ライフサイエンスコーパス: ketamine

1 GLIC in the absence and presence of R- or S-ketamine.

2 change in binding (P<0.04) immediately after ketamine.

3 n factor eEF2, reminiscent of the effects of ketamine.

4 dicating a requirement for mTORC1 similar to ketamine.

5 Mzeta mediated the antidepressant effects of ketamine.

6 without the psychotomimetic side effects of ketamine.

7 drugs, as well as by subanesthetic doses of ketamine.

8 ested this in a randomised trial of low-dose ketamine.

9 rmalities might predict positive response to ketamine.

10 s index (BMI) strongly predicted response to ketamine.

11 kinetic interactions between PF-04958242 and ketamine.

12 d in the sustained antidepressant effects of ketamine.

13 -NK were active but ~4-fold less potent than ketamine.

14 act males enhanced hedonic response low-dose ketamine.

15 ressive episode and following treatment with ketamine.

16 g training, and this effect was prevented by ketamine.

17 iestrus female rats could not be reversed by ketamine.

18 ression and its treatment with imipramine or ketamine.

19 caused by the nonselective NMDAR antagonist ketamine.

20 ice (EmuPADs) for electrochemical sensing of ketamine.

21 ehaviorally to the antidepressant effects of ketamine.

22 ychotomimetic effects and abuse potential of ketamine.

23 mmon and unique effects of imipramine versus ketamine.

24 nthesis and induced behavioral resistance to ketamine.

25 Patients were randomly assigned (1:1) to ketamine (0.5 mg/kg intravenous bolus) or saline adjunct

26 ere randomized to receive either intravenous ketamine (0.5 mg/kg of body weight) or intravenous place

27 and compared the effects between intravenous ketamine (0.5 mg/kg over 40 min) and placebo (normal sal

28 to receive placebo (normal saline), low-dose ketamine (0.5 mg/kg), or high dose ketamine (1.0 mg/kg)

29 then 24 h following intravenous infusion of ketamine (0.5 mg/kg).

30 Mice administered prophylactic ketamine 1 week, but not 1 month or 1 h before CFC, exhi

31 raperitoneal injection with a single dose of ketamine (1, 3, 10, 30 and 80 mg kg(-1)), Ro 25-6981 (1,

32 low-dose ketamine (0.5 mg/kg), or high dose ketamine (1.0 mg/kg) after induction of anaesthesia, bef

33 A single injection of ketamine (10 mg/kg, i.p.) 24 h prior to testing rescued

34 Ketamine (10 mg/kg, i.p.) administered 2 h, 1 week, or 2

35 were administered a single dose of saline or ketamine (30 mg/kg) at varying time points before or aft

36 Ketamine, a non-competitive, voltage-dependent N-Methyl-

37 Ketamine, a pan-NMDA receptor channel blocker, and CP-10

38 rasensitive technique for electroanalysis of ketamine; a date rape drug.

39 Here we report that ketamine accelerates differentiation of doublecortin-pos

40 ism of action of rapid-acting antidepressant ketamine: activation of brain-derived neurotrophic facto

41 hanisms underlying the acute effect, but how ketamine acts at the cellular level to sustain this anti

42 of the mechanisms involved and suggests that ketamine acts at the prelimbic cortex to sensitize neuro

43 However, ketamine administered before reinstatement increased the

44 Moreover, ketamine administration decreased the expression of urot

45 In contrast, ketamine administration following CFC or during extincti

46 Acute ketamine administration in rodents is associated with si

47 n depressive symptoms was observed following ketamine administration in the MDD group (P<0.001), whic

48 es reviewed here provide evidence that acute ketamine administration leads to dopamine release in the

49 We hypothesize that glutamate released after ketamine administration moderates mGluR5 availability; t

50 vation of the basolateral amygdala (BLA) and ketamine administration on VTA DA neuron activity and pa

51 ked activity and was not replicated by acute ketamine administration or pharmacogenetic parvalbumin-i

52 nd primate brain following acute and chronic ketamine administration relative to a drug-free baseline

53 nd cerebellum), or of the effects of chronic ketamine administration, although consistent increases i

54 n the same day-before and during intravenous ketamine administration-and a third scan 1 day later.

55 Moreover, ketamine administration-dependent delayed induction of G

56 tory [BDI]), obtained for up to 1 week after ketamine administration.

