ライフサイエンスコーパス: MK-801

1 MK-801 (0.3 mg/kg) preadministered in the masseter muscl

2 MK-801 also blocked neuronal death induced by activated

3 (+)-MK-801 and NAC attenuated threshold shifts and hair cell

4 MK-801 applied after the transient Ca(2+) elevations blo

5 MK-801 blocked extinction to maintain high levels of con

6 MK-801 did not alleviate reduced Akita mouse body weight

7 (-)-MK-801 did not influence noise-induced 8-isoprostane for

8 MK-801 had no effect on non-androgen-responsive spinal m

9 MK-801 potentiated ethanol's ataxic effects in the grid

10 MK-801 reversed the decreases in the hypothalamic nuclei

11 MK-801 treatment blocked this effect of T on the SNB.

12 MK-801's effects on ethanol sensitization appeared to be

13 MK-801, a non-competitive NMDA receptor antagonist that

14 MK-801, but not control saline, produced significant num

15 MK-801-induced hyperlocomotion was further potentiated i

16 In Experiment 1, MK-801 dose-dependently impaired SDA learning at both ag

17 oduct that retained the ability to bind 125I-MK-801 and is predicted to be active.

18 ed any significant difference in maximal [3H]MK-801 binding between ISO and NH male and female rats,

19 Unlike male rats, maximal [3H]MK-801 binding in the caudate-putamen of female ISO rats

20 Maximal [3H]MK-801 binding in the caudate-putamen of male ISO rats w

21 CH-23390), D2 ([3H]Spiperone), and NMDA ([3H]MK-801) receptor binding (using the method of receptor a

22 Co-incubation of [3H]MK-801 with METH (0.1-100 microM) did not reduce dextrom

23 ined effects of METH (0.1-100 microM) on [3H]MK-801 binding to membranes prepared from adult rat cort

24 Receptor binding experiments with [3H]MK-801 showed significant up-regulation of NMDA receptor

25 -801 microinjection (vehicle, 34.2 +/- 3.4%; MK-801, -2.5 +/- 2.8%), with minimal change in HPR.

26 lly sensitive to pore block by (+)MK-801, (-)MK-801, ketamine, memantine, amantadine, and dextrorphan

27 Acute MK-801 treatment elevated gamma power and reduced beta b

28 evoked beta oscillations observed with acute MK-801, but did not produce changes in gamma band power.

29 In addition, MK-801, microinjected into the MPOA before each of 7 non

30 We found that early adolescent MK-801 exposure elicited an age- and input-specific dysr

31 ulation is absent following early adolescent MK-801 treatment.

32 bserve no recovery of synaptic current after MK-801 synaptic blockade and washout.

33 pulse inhibition of startle was tested after MK-801 (n = 6), NVP-AAM077, and Ro-6891 (n = 5) injectio

34 in spontaneous IPSC frequency and amplitude; MK-801 (40 microm) also reduced evoked IPSC amplitudes.

35 eflective of direct channel inhibition at an MK-801-sensitive site.

36 r, combination treatment with both NRG-1 and MK-801 resulted in greater neuroprotection than either c

37 ed by the ability to reduce amphetamine- and MK-801-induced hyperactivity and apomorphine-induced cli

38 AC-260584 reduced amphetamine- and MK-801-induced hyperactivity and apomorphine-induced cli

39 by the noncompetitive inhibitors cocaine and MK-801 [(+)-dizocilpine, an anticonvulsant] indicated th

40 derivatives) exist that prevent cocaine and MK-801 inhibition of this receptor.

41 he inhibition of the receptor by cocaine and MK-801 led to an inhibition mechanism not previously pro

42 ibition of the neuronal nAChR by cocaine and MK-801 using rapid chemical kinetic techniques was inves

43 and castrated males treated with both EB and MK-801.

