ライフサイエンスコーパス: MDMA

1 MDMA (+/- 3,4-methylenedioxymethamphetamine, 'ecstasy')

2 MDMA (3,4-methylenedioxymethamphetamine) is a popular re

3 MDMA (3,4-methylenedioxymethamphetamine, also popularly

4 MDMA (5-fold) and methadone (7-fold) use showed also an

5 MDMA (Ecstasy) is an illicit drug used by young adults a

6 MDMA and its enantiomers increased affiliative social be

7 MDMA and other similar drugs are reportedly associated w

8 MDMA had a predominantly excitatory effect on neuronal a

9 MDMA induced a 35-fold increase in norepinephrine levels

10 MDMA is showing encouraging results as a treatment for r

11 MDMA pretreatment was hypothesized to enhance the effect

12 MDMA users (N = 65) participated in a 4-session, within-

13 MDMA users had increased serotonin(2A)BP(ND) in occipita

14 MDMA users reported a mean duration of ecstasy use of 8

15 MDMA, a potent monoamine-releaser with particularly pron

16 MDMA, better known as the recreational drug "ecstasy," i

17 MDMA-induced hyperthermia is highly variable, unpredicta

18 MDMA-induced increases in social behaviors are 5-HT2A, b

19 MDMA-treated animals had increased BDNF expression in th

20 memory impairments resulting from P11 to 20 MDMA exposure.

21 Nineteen abstinent MDMA users and 21 control subjects participated in a 5 d

22 toxicity are not fully understood, abstinent MDMA users have been found to have subtle cognitive defi

23 n findings of this study are that: (1) acute MDMA augments locomotor behavior and attenuates the inco

24 us mimicking the clinical situation of acute MDMA intoxication.

25 In addition, MDMA is a potent releaser and reuptake inhibitor of pres

26 iously, we have shown that rats administered MDMA from postnatal (P) days 11-20 had reductions in bod

27 To do this, we administered MDMA-HCl (100 mg p.o.) and, separately, placebo (ascorbi

28 esults indicate that intermittent adolescent MDMA exposure enhances sensitivity of 5-HT(2A/2C) recept

29 tyrosine into the hippocampus did not affect MDMA-induced increases in extracellular DA or the long-t

30 ent profiles than the parent compounds after MDMA administration.

31 Four hours after MDMA treatment, blood was drawn and serum creatine kinas

32 in the ventral midbrain within 4-12 hr after MDMA treatment.

33 Moreover, when administered 1 hr after MDMA, carvedilol completely reversed established hyperth

34 DA and the long-term depletion of 5-HT after MDMA.

35 Plasma catecholamines levels 30 mins after MDMA (40 mg/kg, subcutaneously) were determined by high-

36 Decreased CBF only was observed after MDMA, and this was localized to the right medial tempora

37 neally) administered 15 mins before or after MDMA prevented this hyperthermic response.

38 in cerebral blood flow (CBF) and RSFC after MDMA administration.

39 Speech after MDMA (1.5 mg/kg) had greater semantic proximity than pla

40 cipants completed a 10-min speech task after MDMA (0.75 and 1.5 mg/kg), methamphetamine (20 mg), or p

41 cetate conferred complete protection against MDMA-induced toxicity to DA neurons, and administration

42 Although MDMA administered at either phase did not affect overall

43 s repeated exposure to cocaine, amphetamine, MDMA [(+)-3,4-methylenedioxymethamphetamine], or nicotin

44 restingly, the substitution I333C reveals an MDMA-induced conformation not observed with 5-HT.

45 o hallucinogen-preferring users (n = 10) and MDMA-preferring users (n = 14).

46 .5 mg/kg) and placebo with 88% accuracy, and MDMA (1.5 mg/kg) and methamphetamine with 84% accuracy.

47 reoselectivity was recorded for atenolol and MDMA), treatment technology used (activated sludge showe

48 s/controlled substances such as ketamine and MDMA, indicating the high consumption of ecstasy during

49 motor responses to various doses of MDPV and MDMA, as a function of ambient temperature.

50 , this study assessed the impact of METH and MDMA administration on the DAT protein per se.

51 In animals, MDMA induces 5-HT depletion and toxicity in 5-HT neurons

52 edilol was modestly effective in attenuating MDMA-induced hyperthermia by moderately inhibiting skin

53 At baseline, MDMA users performed less accurately than controls on a

54 traperitoneally) administered 30 mins before MDMA had no effect on the thermogenic response.