57 mechanism that was specifically disrupted by ketamine administration.

58 In the presence of R-ketamine, all subunits showed changes in structure and d

59 Compared with ketamine alone, propofol alone (3.7%; odds ratio [OR], 5

60 , in the present study we determined whether ketamine also corrects the stress-induced reversal learn

61 , in addition to its antidepressant effects, ketamine also has a salutary effect on a major medical c

62 Preclinical studies indicate that ketamine alters expression of circadian clock-associated

63 e expression of inflammatory genes, and that ketamine (an N-methyl-D-aspartate receptor antagonist) w

64 ction of the rapid antidepressant effects of ketamine, an N-methyl-D-aspartate glutamate receptor ant

65 Furthermore, we examined whether ketamine and chlordiazepoxide, pharmacological agents us

66 dance-like phenotype was ameliorated by both ketamine and chlordiazepoxide.

67 The combinations of ketamine and fentanyl (4.1%; OR, 4.0; 95% CI, 1.8-8.1) a

68 6; 95% CI, 2.3-13.1) and the combinations of ketamine and fentanyl citrate (3.2%; OR, 6.5; 95% CI, 2.

69 stinct NMDAR subpopulations by memantine and ketamine and help to explain their differential clinical

70 by three psychedelic substances: psilocybin, ketamine and LSD.

71 Other NMDA open channel blockers ketamine and memantine showed a similar effect.

72 Ketamine and placebo infusions were administered in a ra

73 linear mixed models to assess the impact of ketamine and placebo on anxiety symptoms.

74 itrate (3.2%; OR, 6.5; 95% CI, 2.5-15.2) and ketamine and propofol (2.1%; OR, 4.4; 95% CI, 2.3-8.7) h

75 entanyl (4.1%; OR, 4.0; 95% CI, 1.8-8.1) and ketamine and propofol (2.5%; OR, 2.2; 95% CI, 1.2-3.8) h

76 We found a clear dose-dependent effect of ketamine and Ro 25-6981 on behavior and the percentage o

77 Ketamine and the two NMDA NR2B NAMs produced selective i

78 MDD patients received a single infusion of ketamine and underwent repeated rs-fcMRI at 24 h posttre

79 tively (36.9% in placebo, 39.6% in 0.5 mg/kg ketamine, and 40.8% in 1.0 mg/kg ketamine groups, p=0.69

80 d the potential antidepressant properties of ketamine, and comparisons with stimulants and other NMDA

81 ity patterns indicate rapid mood response to ketamine, and that mediators of continuing ketamine-indu

82 Memantine and ketamine are clinically useful NMDA receptor (NMDAR) ope

83 Agents such as the glutamatergic modulator ketamine are effective in treatment-resistant mood disor

84 lopment.SIGNIFICANCE STATEMENT Memantine and ketamine are NMDA receptor (NMDAR) channel-blocking drug

85 The antidepressant effects of ketamine are thought to depend on brain-derived neurotro

86 e studies, they have led to increased use of ketamine as an off-label treatment for mood and other ps

87 of cocaine now vs money later, we found that ketamine, as compared to the control, significantly decr

88 e-weekly and thrice-weekly administration of ketamine at 0.5 mg/kg similarly maintained antidepressan

89 ne/glutamate increase in the pgACC caused by ketamine at 24 h post infusion was reproduced in an enla

90 We systematically administered ketamine at different time points relative to a fear exp

91 cient rodent studies of the acute effects of ketamine at sub-anaesthetic doses for meta-analysis.

92 ich included two (6%) of 33 patients who had ketamine-attributable transient psychological effects.

93 re, differential inhibition by memantine and ketamine based on NMDAR location is likely to result fro

94 Ketamine binding decreases occupancy of desensitized sta

95 R-ketamine binding promoted a conformational shift toward

96 imentally measured negative cooperativity of ketamine binding to GLIC.

97 nt electrostatic interactions to stabilize R-ketamine binding.