44 Both lorazepam and MK-801 treatment conditions resulted in enhanced BSE act

45 als to evaluate the ability of lorazepam and MK-801 treatments to antagonize behavioral and electroen

46 ntensified effect was blocked by M100907 and MK-801, suggesting that variation in syndrome intensity

47 t conditions on the one hand and the NAc and MK-801 conditions on the other hand for any of these reg

48 Pharmacologic challenges with NAc and MK-801 did not affect the (11)C-ABP688 BPND in the rat b

49 c challenges with N-acetylcysteine (NAc) and MK-801.

50 Phenobarbital and MK-801 were superior to phenytoin in suppressing SE and

51 trazepam and diazepam (GABA(A) receptor) and MK-801 and NMDA (NMDA receptor).

52 , and no significant changes in the test and MK-801 conditions were observed.

53 2 kHz but increased them at 20 kHz, and (-)-MK-801 was ineffective.

54 ethyl-d-aspartate (NMDA) receptor antagonist MK 801, and calcium channel blockers.

55 oncurrent treatment with the NMDA antagonist MK-801 and by a membrane-permeable scavenger ofROS.

56 beling persisted if both the NMDA antagonist MK-801 and the VSCC blocker Gd3+ were present during OGD

57 st AP5 or the noncompetitive NMDA antagonist MK-801 does not selectively disrupt reconsolidation, ind

58 We report here that the NMDA antagonist MK-801, microinjected into the MPOA, impaired copulatory

59 f the N-methyl-D-aspartate (NMDA) antagonist MK-801 on acute responses to ethanol and its ability to

60 d the N-methyl-D-aspartate (NMDA) antagonist MK-801 similarly reduced infarct size following pMCAO.

61 because the noncompetitive NMDAR antagonist MK-801 blocked both morphine tolerance and thermal hyper

62 Finally, the NMDAR antagonist MK-801 blocked the LTD facilitation seen 3 h after train

63 injections of saline or the NMDAR antagonist MK-801 from postnatal day 35 (P35) to P40.

64 ion with the noncompetitive NMDAR antagonist MK-801 reversed neuropathic pain behaviors exacerbated b

65 (as control) or the NMDA receptor antagonist MK-801 (0.2 mg kg(-1), i.p.) was systemically injected a

66 the N-methyl-d-aspartate receptor antagonist MK-801 (0.5 nmol bilaterally) into the ventral tegmental

67 tly reversed by the NMDA receptor antagonist MK-801 [(+)-5-methyl-10,11-dihydro-5H-dibenzo [a,d] cycl

68 R inhibition or the NMDA receptor antagonist MK-801 [(+)-5-methyl-10,11-dihydro-5H-dibenzo [a,d] cycl

69 The NMDA receptor antagonist MK-801 [(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cycloh

70 ethyl-D-aspartate (NMDA) receptor antagonist MK-801 attenuated hyperalgesia in naltrexone-treated mic

71 ral response to the NMDA receptor antagonist MK-801 in mGlu5 KO mice was seen.

72 nurenic acid or the NMDA receptor antagonist MK-801 into the vPAG did not affect nociception.

73 The NMDA receptor antagonist MK-801 produces different effects on timing tasks.

74 tment with the glutamate receptor antagonist MK-801 strongly reduced bioluminescence and pathology.

75 ection in rats of a NMDA receptor antagonist MK-801((+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohe

76 was reversed by the NMDA receptor antagonist MK-801, and was neuron-dependent, since NMDA had no effe

77 ate N-methyl-D-aspartate receptor antagonist MK-801, as well as deficits in social behaviors (social

78 ated daily with the NMDA receptor antagonist MK-801, castrated males treated with estradiol benzoate

79 the noncompetitive NMDA receptor antagonist MK-801, indicating that the initial GT upregulation hamp

80 A (N-methyl-D-aspartate) receptor antagonist MK-801, is reduced by presynaptic inactivation of presen

81 partate (NMDA) glutamate receptor antagonist MK-801, when applied locally to the CA1 recording site b

82 were reduced by the NMDA receptor antagonist MK-801.

83 the addition of the NMDA receptor antagonist MK-801.

84 as prevented by the NMDA receptor antagonist MK-801.