55 nclude that the negative association between MDMA use and cerebral SERT binding is mediated through a

56 Classifiers discriminated between MDMA (1.5 mg/kg) and placebo with 88% accuracy, and MDMA

57 Although multiple parallels exist between MDMA abuse and stress, including effects on 5-HTergic ne

58 was shifted to a new location, however, both MDMA males and females were impaired when the location o

59 nt release of DA in the striatum elicited by MDMA appears to involve 5-HT2 receptor activation.

60 mpathetic and behavioral responses evoked by MDMA.

61 Furthermore, hyperthermia induced by MDMA during preconditioning appears not to contribute to

62 The release of DA induced by MDMA is thought to involve both transporter and impulse-

63 ocrine and neurochemical changes produced by MDMA treatment on P11.

64 increases in positive mood were produced by MDMA.

65 of PKC activity on DA release stimulated by MDMA.

66 T transmission in recently abstinent chronic MDMA users compared with matched healthy controls.

67 ed to study the effects of acute and chronic MDMA on locomotor activity and sensory evoked field pote

68 In contrast, MDMA pretreatment led to CUS-induced learning impairment

69 In rats previously microinjected with CSF, MDMA elicited significant increases from baseline in cor

70 esults showed, for drugs with weekly cycles (MDMA, methamphetamine and cocaine in this sample), sampl

71 During sleep deprivation, MDMA users, but not controls, became increasingly impuls

72 luated in 13 current and recently detoxified MDMA users and 13 matched healthy controls.

73 oach, analysis was performed for four drugs (MDMA, methamphetamine, cocaine, methadone) collected thr

74 sine into the striatum or hippocampus during MDMA administration potentiated the acute increase in ex

75 have assessed the long-term impact of early MDMA exposure on serotonin (5-HT) and dopamine (DA) neur

76 Results indicated that early MDMA exposure caused a decrease in PKA activity and 5-HT

77 These data indicate that early MDMA exposure has long-term effects on the 5-HT and DA n

78 3,4 methylenedioxymethamphetamine (ecstasy, MDMA) elicits hyperthermia, hyperactivity, tachycardia,

79 atum, intracortical infusion of BIM enhanced MDMA-induced release of DA in the mPFC.

80 eat dissipation to the external environment, MDMA at a moderate nontoxic dose (9 mg/kg or ~1/5 of LD5

81 As expected, MDMA dose-dependently increased heart rate and blood pre

82 In the first experiment, MDMA pretreatment increased the frequency of head twitch

83 es in affiliative social behaviors following MDMA administration, in concordance with human and roden

84 atic ACTH was elevated immediately following MDMA and remained elevated for at least 1 h after the la

85 erotonin transporter were observed following MDMA treatment, although females had lower levels than m

86 learning and memory deficits seen following MDMA treatment.

87 preconditioning-induced neuroprotection for MDMA remain to be determined.

88 A exposures, and the time of abstinence from MDMA was positively correlated with subcortical, but not

89 Case participants were abstinent from MDMA use for at least 90 days as verified by analysis of

90 On measures of social function, MDMA impaired recognition of angry and fearful facial ex

91 ssant medications and psychostimulants (e.g. MDMA, cocaine).

92 In the Encoding group, MDMA reduced recollection estimates for negative and pos

93 Neuroimaging data indicate that some human MDMA users develop persistent deficits in brain 5-HT neu

94 exclude the possibility that alterations in MDMA pharmacokinetics or MDMA-induced hyperthermia in ra

95 n SERT(ir) also was completely attenuated in MDMA-preconditioned animals.

96 bance and suggest that cognitive deficits in MDMA users may become more prominent in situations assoc

97 rbance plays a role in cognitive deficits in MDMA users.

98 rged as candidate genes possibly involved in MDMA-induced toxicity to DA neurons.

99 sterone responses to DOI were potentiated in MDMA-pretreated animals.

100 first to demonstrate that memory problems in MDMA users may be related, at least in part, to sleep di

101 neuronal activity in the DMH plays a role in MDMA-evoked sympathetic and behavioral responses by micr

102 ta, and trkB was elevated in the striatum in MDMA-treated animals.

103 lter affiliative vocalizations and increased MDMA-induced social contact.

104 e into the striatum, significantly increased MDMA-induced DA release.

105 Rats were treated with saline or 20 mg/kg MDMA (two injections per day) from postnatal day (PD) 11

106 ated intermittent administration of 10 mg/kg MDMA during adolescence on behavioral (Experiment 1) and

107 Lifetime MDMA use was positively associated with serotonin(2A)BP(

108 ively correlated with the number of lifetime MDMA exposures, and the time of abstinence from MDMA was

109 or levels correlate positively with lifetime MDMA use and do not decrease with abstinence.