98 Conformational changes near the ketamine-binding site were propagated to the interface b

99 In the CORT model, a single dose of ketamine blocked stress-induced behavior in the forced s

100 The crystal structure of GLIC shows R-ketamine bound to an extracellular intersubunit cavity.

101 antidepressant effect of an anesthetic drug, ketamine, by Inverse-Frequency Analysis of eight million

102 Moreover, it is unknown whether ketamine can be prophylactic against subsequent stressor

103 These data indicate that ketamine can buffer a fear response when given a week be

104 Our study also suggests that ketamine causes less protein damage by rapidly decreasin

105 as significantly and similarly diminished by ketamine (Cohen's d = 1.14) and schizophrenia (Cohen's d

106 nificantly fewer SAEs and interventions than ketamine combined with propofol or fentanyl.

107 ndomly ordered test days, a saline day and a ketamine day.

108 Adjunctive ketamine demonstrated a greater reduction in clinically

109 Ketamine depressed local field potentials evoked in the

110 ERPRETATION: A single subanaesthetic dose of ketamine did not decrease delirium in older adults after

111 We found that memantine and ketamine differentially alter NMDAR desensitization and

112 .01) and nightmares (p=0.03) with increasing ketamine doses compared with placebo.

113 This study found a significant dose-related ketamine effect on scores on the Hamilton Depression Rat

114 tabolite (2R,6R)-hydroxynorketamine mimicked ketamine effects at sub-micromolar concentrations.

115 ant depression and the first to characterize ketamine effects in a genotyped Chinese population in wh

116 Sixty minutes exposure to ketamine elicited concentration-dependent increases of d

117 We evaluated whether ketamine elicits similar molecular events in dopaminergi

118 These data indicate that ketamine elicits structural plasticity by recruitment of

119 gnostic samples are required to confirm that ketamine exerts a specific effect on suicidal ideation.

120 naling pathway is a novel mechanism by which ketamine exerts its therapeutic effects on stress-induce

121 Upon ketamine exposure in utero, PFC neurons at P30 showed mo

122 Our previous work demonstrated that ketamine exposure of pregnant rats induces affective dis

123 his trial was to assess the effectiveness of ketamine for prevention of postoperative delirium in old

124 a general overview of the data on the use of ketamine for the treatment of mood disorders and highlig

125 demonstrate the dose-related efficacy of R/S-ketamine for treatment-resistant depression and the firs

126 roperties; like the NMDA receptor antagonist ketamine GLYX-13 produces rapid antidepressant actions i

127 /=50% in SSI score) at day 1 was 55% for the ketamine group and 30% for the midazolam group (odds rat

128 ore at day 1 was 4.96 points greater for the ketamine group compared with the midazolam group (95% CI

129 ession subscale was greater at day 1 for the ketamine group compared with the midazolam group (estima

130 re randomly assigned to treatment (40 in the ketamine group vs 39 in the saline group).

131 roups (six [27%] of 22 adverse events in the ketamine group vs seven [54%] of 13 in the saline group)

132 2 in the placebo group, 227 in the 0.5 mg/kg ketamine group, and 223 in the 1.0 mg/kg ketamine group.

133 utamate ratio increased significantly in the ketamine group, compared with placebo, specifically in t

134 /kg ketamine group, and 223 in the 1.0 mg/kg ketamine group.

135 m incidence between patients in the combined ketamine groups and the placebo group (19.45% vs 19.82%,

136 n 0.5 mg/kg ketamine, and 40.8% in 1.0 mg/kg ketamine groups, p=0.69), did not differ significantly a

137 rated that compared with control treatments, ketamine had significant benefits on the individual suic

138 ale data revealed that patients who received ketamine had significantly lower frequency of reports of

139 nalysis also revealed that patients who took ketamine had significantly lower frequency of reports of

140 Most recently, ketamine has also been shown to be prophylactic against

141 Ketamine has been reported to be an efficacious antidepr

142 with nanocrystalline Zeo-GO for detection of ketamine has immense prospective for field-testing platf

143 ntidepressant response to subanesthetic-dose ketamine has led to a collection of studies that have ex

144 Ketamine has rapid antidepressant efficacy, but it is un

145 Here, we show that memantine and ketamine have contrasting effects on NMDAR desensitizati

146 Use of ketamine hydrochloride alone resulted in the lowest inci

147 Several studies now provide evidence of ketamine hydrochloride's ability to produce rapid and ro

148 ntidepressant efficacy, but it is unknown if ketamine improves cognitive symptoms.

149 support safe, effective, and ethical use of ketamine in depression.

