine and citalopram treatment also inhibited the signaling of TLR

256 ants who completed an average of 10 weeks of citalopram treatment and provided DNA samples.

257 other neuropsychiatric symptoms improve with citalopram treatment compared with placebo.

258 In contrast to fluoxetine, citalopram treatment did not increase BLA eCBs or facili

259 ups by their index scores; and estimated the citalopram treatment effect for each.

260 Across the postsynaptic brain regions, citalopram treatment induced a mean 7% in [(11)C]CUMI-10

261 ation of 5-HT input to the VTA combined with citalopram treatment produced a synergistic decrease in

262 Fluoxetine and citalopram treatment selectively inhibit endosomal TLR s

263 odel predicted nonremission after 8 weeks of citalopram treatment with 76% corrected accuracy in an i

264 o Relieve Depression (STAR*D) study (12-week citalopram treatment) were used as the basis for calcula

265 ne density in CA1 was moderately improved by citalopram treatment, but not fully restored.

266 domly assigned to open or placebo-controlled citalopram treatment.

267 nfluence population variation in response to citalopram treatment.

268 c variation in the HTR2A gene and outcome of citalopram treatment.

269 domly assigned to open or placebo-controlled citalopram treatment.

270 ene expression to predict nonremission after citalopram treatment.

271 Depression (STAR*D) trial were treated with citalopram under a standard protocol for up to 14 weeks.

272 he risk of cataract surgery was highest with citalopram use (OR = 1.53; 95% CI, 1.33-1.77; P < .001).

273 The authors assessed relationships between citalopram use and ventricular arrhythmias and mortality

274 Citalopram use was significantly more likely to be assoc

275 Furthermore, the prosocial effects of citalopram varied as a function of trait empathy.

276 Several compounds (citalopram, venlafaxine, O-desmethyl-venlafaxine) were n

277 of the selective serotonin-uptake inhibitor citalopram vs placebo in volunteers (n=29) at a high ris

278 The mean (SD) maximum dose of citalopram was 16.5 (6.5) mg by mouth daily (maximum dos

279 This harm-avoidant bias after citalopram was also evident in behavior during the ultim

280 Intolerance to citalopram was associated with intolerance to sertraline

281 Patients for whom citalopram was more effective were more likely to be out

282 ; the selective serotonin reuptake inhibitor citalopram was used as a positive control.

283 Citalopram was well-tolerated, with no significant negat

284 prasidone, valproic acid, carbamazepine, and citalopram were associated with higher mortality indices

285 actory outcomes after initial treatment with citalopram were eligible for a randomized second-step tr

286 r a lower reduction in symptom severity with citalopram were more likely to accept a switch strategy

287 pitalizations and mortality after dosages of citalopram were or were not reduced to </=40 mg/day were

288 zations and mortality when higher dosages of citalopram were or were not reduced to </=40 mg/day.

289 patients who did not remit with or tolerate citalopram were randomly assigned either to switch to su

290 At week 9, participants treated with citalopram were significantly less likely to be reported

291 The effects of citalopram were stronger than those of levodopa.

292 Fluoxetine and N-desmethyl citalopram were the most rapidly attenuated compounds (t

293 nd acutely medicated with the antidepressant citalopram, were scanned using fMRI during a reward-lear

294 red sexual behavior similar to the effect of citalopram, whereas exposure to 5-HT(1A) receptor agonis

295 ctive than cognitive therapy augmentation of citalopram, whereas switching to cognitive therapy was b

296 increases dopamine levels in the brain), or citalopram (which has a selective, if complex, effect on

297 We found that citalopram (which increases levels of 5-HT) caused susta

298 ring the dosages used and the association of citalopram with cardiac QT prolongation, use of this age

299 ssign participants to either augmentation of citalopram with cognitive therapy (N=65) or medication (

300 Augmentation of citalopram with either sustained-release bupropion or bu