ライフサイエンスコーパス: ketamine

1 ls (HCs) at baseline, post-placebo, and post-ketamine.

2 olely on the receptor or regional targets of ketamine.

3 nd canceled the analgesic effect of low-dose ketamine.

4 gh-frequency qEEG power increases induced by ketamine.

5 set based on when they were first exposed to ketamine.

6 ubunit, GluN2B, implicated in the actions of ketamine.

7 re central to the antidepressant activity of ketamine.

8 mma power elicited by subanesthetic doses of ketamine.

9 riven by the administration of subanesthetic ketamine.

10 lly meaningful efficacy of lower doses of IV ketamine.

11 l role in the antidepressant-like actions of ketamine.

12 nical biomarkers or novel treatments, beyond ketamine.

13 her this activity was altered by single-dose ketamine.

14 cin, an mTORC1 inhibitor, prior to receiving ketamine.

15 ocortical activity was strongly inhibited by ketamine.

16 k2a-expressing neurons blocks the actions of ketamine.

17 is necessary for antidepressant response to ketamine.

18 re-infusion), 230 min, day 1, and day 3 post-ketamine.

19 ociative and psychotomimetic side effects of ketamine.

20 receptor antagonists phencyclidine (PCP) and ketamine.

21 imals treated with the psychotomimetic agent ketamine.

22 for dosing, outcomes, and adverse effects of ketamine.

23 :1:1:1 fashion: a single intravenous dose of ketamine 0.1 mg/kg (n = 18), a single dose of ketamine 0

24 etamine 0.1 mg/kg (n = 18), a single dose of ketamine 0.2 mg/kg (n = 20), a single dose of ketamine 0

25 etamine 0.2 mg/kg (n = 20), a single dose of ketamine 0.5 mg/kg (n = 22), a single dose of ketamine 1

26 h prior to the intravenous administration of ketamine 0.5 mg/kg in a double-blind cross-over design w

27 baseline and following a 40 min infusion of ketamine (0.5 mg/kg).

28 to a 52-minute intravenous administration of ketamine (0.71 mg/kg, N=17) or the active control midazo

29 etamine 0.5 mg/kg (n = 22), a single dose of ketamine 1.0 mg/kg (n = 20), and a single dose of midazo

30 g rapamycin + ketamine compared to placebo + ketamine (13%, p = 0.04, and 7%, p = 0.003, respectively

31 We found ketamine 20 mg/kg provoked "fast" theta sniffing in rode

32 as conducted following the administration of ketamine (20 mg) or placebo (saline).

33 escent male and female C57BL/6 mice received ketamine (20 mg/kg) for 15 consecutive days (Postnatal D

34 Mice were treated with sub-chronic ketamine (30 mg/kg) or saline and then received in vivo

35 These data show that in addition to (R,S)-ketamine, 5-HT(4)R agonists are also effective prophylac

36 LBNP test was not different between trials (Ketamine: 635 +/- 391 vs. Placebo: 652 +/- 360 mmHg min,

37 Ketamine, a dissociative anesthetic, is experiencing a c

38 Sub-anaesthetic doses of ketamine, a non-competitive N-methyl-D-aspartate recepto

39 rtant for the antidepressant-like effects of ketamine, a non-competitive N-methyl-D-aspartate recepto

40 d experimentally using the NMDA-R antagonist ketamine, a pharmacological model of schizophrenia.

41 We employed MRI to assess the effects of ketamine abuse on cerebral gray matter volume (GMV) and

42 ar death experience that is keenly sought by ketamine abusers.

43 partate receptor (NMDAR) antagonists such as ketamine act preferentially on GABAergic neurons.

44 It has been hypothesized that ketamine activates mTORC1-4E-BP signalling in pyramidal

45 d others have previously reported that (R,S)-ketamine acts as a prophylactic against stress when admi

46 In the central nervous system, ketamine acts primarily by blocking NMDA receptor curren

47 Here, we report that ketamine acutely suppresses the activity of SST interneu

48 d whether a single subanesthetic infusion of ketamine administered to adults with alcohol dependence

49 t this relation was effectively absent after ketamine administration (r = -0.12, P = 0.5885).