150 Ketamine in low doses produces both rapid and sustained

151 e the dose-related antidepressant effects of ketamine in patients with treatment-resistant depression

152 o not support the use of adjunctive low-dose ketamine in routine ECT treatment.

153 thrice-weekly intravenous administration of ketamine in sustaining initial antidepressant effects in

154 No stable binding of S-ketamine in the original cavity was observed in the simu

155 ncourage an evidence-based approach to using ketamine in the treatment of psychiatric disorders consi

156 acting, non-monoamine-based antidepressant, ketamine, in mice subjected to chronic social defeat str

157 artate (NMDA) antagonists like memantine and ketamine increase PPI, and under some conditions, memant

158 In contrast, both GLYX-13 and ketamine increased attention in the SRTT task, which is

159 OFC and primary cortical neurons in culture, ketamine increased expression of the neural plasticity-r

160 antidepressants fluoxetine, desipramine and ketamine increased PKMzeta expression in mPFC and PKMzet

161 a serial reaction time task (SRTT), whereas ketamine increased responses in both tests.

162 e discuss the inter-species variation in the ketamine induced dopamine release as well as the implica

163 Ketamine induced more expression changes in the hippocam

164 ition of adult neurogenesis, each blocks the ketamine-induced behavioral responses.

165 There were no differences in ketamine-induced changes between MDD and control groups

166 A ketamine-induced decrease in resistin was also observed;

167 MPAR potentiator PF-04958242 would attenuate ketamine-induced deficits in verbal learning and memory

168 PF-04958242 significantly reduced ketamine-induced impairments in immediate recall and the

169 We observed a ketamine-induced increase in hippocampal Glx (glutamate+

170 o ketamine, and that mediators of continuing ketamine-induced mood changes include altered timing and

171 We then tested the role of JAK2/STAT3 in ketamine-induced plasticity in the OFC.

172 Battery), without significantly attenuating ketamine-induced psychotomimetic effects.

173 We observed a significant ketamine-induced reduction in mGluR5 availability (that

174 Ketamine-induced ulcerative cystitis (KIC) initially dam

175 ects of PF-04958242/placebo were assessed on ketamine-induced: (1) impairments in verbal learning and

176 a major depressive episode received a single ketamine infusion (0.5 mg kg(-1) for 40 min).

177 -group, placebo-controlled trial of a single ketamine infusion (saline, 0.2 mg/kg, 0.5 mg/kg).

178 each treatment period, subjects underwent a ketamine infusion for 75 min during which the effects of

179 bone marker levels and their responses to IV ketamine infusion in MDD patients and HCs were measured

180 likely to exhibit a treatment response after ketamine infusion relative to placebo in the first 2 wee

181 Ketamine inhibits pentameric ligand-gated ion channels (

182 systemically or into the OFC at the time of ketamine injection prevented its beneficial effect on re

183 Moderate doses of IP ketamine, IP memantine, or intra-PLmPFC memantine increa

184 Ketamine is a non-competitive antagonist at the N-methyl

185 Ketamine is a potent N-methyl-D-aspartate receptor antag

186 , suggesting that the prophylactic effect of ketamine is a result of altered functioning of this proj

187 Ketamine is an N-methyl-D-aspartate receptor antagonist,

188 hippocampus, the antidepressant response to ketamine is associated with rapid VGF translation, is im

189 fear experience, in order to determine when ketamine is most effective at reducing fear expression o

190 Subanaesthetic ketamine is often administered intraoperatively for post

191 ophrenia-relevant disease processes: chronic ketamine (KET) administration and Df(16)A(+/-), modeling

192 d-acting antidepressant strategies, low-dose ketamine (KT) and sleep deprivation (SD) therapies, dram

193 In addition, administration of ketamine led to differential regulation of CaMKII functi

194 Plasma ketamine levels and BDNF genotypes were assessed.

195 While ketamine may be beneficial to some patients with mood di

196 ssant effects of the glutamatergic modulator ketamine may be due to its ability to restore synaptic p

197 concept trial provides initial evidence that ketamine may be effective in reducing anxiety.