110 om saline and that cumulative doses of MDPV, MDMA, and METH fully substituted for the MDPV training s

111 ts of a range of substitution doses of MDPV, MDMA, and METH were then assessed.

112 ursor to DA biosynthesis, tyrosine, mediates MDMA-induced 5-HT depletions.

113 rugs of abuse (amphetamine, methamphetamine, MDMA, MDA), ephedrines (ephedrine and pseudoephedrine),

114 ough 3,4-methylenedioxy-N-methylamphetamine (MDMA) or ecstasy is currently classified as a type of ha

115 used 3,4-methylenedioxy-N-methylamphetamine (MDMA), 221 (10%) used gamma-hydroxybutyrate or gamma-but

116 DA), 3,4-methylenedioxy-N-methylamphetamine (MDMA), 3,4-methylenedioxy-N-ethylamphetamine (MDEA), mor

117 g of 3,4-methylenedioxy-N-methylamphetamine (MDMA).

118 silocybin) and methylenedioxymethamfetamine (MDMA), best known for their illegal use as psychedelic d

119 Methylenedioxymethamphetamine (MDMA; "Ecstasy") is a popular recreational drug and brai

120 f illicit 3,4-methylenedioxymethamphetamine (MDMA or "ecstasy") has been a global target of law enfor

121 ogens and 3,4-methylenedioxymethamphetamine (MDMA or "ecstasy") have direct agonistic effects on post

122 3,4-methylenedioxymethamphetamine (MDMA or 'Ecstasy'), which is widely used as a recreation

123 mericans, 3,4-methylenedioxymethamphetamine (MDMA) (commonly referred to as ecstasy) is popular in th

124 ompounds, 3,4-methylenedioxymethamphetamine (MDMA) and methamphetamine.

125 imilar to 3,4-methylenedioxymethamphetamine (MDMA) and share many of its physiological and behavioral

126 ration of 3,4-methylenedioxymethamphetamine (MDMA) elevates extracellular concentrations of dopamine

127 3,4-Methylenedioxymethamphetamine (MDMA) increases sociality in humans and animals.

128 3,4-Methylenedioxymethamphetamine (MDMA) is a drug of abuse worldwide and a selective serot

129 compound 3,4-methylenedioxymethamphetamine (MDMA) is a potent monoamine releaser that produces an ac

130 3,4-Methylenedioxymethamphetamine (MDMA) is a widely abused amphetamine derivative that inc

131 e drug +/-3,4-methylenedioxymethamphetamine (MDMA) is increasingly used for its perceived emotional e

132 stion of 3, 4-methylenedioxymethamphetamine (MDMA) leads to heightened response to sensory stimulatio

133 ffects of 3,4-methylenedioxymethamphetamine (MDMA) on large-scale patterns of brain activity.

134 ollowing: 3,4-methylenedioxymethamphetamine (MDMA) tablets resulting in the detection of 12-40 ng of

135 n that +/-3,4-methylenedioxymethamphetamine (MDMA) treatment from P11 to P20 in rats produces deficit

136 ed by (+)-3,4-methylenedioxymethamphetamine (MDMA) with E effects on cocaine-evoked hyperactivity in

137 (+/-)3,4-Methylenedioxymethamphetamine (MDMA), a widely used drug of abuse, rapidly reduces sero

138 of abuse 3,4-methylenedioxymethamphetamine (MDMA), and methamphetamine (METH) suggest that it may ha

139 hetamine, 3,4-methylenedioxymethamphetamine (MDMA), phentermine, and mephedrone) in one method using

140 3,4-Methylenedioxymethamphetamine (MDMA), the main psychoactive component of the recreation

141 ribute to 3,4-methylenedioxymethamphetamine (MDMA)-induced 5-HT toxicity.

142 lying (+)-3,4-methylenedioxymethamphetamine (MDMA)-induced damage to 5-HT terminals are unknown.

143 5-HT and 3,4-methylenedioxymethamphetamine (MDMA).

144 g adults, 3,4-methylenedioxymethamphetamine (MDMA, "ecstasy") is a popular drug of abuse, and anecdot

145 larity to 3,4-methylenedioxymethamphetamine (MDMA, "Ecstasy") prompted the current investigation of t

146 of severe 3,4-methylenedioxymethamphetamine (MDMA, Ecstasy) intoxication.