50 These data suggest that low dose ketamine administration attenuates perceived pain and pr

51 Our data suggest that low dose ketamine administration blunts pain perception and reduc

52 Following ketamine administration, EEG changes were immediate and

53 Two weeks following ketamine administration, we found higher response (41%)

54 that contribute to depression relapse after ketamine administration.

55 Similar to previous results with R,S-ketamine, administration of L-655,709 increased levels o

56 Therefore, it is unknown whether ketamine adversely affects physiological mechanisms resp

57 This study examined whether ketamine affects the brain's fronto-striatal system, whi

58 At the neurocircuitry level, ketamine affects the brain's reward and mood circuitry l

59 d the size and duration of avalanches, while ketamine allowed for more awake-like dynamics to persist

60 Ketamine also has short term dissociative effects, in wh

61 f a broad range of subanesthetic doses of IV ketamine among outpatients with treatment-resistant depr

62 Ketamine, an N-methyl-d-aspartate (NMDA) receptor antago

63 A single subanesthetic dose of ketamine, an NMDA receptor (NMDAR) antagonist, produces

64 led studies have demonstrated the ability of ketamine, an NMDA receptor antagonist, to induce rapid (

65 ssary for the prophylactic efficacy of (R,S)-ketamine and (2R,6R)-HNK in female mice.

66 esis, we studied the behavioural response to ketamine and (2R,6R)-HNK in mice lacking 4E-BPs in eithe

67 The antidepressant effects of ketamine and (2R,6R)-HNK in rodents require activation o

68 effectors of the antidepressant activity of ketamine and (2R,6R)-HNK, and that ketamine-induced hipp

69 (R,S)-ketamine and (2R,6R)-HNK, but not (2S,6S)-HNK, attenuate

70 er highlighted approaches involve the use of ketamine and 3,4-methylenedioxymethamphetamine-assisted

71 eproduces some of the therapeutic effects of ketamine and appears to lack abuse liability.

72 Rats were anesthetized using ketamine and chlorpromazine.

73 rovide a historical note on the discovery of ketamine and its putative mechanisms.

74 mimics some of the neuroactive properties of ketamine and may lack its abuse liability.

75 g/kg and 1.0 mg/kg subanesthetic doses of IV ketamine and no clear or consistent evidence for clinica

76 nd longer-lasting antidepressant response to ketamine and other N-methyl-D-aspartate (NMDA) receptor

77 These data suggest that ketamine and other RAADs mediate a specific effect on af

78 nconsciousness under different anaesthetics (ketamine and propofol).

79 mediate the rapid antidepressant actions of ketamine and rapastinel.

80 ed or occluded the antidepressant actions of ketamine and revealed sex-specific differences that are

81 ptual framework that suggests the actions of ketamine and serotonergic psychedelics may converge at t

82 gger for the rapid antidepressant actions of ketamine and show sex-specific adaptive mechanisms to Gl

83 escent male mice were exposed to concomitant ketamine and social stressors (PD35-44), namely the soci

84 rt on the downstream molecular mechanisms of ketamine and their effects on the brain circuitry and ne

85 ce that rapamycin may extend the benefits of ketamine, and thereby potentially sheds light on mechani

86 ecessary for and sufficient to restore (R,S)-ketamine- and (2R,6R)-HNK-mediated prophylaxis in female

87 a depression-related phenotype (along with a ketamine antidepressant-like response).

88 ulation or rapid-acting antidepressants like ketamine, appear to reverse depression associated circui

89 ts treatment has advanced with the advent of ketamine as a rapid-acting antidepressant and the develo

90 observed when male and female mice received ketamine as adults (PD70-84) and tested for sucrose and

91 cluding using rapid-acting treatments (e.g., ketamine) as a means to test this integrative model by a

92 timized conditions, the calibration curve of ketamine at buffer solution (pH 12) exhibits a sensitivi

93 did not alter the antidepressant effects of ketamine at the 24-h timepoint.

94 detail the molecular and circuits effect of ketamine based on preclinical findings, followed by a su

95 ssfully identified a robust and reproducible ketamine biomarker that is related to the mechanisms of

96 ithout any effect on glutamate efflux, while ketamine blocks NMDAR on GABA interneurons to cause glut

97 We tested the hypothesis that low dose ketamine blunts perceived pain, and blunts subsequent sy

98 pioid system does not mediate the actions of ketamine but rather is permissive.