198 Thus, ketamine may be most useful in the clinic if administere

199 For example, memantine but not ketamine may inhibit extrasynaptic NMDARs more effective

200 the N-methyl-D-aspartate receptor antagonist ketamine may work to correct these neuroadaptations and

201 Although we recently showed that ketamine may work, in part, through significant mGluR5 m

202 er common anesthetics, such as etomidate and ketamine, may target additional protein networks of the

203 Ketamine (mean 5.17, SD 2.92), when compared with saline

204 uggest safety of other agents (eg, riluzole, ketamine, memantine, N-acetylcysteine, lamotrigine, cele

205 Finally, the ketamine metabolite (2R,6R)-hydroxynorketamine mimicked

206 nlike the rapidly acting glutamatergic agent ketamine, mGluR5-specific modulation has not yet shown a

207 ic binding shown in the crystal structure, R-ketamine moved away from some of the binding sites and w

208 e glutamine/glutamate ratios (placebo, n=14; ketamine, n=12).

209 oduced in an enlarged sample (placebo, n=24; ketamine, n=20).

210 On D1, ketamine nonresponders had a lower mesor and a blunted 2

211 umulation of novel visualizable analogues of ketamine/norketamine.

212 ted 10 to 20 minutes after administration of ketamine, occurred concurrently with eEF2K-dependent inc

213 antidepressant response in association with ketamine occurs, in part, by reversing these neurochemic

214 d to result from inhibition by memantine and ketamine of overlapping but distinct NMDAR subpopulation

215 fect of adjunctive subanesthetic intravenous ketamine on clinically significant suicidal ideation in

216 Here, we explored the effects of ketamine on contingency learning using a placebo-control

217 ect of anaesthetic doses (>100 mg kg(-1)) of ketamine on dopamine levels ex vivo, although this remai

218 onance imaging (MRI) to study the effects of ketamine on hippocampal neurometabolite levels and funct

219 This study examined the effects of ketamine on ligand binding to a metabotropic glutamaterg

220 acologic and rapid antidepressant effects of ketamine on markers of circadian timekeeping (amplitude

221 ssociated molecules, and clinical studies of ketamine on plasticity-related biomarkers further sugges

222 amics basis for the inhibitory modulation of ketamine on pLGICs.

223 is examining the effects of a single dose of ketamine on suicidal ideation.

224 To examine the effect of ketamine on the dopamine systems, we carried out a syste

225 xamined the effects of the NMDAR antagonist, ketamine, on predictive coding during vocalization in he

226 Use of ketamine only was associated with the best outcomes, res

227 eptin-as potential predictors of response to ketamine or as possible transducers of its therapeutic e

228 vented induction of structural plasticity by ketamine or CX614.

229 at adipokines may either predict response to ketamine or have a role in its possible therapeutic effe

230 umbers of responders and nonresponders after ketamine or imipramine treatment.

231 may trigger ketamine's psychoactive effects, ketamine or its major metabolite norketamine could act i

232 re receiving intraperitoneal (i.p.) doses of ketamine or memantine, or infusions of memantine directl

233 intake blocked the pro-aggressive effects of ketamine or memantine.

234 edication, were randomly assigned to receive ketamine or midazolam infusion.

235 e analgesia, and some evidence suggests that ketamine prevents delirium.

236 Ketamine rapidly (within 1 day) reduced suicidal ideatio

237 Ketamine rapidly reduced suicidal thoughts, within 1 day

238 g reward anticipation was observed following ketamine relative to placebo during performance of a mon

239 nism underlying the antidepressant action of ketamine remains unclear.

240 Furthermore, the actions of ketamine required functionally intact dopamine D3 recept

241 Although both doses of ketamine rescued depression-like behavior in female rats

242 ng antidepressant action including the rapid ketamine response.

243 efense system as downstream effectors of the ketamine response.

244 creased JAK2 phosphorylation in the OFC, and ketamine restored pJAK2 levels within 2 h post injection

245 We found ketamine resulted in a significantly greater reduction i

246 matory compound, this decrease suggests that ketamine's anti-inflammatory effects may be transduced,

247 evels of adiponectin significantly predicted ketamine's antidepressant efficacy, suggesting an advers

248 he specific role of mGluR5 downregulation in ketamine's antidepressant response is unclear.

249 )-medial prefrontal cortex (mPFC) pathway in ketamine's antidepressant response.

250 first to demonstrate an association between ketamine's clinical antidepressant effects and circadian

251 6, 13.94), and this effect mediated 33.6% of ketamine's effect on SSI score.