147 sant) and 3,4-methylenedioxymethamphetamine (MDMA; "Ecstasy") revealed them as being similar to the e

148 after +/-3,4-methylenedioxymethamphetamine (MDMA; 'ecstasy') and methamphetamine in 13 ecstasy users

149 istrations of methylenedioxymethamphetamine (MDMA) cause less of an acute reduction in DA uptake and

150 tional use of methylenedioxymethamphetamine (MDMA) has dramatically increased among juveniles and you

151 /-)-3,4-methylenedioxymethamphetamine ((+/-)-MDMA, commonly called ecstasy) can lead to life-threaten

152 drug (+/-)3,4-methylenedioxymethamphetamine [MDMA ("ecstasy")] produces a selective toxic effect on b

153 ecstasy (3,4 methylenedioxymethamphetamine; MDMA) have been implicated.

154 d signaling pathways differentially modulate MDMA-induced DA release from mesocorticolimbic and nigro

155 dentify genes potentially involved in murine MDMA-induced toxicity to DA neurons.

156 rning and memory deficits following neonatal MDMA exposure.

157 Compared with nonusers, MDMA-preferring users showed significant decreases in SE

158 lly implicated in the mechanism of action of MDMA, but further work is required to elucidate how the

159 s produced by the systemic administration of MDMA (10 mg/kg i.p. x4).

160 d adrenal output following administration of MDMA (10 mg/kg, 4 times) on postnatal day 11.

161 The effect of systemic administration of MDMA on ATP levels in the striatum and hippocampus also

162 Finally, the systemic administration of MDMA produced a 30% decrease in the concentration of ATP

163 sensitization, (3) chronic administration of MDMA results in attenuation of the baseline activity of

164 ys were examined following administration of MDMA, its enantiomers, and methamphetamine.

165 s produced by the systemic administration of MDMA.

166 l before or after a thermogenic challenge of MDMA.

167 ical studies that report the consequences of MDMA on sensory input.

168 Although the consequences of MDMA-induced 5-HT neurotoxicity are not fully understood

169 Reverse dialysis of MDMA and malonate directly into the striatum resulted in

170 e isotope ratios allow the discrimination of MDMA.HCl batches according to synthetic route used for m

171 A serotonergic-depleting dose of MDMA (10 mg/kg x 4 at 2-hour intervals on a single day)

172 ected rats with a moderate non-toxic dose of MDMA (9 mg/kg) during social interaction, and we adminis

173 onditioning) to a non-5-HT depleting dose of MDMA in adult rats provides neuroprotection against subs

174 Our results demonstrate that doses of MDMA that are nontoxic under cool, quiet conditions can

175 ng the administration of neurotoxic doses of MDMA.

176 cally significant effects of the duration of MDMA abstinence on serotonin(2A)BP(ND).

177 Here, we examined the effect of MDMA on temperature homeostasis in male rats under stand

178 study, we investigated the acute effects of MDMA and oxytocin on social and emotional processing in

179 erapeutics with the unique social effects of MDMA but fewer of its limitations.

180 echanisms mediating the prosocial effects of MDMA could help in the development of novel therapeutics

181 ined the mechanisms of the social effects of MDMA in nonhuman primates.

182 o-controlled study to examine the effects of MDMA on emotional memory separately during encoding and

183 been little investigation of the effects of MDMA on sexual function in rodents.

184 In this study, we examined the effects of MDMA on the expression of brain-derived neurotrophic fac

185 elatively weak brain hyperthermic effects of MDMA under standard control conditions (quiet rest, 22-2

186 an by the serotonin(2A) agonistic effects of MDMA.

187 he intensity of global subjective effects of MDMA.

188 t oxytocin produces the prosocial effects of MDMA.

189 Failure of MDMA-treated rats to form CPP to sex may be due to MDMA-

190 injection of METH or multiple injections of MDMA caused little or no formation of these DAT complexe

191 duct the first comprehensive localization of MDMA induced neuronal degeneration throughout the entire

192 bolism which contributes to the mechanism of MDMA-induced 5-HT neurotoxicity.

193 receptors may contribute to the mediation of MDMA-induced hyperthermia and that drugs targeting these

194 the requirement for peripheral metabolism of MDMA to a neurotoxic metabolite.

195 d for BE, cocaine, and a major metabolite of MDMA (i.e., 4-hydroxy-3-methoxymethamphetamine).

196 Using a rat model of MDMA hyperthermia, we evaluated the acute drug-induced c

197 ing might take place after several months of MDMA abstinence.