99 and sustained antidepressant-like actions of ketamine, but is spared its dissociative-like properties

100 ailed to block the antidepressant effects of ketamine, but it prolonged ketamine's antidepressant eff

101 their differential effects on consciousness (ketamine, but not propofol, is known to induce an unusua

102 imilar positive biases in decision-making to ketamine, but the same effects were not seen with other

103 tem allows for the on-site identification of ketamine by law enforcement agents in an easy-to-use and

104 rolongation of the antidepressant effects of ketamine by rapamycin.

105 s still unknown whether metabolites of (R,S)-ketamine can be prophylactic in both sexes.

106 A subanesthetic dose of ketamine causes acute psychotomimetic symptoms and susta

107 Finally, we investigated the ketamine CFP connectivity at 1-week post treatment in ma

108 Compared to placebo, the ketamine CFP connectivity changes at 1 week predicted re

109 stness and reproducibility of the discovered ketamine CFP in two separate healthy samples (Cohort B,

110 ound a significant, robust, and reproducible ketamine CFP, consistent with reduced connectivity withi

111 remission rates (29%) following rapamycin + ketamine compared to placebo + ketamine (13%, p = 0.04,

112 For the post-drug CPT, ketamine compared to placebo administration attenuated p

113 on-making task are differentially altered by ketamine, compared to conventional, delayed onset antide

114 ravenous infusion of a subanesthetic dose of ketamine, compared to normal saline.

115 First, ketamine concentration positively predicted distal antid

116 vation of Cav1.2 in smooth muscle mimics the ketamine cystitis phenotype.

117 signaling is an important pathway mediating ketamine cystitis.

118 se extensive pathological changes, including ketamine cystitis.

119 Consistent with ketamine-dependent HFO being driven by nasal respiration

120 findings suggest that nasal airflow entrains ketamine-dependent HFO in diverse brain regions, and tha

121 blockade led to an ipsilateral reduction in ketamine-dependent HFO power compared to the control sid

122 Bursts of ketamine-dependent HFO were coupled to "fast" theta freq

123 Haloperidol 1 mg/kg pretreatment prevented ketamine-dependent increases in fast sniffing and instea

124 Uses of ketamine discussed focused on critically ill patients in

125 Thus, ketamine does not act as an opiate but its effects requi

126 t the administration of an analgesic dose of ketamine does not compromise tolerance to a simulated ha

127 sent study aimed to test the hypothesis that ketamine does not impair haemorrhagic tolerance in human

128 onstrate that the administration of low-dose ketamine does not impair tolerance to simulated haemorrh

129 A range of IV ketamine doses were compared to active placebo in the tr

130 At the same time, ketamine elicits a unique form of functional synaptic pl

131 pinnings of the antidepressant efficacy of S-ketamine (esketamine) nasal spray in major depressive di

132 Subanesthetic ketamine evokes rapid and long-lasting antidepressant ef

133 findings suggest a neural mechanism by which ketamine exerts its antidepressant efficacy, via rapid b

134 Twenty-four hours after administration, ketamine exerts rapid and robust antidepressant effects

135 Ketamine exerts rapid antidepressant action in depressed

136 ingle, subanesthetic dose of (R,S)-ketamine (ketamine) exerts rapid and robust antidepressant effects

137 ever, the potential enduring consequences of ketamine exposure have not been thoroughly evaluated.

138 physical or psychological stress, adolescent ketamine exposure increases later life preference for th

139 rent study, we examined the effects of early ketamine exposure on brain structure and function.

140 vioral consequences associated with juvenile ketamine exposure.

141 ularly vulnerable to the influences of early ketamine exposure.

142 ce imaging (rsfMRI) was acquired 2 days post-ketamine (final sample: TRD n = 27, HV n = 19) and post-

143 Mice were administered saline, (R,S)-ketamine, Flx, RS-67,333, prucalopride, or PF-04995274 a

144 pid and robust antidepressant effects of r/s-ketamine for the treatment of antidepressant-resistant s

145 Repurposing of ketamine for treating TRD provided a new understanding o

146 he N-methyl-D-aspartate receptor antagonist, ketamine, for treating major depressive disorder (MDD);

147 Pain creams compounded for neuropathic pain (ketamine, gabapentin, clonidine, and lidocaine), nocicep

148 lobenzaprine, and lidocaine), or mixed pain (ketamine, gabapentin, diclofenac, baclofen, cyclobenzapr