252 Ketamine's effect on suicidal ideation remained signific

253 Ketamine's effects on suicidal ideation were partially i

254 Additional research on ketamine's long-term safety and its efficacy in reducing

255 To elucidate ketamine's mechanism of action, we tested whether the cl

256 in and opioid induced side effects, implying ketamine's potential to act as a beneficial adjunct agen

257 -surface NMDA receptors (NMDARs) may trigger ketamine's psychoactive effects, ketamine or its major m

258 convulsive shock therapy, sleep deprivation, ketamine, scopolamine, GLYX-13 and pindolol used in conj

259 It remains unknown, however, when ketamine should be administered relative to a stressor i

260 Responders to ketamine showed increased GBCr in the lateral PFC, cauda

261 Ketamine significantly increased both the OPG/RANKL rati

262 Ketamine significantly increased GBCr in the PFC and red

263 isms underlying antidepressant properties of ketamine, structural remodeling of prefrontal and hippoc

264 conducted following a cross-over placebo and ketamine study in human subjects, an attenuated ventral

265 jecting neurons from the PL, IS did so after ketamine, suggesting that the prophylactic effect of ket

266 Specifically, ketamine tended to downregulate the adenosine triphospha

267 ces linking the rapid-acting antidepressant, ketamine, to BDNF translation and BDNF-dependent signali

268 d fibrosis markers was also increased in the ketamine-treated group.

269 Hippocampi of ketamine-treated mice were analysed by metabolome and pr

270 15 (45%) of 33 ketamine-treated patients compared with 10 (27%) of 37 p

271 agonist, normalized MSO task performance in ketamine-treated rats and this effect was blocked by GAB

272 ergic currents were also decreased in OFC of ketamine-treated rats and were normalized by activation

273 alysis of voiding behavior revealed that the ketamine-treated rats exhibited significant bladder hype

274 l registries, and that the risk potential of ketamine treatment continues to be monitored and modelle

275 ties associated with MDD and, if so, whether ketamine treatment corrected the abnormalities.

276 Rapid reduction in suicidal thoughts after ketamine treatment has mostly been studied in patients w

277 eptibility to CSDS and impaired responses to ketamine treatment in the forced swim test.

278 In cohort B, ketamine treatment reduced left NAc, but increased left

279 in patients who achieved remission following ketamine treatment, an intriguing preliminary finding th

280 radigm of rapid mood normalization following ketamine treatment, the current study investigated intri

281 tabolome and proteome profiling to delineate ketamine treatment-affected molecular pathways and biosi

282 cadian value (mesor) was present on D1 after ketamine treatment.

283 are of likely relevance to the influence of ketamine upon mood and its other functional actions in v

284 We find that, based on current evidence, ketamine use for severe, treatment-resistant depression

285 s of the ethical considerations in off-label ketamine use for severe, treatment-resistant depression.

286 xtualised in an overview of the evidence for ketamine use in depression, and a review of the drug's s

287 fusion measured on the LSAS (33.33% response ketamine vs 0% response placebo, Wilcoxon signed-rank te

288 st z=2.24, p=0.025) and VAS (88.89% response ketamine vs 52.94% response placebo, Wilcoxon signed-ran

289 INTERPRETATION: No evidence of benefit for ketamine was found although the sample size used was sma

290 Recently, ketamine was found to normalize this stress-induced NAc

291 hways mediating the antidepressant action of ketamine was reduction of phosphorylation of eEF2 via eE

292 Direct evidence of mTOR activation by ketamine was revealed by its induction of p70S6 kinase.

293 ebo-controlled intravenous infusion study of ketamine, we measured glutamate and glutamine in the pre

294 To unravel the mechanism of action of ketamine, we treated wild-type C57BL/6 mice with calcium

295 All effects of ketamine were abolished by AMPA receptor antagonists and

296 effects of conventional antidepressants and ketamine were also investigated.

297 Subanesthetic doses of ketamine were repeatedly shown to improve depressive sym

298 imetic side effects of GLYX-13 compared with ketamine, whereas regulation of the hypocretin responses

299 ate ratios to a single subanesthetic dose of ketamine, which mirrors the time course of the antidepre

300 that administering the glutamate antagonist ketamine with ECT might alleviate cognitive adverse effe

301 optional 2-week open-label phase to receive ketamine with the same frequency as in the double-blind