198 dopamine produced by the local perfusion of MDMA (100 microM) and malonate (100 mM) and the depletio

199 ctivity- and state-dependent potentiation of MDMA-induced brain hyperthermia.

200 In contrast to the powerful potentiation of MDMA-induced hyperthermia by social interaction and warm

201 s that received a preconditioning regimen of MDMA (10 mg/kg, ip daily for 4 days).

202 The 5-HT depleting regimen of MDMA also resulted in a 40-80% reduction in 5-HT transpo

203 n of a serotonin (5-HT)-depleting regimen of MDMA did not produce a change in mount, intromission, an

204 ic response to the 5-HT depleting regimen of MDMA in rats that had earlier received 4 daily injection

205 inistration of the 5-HT depleting regimen of MDMA, there was no difference in the extracellular conce

206 e induced a marked and immediate reversal of MDMA-induced hyperthermia via inhibition of brain metabo

207 tive effects of MDPV are similar to those of MDMA and METH, direct effects on thermoregulatory proces

208 diated by different mechanisms than those of MDMA.

209 ming sensory input, (2) chronic treatment of MDMA elicits behavioral sensitization, (3) chronic admin

210 er conditions that mimic recreational use of MDMA at rave parties or other hot, crowded venues.

211 The recreational use of MDMA is associated with long-lasting increases in seroto

212 otal evidence indicates that repeated use of MDMA may result in impairments in sexual function and de

213 esults indicate that the delta(2)H values of MDMA.HCl are affected by the length of imine stir time,

214 Based on MDMA-induced changes in plasma catecholamine levels, rat

215 Recent findings on MDMA use further question the current drug classificatio

216 inhibitory effects of the PKC inhibitors on MDMA-induced DA release in the striatum, intracortical i

217 Speech on MDMA (0.75 mg/kg) had greater proximity to empathy than

218 rom those established for methamphetamine or MDMA in prior work, despite recent evidence of neurophar

219 that alterations in MDMA pharmacokinetics or MDMA-induced hyperthermia in rats previously exposed to

220 H prior to intravenous infusion of saline or MDMA in conscious rats.

221 ived 4 prior, daily injections of vehicle or MDMA.

222 er received 4 daily injections of vehicle or MDMA.

223 (mAbs) against (+)-METH, (+)-AMP, and/or (+)-MDMA.

224 n-subjects study in which they received oral MDMA (0.75, 1.5 mg/kg), intranasal oxytocin (20 or 40 IU

225 Current strategies to treat pathological MDMA-induced hyperthermia in humans are palliative and m

226 ing is mediated through a direct presynaptic MDMA effect rather than by the serotonin(2A) agonistic e

227 In contrast to vehicle-treated rats, MDMA-treated rats did not form a conditioned place prefe

228 assigned to one of three groups who received MDMA (1 mg/kg) either during encoding (Encoding group; N

229 ntial, and (4) administration of rechallenge MDMA result in enhancement of the PFC sensory evoked fie

230 Current recreational MDMA use was significantly associated with lower SERT BP

231 ugs, might be highly effective for reversing MDMA-induced brain and body hyperthermia in emergency cl

232 ypical antipsychotic clozapine, in reversing MDMA-induced brain and body hyperthermia.

233 dependent scans in a 90-minute scan session; MDMA and placebo study days were separated by 1 week.

234 Nonhuman primates show MDMA-specific increases in affiliative social behaviors

235 d, placebo-controlled, balanced-order study, MDMA was orally administered to 25 physically and mental

236 provides neuroprotection against subsequent MDMA-induced 5-HT depletion.

237 rmia and significantly attenuated subsequent MDMA-induced creatine kinase release.

238 pletion of brain 5-HT produced by subsequent MDMA administration.

239 th these changes might contribute to sustain MDMA use.