149 nd to moderate the relationship between post-ketamine gamma power and antidepressant response; specif

150 pressant response; specifically, higher post-ketamine gamma power was associated with better response

151 The ketamine group had a lower risk of post-intubation hypot

152 ed-based correlation analysis show that both ketamine groups had higher functional connectivity betwe

153 Ketamine had no effect compared to baseline or placebo i

154 f the rapid-acting antidepressant effects of ketamine has 1) led to a paradigm shift in our perceptio

155 Recently, ketamine has also been proposed as a novel treatment for

156 In humans, ketamine has been demonstrated to raise resting BP, alth

157 Ketamine has been proposed to exert its antidepressant e

158 The general anesthetic ketamine has been repurposed by physicians as an anti-de

159 Ketamine has been used for medical purposes, most typica

160 Ketamine has emerged as a widespread treatment for a var

161 anisms, the focus on the receptor targets of ketamine has failed in several clinical trials over the

162 Ketamine has shown promising antidepressant efficacy for

163 Ketamine has suggested potential benefit in several dise

164 We found that, like ketamine, HNK reduced NMDA receptor currents in a dose-,

165 vity are widely reported after subanesthetic ketamine, however their mechanisms of generation are unc

166 Ketamine improves motivation-related symptoms in depress

167 lind, placebo-controlled, crossover trial of ketamine in 33 individuals with treatment-resistant majo

168 ther sex who received the NMDAR antagonist S-ketamine in a placebo-controlled, double-blind, within-s

169 180 Hz, HFO) and behavioral activation after ketamine in freely moving rats.

170 alysis for clinicians administering low dose ketamine in humans.

171 rochemical approach for the determination of ketamine in street samples and seizures is presented by

172 antidepressant-like (AD-like) effect of R,S-ketamine in the absence of any psychotomimetic or abuse-

173 nical studies have confirmed the efficacy of ketamine in the treatment of depression.

174 rmulation of esketamine, the S enantiomer of ketamine, in conjunction with an oral antidepressant, ha

175 Ketamine increased fronto-striatal functional connectivi

176 Sub-chronic ketamine increased striatal dopamine synthesis capacity

177 High-dose POMA significantly reduced ketamine-induced BPRS total symptoms within and between-

178 Primary outcomes were ketamine-induced changes in pharmacoBOLD in the dorsal a

179 t neither POMA dose significantly suppressed ketamine-induced dACC pharmacoBOLD.

180 tivity of ketamine and (2R,6R)-HNK, and that ketamine-induced hippocampal synaptic plasticity depends

181 Bilateral nares blockade reduced ketamine-induced hyperactivity and HFO power and frequen

182 ne D(2) receptors, significantly reduced the ketamine-induced increase in dopamine synthesis capacity

183 lly in inhibitory neurons also prevented the ketamine-induced increase in hippocampal excitatory neur

184 The ketamine-induced increase in intracellular cAMP persiste

185 y be particularly relevant for understanding ketamine-induced shifts in motivational symptoms.

186 contrast, Cav1.2 agonist Bay k8644 abrogates ketamine-induced smooth muscle dysfunction.

187 Notably, it is unknown if low dose ketamine influences autonomic cardiovascular responses d

188 stant depression (TRD) who received a single ketamine infusion (0.5 mg/kg) over 40 min.

189 A single ketamine infusion was found to improve measures of drink

190 stinence from alcohol over the 21 days after ketamine infusion.

191 therapy, transcranial magnetic stimulation, ketamine infusions, and, more recently, glabellar botuli

192 Our results demonstrate that ketamine inhibition of Cav1.2 signaling is an important

193 Low dose ketamine is a leading medication used to provide analges

194 Ketamine is a valuable anaesthetic and analgesic that in

195 Low dose ketamine is an effective analgesic medication.

196 Here we present evidence that ketamine is an effective L-type Ca(2+) channel (Cav1.2)

197 The mechanism of action of ketamine is currently unclear but one hypothesis is that

198 Low dose ketamine is increasingly used off-label to treat conditi

199 riguingly, another psychotomimetic compound, ketamine, is a fast-acting antidepressant and induces sy