240 These results support the conclusion that MDMA produces a dysregulation of energy metabolism which

241 We also demonstrate that MDMA and MDA, like fenfluramine and its N-deethylated me

242 In the present study, we demonstrate that MDMA causes increased susceptibility to herpes simplex v

243 We also demonstrate that MDMA has an effect on the cytokines of the innate immune

244 It is well established that MDMA metabolism produces bioactive metabolites.

245 We found evidence that MDMA but not hallucinogen use is associated with changes

246 We hypothesized that MDMA use is associated with lower SERT density and conco

247 These findings indicate that MDMA attenuates the encoding and retrieval of salient de

248 ngs from latent class analysis indicate that MDMA users have a significantly higher risk of dependenc

249 Collectively, these results indicate that MDMA-induced toxicity to DA neurons is associated with i

250 These results show that MDMA increases the concentration of tyrosine in the brai

251 Previous work has shown that MDMA exposure can alter circadian clock function both in

252 Overall, the findings suggest that MDMA depletes 5-HT by increasing tyrosine and its eventu

253 These data suggest that MDMA may play an important biological role in infection.

254 These results suggest that MDMA use produces chronic serotonin neurotoxicity in hum

255 One line of evidence suggests that MDMA produces these effects by releasing oxytocin, a pep

256 odialysis probe significantly attenuated the MDMA (10 mg/kg, i.p.)-induced increase in the extracellu

257 and a 5-HT2C receptor agonist attenuated the MDMA-induced increase in social behaviors, while a 5-HT1

258 rship) as a neurobiological signature of the MDMA experience, and relate this brain effect to trait a

259 Only the MDMA females showed deficits when the platform was shift

260 in function, the possibility for therapeutic MDMA use, and the widespread recreational popularity of

261 Thus, MDMA increased euphoria and feelings of sociability, per

262 tened response to sensory stimulation; thus, MDMA is referred to as "ecstasy" because it produces ple

263 transmitter-releasing activity comparable to MDMA.

264 s pattern of effects is in sharp contrast to MDMA, where ambient temperature interacts with thermoreg

265 reated rats to form CPP to sex may be due to MDMA-induced impairments in circuits mediating sexual re

266 d hyperthermia in rats previously exposed to MDMA contribute towards neuroprotection.

267 Thus, prior exposure to MDMA affords protection against the long-term depletion

268 ted the consequences of combined exposure to MDMA and chronic stress.

269 as to determine whether repeated exposure to MDMA during the preweanling period would cause long-term

270 interpretation is that repeated exposure to MDMA in humans, even in moderate amounts, leads to damag

271 These results show that prior exposure to MDMA leads to stress-induced impairments in learning beh

272 icroinjecting muscimol into the DMH prior to MDMA prevented increases in core temperature and locomot

273 ness suggest that these initial responses to MDMA may contribute to the long-term learning and memory

274 ses to oxytocin were related to responses to MDMA with subjects on two subjective measures of sociabi

275 membrane monoamine transporters, similar to MDMA in potency and selectivity.

276 together, despite structural similarities to MDMA, exposure to methylone or MDPV under conditions com

277 rontal cortex was particularly vulnerable to MDMA-induced alterations in that BDNF, NT-3, trkB, and t

278 ouble knock-out mice were more vulnerable to MDMA-induced toxicity to DA neurons than corresponding w

279 jection whereas the enhanced response to (+)-MDMA was delayed for approximately 30 min.

280 For the two MDMA doses, the classifier performed at chance.

281 lience network functional connectivity under MDMA.

282 periences of altered bodily sensations under MDMA.

283 d heat loss via skin surfaces) that underlie MDMA-induced brain temperature responses.

284 eductions were significantly attenuated when MDMA and malonate were co-perfused with nicotinamide (1

285 Whereas MDMA alone increased anxiety-like behavior on the elevat

286 Whether MDMA produces chronic reductions in serotonin signaling

287 In contrast, there were no regions in which MDMA use was inversely associated with receptor levels.

288 ediating this damage, it remains unclear why MDMA produces long-term depletions of 5-HT in brain regi

289 iction, two critical factors associated with MDMA toxicity.

290 plus maze, CUS alone or in combination with MDMA pretreatment did not increase anxiety-like behavior

291 Preconditioning with MDMA (10 mg/kg, ip) daily for 4 days provided neuroprote

292 protection, inasmuch as preconditioning with MDMA at a low ambient temperature at which hyperthermia

293 Therefore, rats were pretreated with MDMA and exposed 7 days later to 10 days of mild chronic

294 Treatment of rats with MDMA (10 mg/kg, ip every 2 h for 4 injections) resulted

295 ence of neuropharmacological similarity with MDMA.

296 the association of withdrawal symptoms with MDMA abstinence.

297 analysis revealed that animals treated with MDMA showed reduced serotonin staining, as evidenced by

298 iatal amines, whereas similar treatment with MDMA (2.5 and 7.5 mg/kg, s.c., 3 doses) evoked robust hy

299 Treatment with MDMA significantly diminished the TRZ induced phase shif

300 Following treatment with MDMA, these animals took an average of 8.3 +/- 0.1 days