200 Relative to ketamine, it had 100-fold-lower potency (46 uM at pH 7.2

201 NMDA receptor (NMDAR) blockade with ketamine (KET) during development causes oxidative stres

202 lopment [subcutaneous injections of 30 mg/kg ketamine (KET) on postnatal days 7, 9, and 11] results i

203 A single, subanesthetic dose of (R,S)-ketamine (ketamine) exerts rapid and robust antidepressa

204 Unlike R,S-ketamine, L-655,708 did not cause an increase in the pho

205 receptors alone is not sufficient to produce ketamine-like effects, nor does ketamine mimic the hedon

206 for ketamine's effects remains elusive, but ketamine may broadly modulate brain plasticity processes

207 al the neural plasticity-based mechanism for ketamine-mediated functional recovery from adult amblyop

208 2R,6R-Hydroxynorketamine (HNK), a ketamine metabolite, reproduces some of the therapeutic

209 Linear mixed models evaluated ketamine metabolites as mediators of antidepressant and

210 tory study examined the relationship between ketamine metabolites, clinical response, psychotomimetic

211 ponse (with 95% CI) yielded similar results: ketamine (midazolam), 45% (34-56%); ketamine (saline), 4

212 t to produce ketamine-like effects, nor does ketamine mimic the hedonic effects of an opiate, indicat

213 2R,6R-Hydroxynorketamine, a metabolite of ketamine, mimics some of the neuroactive properties of k

214 liminary results characterize the effects of ketamine misuse on brain structure and function and high

215 Ketamine, N,N-dimethyltryptamine (DMT), and other psycho

216 , in 5/6 sheep we observed a novel effect of ketamine, namely the complete cessation of cortical EEG

217 Non-ketamine NMDA antagonists lacked efficacy and we also fo

218 Second, ketamine, norketamine, and (2S,6S;2R,6R)-HNK concentrati

219 Plasma concentrations of ketamine, norketamine, and HNKs were measured at 40, 80,

220 ies found that antidepressant treatment with ketamine normalized aberrant GBC changes in the prefront

221 cal electroencephalography (EEG) response to ketamine of 12 sheep.

222 However, our knowledge of the effects of ketamine on autonomic cardiovascular regulation is prima

223 anaesthetic actions, however, the effects of ketamine on brain activity have rarely been probed.

224 NMDAR PAM (rapastinel) or NMDAR antagonist, ketamine on NMDAR function and disinhibition-mediated gl

225 Besides, the oxidation pathway of ketamine on SPE is investigated for the first time with

226 Thus, identifying the effect of ketamine on the brain circuitry and networks is becoming

227 ghlight the influence of earlier exposure to ketamine on the development of the brain.

228 The effect of ketamine on the electrophysiological activity of the OB

229 Specifically, the influence of low-dose ketamine, one of three analgesics employed in the pre-ho

230 We administered (R,S)-ketamine or its metabolites (2R,6R)-hydroxynorketamine (

231 induced by precisely-dosed administration of ketamine or phencyclidine.

232 ctrophysiological recordings following (R,S)-ketamine or prucalopride administration revealed that bo

233 e- and 5 min post-drug administration (20 mg ketamine or saline).

234 Moreover, electroconvulsive therapy, ketamine, physical exercise, and certain non-steroidal a

235 We found that juvenile ketamine-pretreatment increased preference for sucrose a

236 Ketamine prevents Cav1.2-mediated induction of immediate

237 ly reported that the administration of (R,S)-ketamine prevents stress-induced depressive-like behavio

238 Ketamine produces a rapid increase in extracellular glut

239 Ketamine produces immediate antidepressant effects and h

240 Ketamine produces rapid and robust antidepressant effect

241 e of mTORC1 in the antidepressant effects of ketamine, provides preliminary evidence that rapamycin m

242 We show that single-dose ketamine reactivates adult mouse visual cortical plastic

243 Thus, ketamine reactivation of adult visual cortical plasticit

244 er, there are several pain medications (e.g. ketamine) recommended for use in the prehospital, field

245 Sub-chronic ketamine reduced PV expression in these cortical and hip

246 Finally, ketamine reduced sgACC hyper-activation to positive ince

247 n patients with schizophrenia and effects of ketamine relevant to its therapeutic use for treating ma

248 signaling via GluN2B knockdown, we show that ketamine's actions on the dendritic inhibitory mechanism

249 The mechanisms of ketamine's anti-depressant and adverse effects remain po

250 essant effects of ketamine, but it prolonged ketamine's antidepressant effects.

251 Ketamine's antidepressant mechanism is predominantly med

252 lar trigger that initiates this increase and ketamine's behavioral actions has not been identified.

253 However, whether ketamine's dissociative side effects are necessary for i

254 The mechanism for ketamine's effects remains elusive, but ketamine may bro

255 potential importance of reward circuitry in ketamine's mechanism of action, which may be particularl

256 results: ketamine (midazolam), 45% (34-56%); ketamine (saline), 46% (34-58%); midazolam, 18% (6-30%);

257 Ketamine, shown to have rapid antidepressant effects, fa

258 In contrast to traditional antidepressants, ketamine shows a rapid (within 2 h) and sustained (~7 da

259 Furthermore, we find that ketamine significantly diminished the expression of high

260 In each of Cohorts A-C, ketamine significantly increased connectivity in a previ

261 Ketamine significantly increased the likelihood of absti

262 kely to underlie the dissociative actions of ketamine, since it is during this phase that ketamine us

263 Ketamine specifically induces downregulation of neuregul

264 In animals, ketamine stimulates the sympathetic nervous system and i

265 FC did not fully recapitulate the effects of ketamine, suggesting a specific mechanism.

266 However, ketamine tends to be abused by adolescents and young adu

267 m as a comparator yielded smaller effects of ketamine than those which used saline, which was account

268 Ketamine thus normalized fronto-striatal connectivity in

269 this effect concurred with the inability of ketamine to induce a long-lasting decrease in inhibitory

270 (HCN1) pacemakers were required for systemic ketamine to induce this rhythm and to elicit dissociatio

271 n, opioid antagonists abolish the ability of ketamine to reduce the depression-like behavioral and LH

272 These results show that sub-chronic ketamine treatment in mice mimics the dopaminergic alter

273 Thus, we examined if juvenile ketamine treatment results in long-lasting changes for t

274 rons in vitro and in vivo following a single ketamine treatment.

275 Subsequent to the ketamine treatments, participants remained on lithium or

276 apid acting antidepressant (RAAD) effects of ketamine, treatments were limited to drugs that have del

277 In addition, propofol, but not ketamine, triggered a large reduction in the complexity

278 However, ketamine use can cause extensive pathological changes, i

279 ketamine, since it is during this phase that ketamine users report hallucinations.

280 Compared to controls, ketamine users showed decreased GMV in the right insula,

281 Ketamine users were categorized as adolescent-onset and

282 revealed lower GMV in the left precuneus in ketamine users, with a larger decrease in the adolescent

283 ere higher during moderate hypovolemia after ketamine vs. placebo administration (P < 0.05 for all, p

284 ere higher during moderate hypovolemia after ketamine vs. placebo administration.

285 The response rate for ketamine was higher than the control condition for both

286 ic symptoms; post-hoc analysis revealed that ketamine was the predominant contributor.

287 onstrated that the antidepressant actions of ketamine were blocked by GluN2B-NMDAR knockdown on GABA

288 ive setting using either IV or intramuscular ketamine were included for analysis.

289 The infusions of ketamine were relatively well tolerated compared to acti

290 Propofol and ketamine were selected due to their differential effects

291 g/kg) and high dose (1 mg/kg) of intravenous ketamine were superior to active placebo; a low dose (0.

292 e evidence was organized according to use of ketamine, which included pain, sedation, status asthmati

293 Subsequently, binary mixtures of ketamine with adulterants and illicit drugs are analyzed

294 rther investigate these effects by comparing ketamine with other NMDA antagonists using this decision

295 were acquired at 3 and 7 d after TAC, under ketamine-xylazine anesthesia to suppress cardiomyocyte g

296 hanced at 30 d postsurgery in both awake and ketamine-xylazine anesthetized mice with electrodes, sup

297 In Ketamine/Xylazine (KX) anesthetized mice, glymphatic tra

298 dependent changes in glymphatic influx under ketamine/xylazine anesthesia were not altered by sex.

299 or responses in olfactory bulb degrade under ketamine/xylazine anesthesia while responses immediately

300 Ketamine yielded an increase in subjects' PVB, consisten