85 the N-methyl-d-aspartate receptor antagonist MK-801.

86 neuroserpin or the NMDA receptor antagonist MK-801.

87 etreatment with the NMDA receptor antagonist MK-801.

88 ive N-methyl-D-aspartate receptor antagonist MK-801; the adenosine A1 receptor agonist 2-chloro-N6-cy

89 0 micromol/L) with or without the antagonist MK-801 or AP-5 (50 micromol/L); and (2) neuromuscular pr

90 (lorazepam) or an NMDA receptor antagonist (MK-801) may have some initial benefits in ameliorating t

91 l-D-aspartate (NMDA) receptor antagonist (+)-MK-801, its inactive isomer (-)-MK-801, the selective NR

92 the selective and powerful NMDA antagonist, MK-801, from producing NAN in adult animals, suggesting

93 lay greater responses to an NMDA antagonist, MK-801, in open field and pre-pulse inhibition of the ac

94 urotoxic dose of the potent NMDA antagonist, MK-801.

95 ion induced by the powerful NMDA antagonist, MK-801.

96 vented by treatment with an NMDA-antagonist, MK-801.

97 e (NMDA)-type glutamate receptor antagonist, MK-801, and a non-NMDA-type glutamate receptor antagonis

98 6, and a selective NMDA receptor antagonist, MK-801, inhibit the dephosphorylation of DAPK after in v

99 Pretreatment with NMDA glutamate antagonists MK-801 or CPP dose-dependently attenuates these quinpiro

100 ed by the NMDA and AMPA receptor antagonists MK-801 and CNQX, respectively.

101 bition of the receptor by the anticonvulsant MK-801 [(+)-dizocilpine] and the abused drug cocaine led

102 In the PCC/RSC, bath-applied MK-801 (10-40 microm) produced disinhibition, shown as a

103 cause of downregulation of NMDA receptors as MK-801 binding and NMDA receptor complexes in postsynapt

104 electivity over other PDEs, fully attenuates MK-801-induced hyperlocomotor activity after ip dosing.

105 when the noncompetitive NMDA channel blocker MK-801 was added to the patch-pipette saline, suggesting

106 f NMDA receptors by the open channel blocker MK-801, we confirmed that the initial release probabilit

107 in the presence of the open channel blocker MK-801.

108 of oscillations in response to NMDAR blocker MK-801.

109 of the N-methyl-d-aspartate receptor blocker MK-801 directly into the caudomedial nucleus of the soli

110 -TG secretion, whereas NMDA receptor blocker MK-801 fully negated glycine's effect.

111 o-application with the NMDA receptor blocker MK-801 increased protection.

112 e experiments used the NMDA receptor blocker MK-801.

113 owing injection of an NMDA receptor blocker (MK-801) before, but not after training.

114 artial agonists and the ion channel blocker, MK-801.

115 lular injection of the NMDA channel blocker, MK-801.

116 iments with the use-dependent NMDAR blocker, MK-801, indicate that potentiated NMDARs reside on the p

117 Pretreatment with channel blockers MK-801 and ketamine, NMDA NR2B receptor subunit antagoni

118 of administering the NMDA receptor blockers MK-801 and memantine, the AMPA/kainate receptor blockers

119 neurons using the open-channel blockers (+)-MK-801 and ketamine to tag synaptic NMDA receptors.

120 equired for clozapine's efficacy in blocking MK-801- and PCP-induced models of schizophrenic behavior

121 ressing electrographic seizure activity, but MK-801 had a slightly wider window for the prevention of

122 into an experimental group (administered by MK-801) and a positive control group (administered by sa

123 hough OGD-induced toxicity was attenuated by MK-801 only in slices from young rats.

124 hemia model and this effect was augmented by MK-801.

125 pression did not change the rate of block by MK-801 of NMDA-mediated currents in excised patches from

126 ed castrates, but this growth was blocked by MK-801 treatment.

127 activated T cells, which could be blocked by MK-801, by scavenging ROS, by the calcineurin inhibitor

128 ed a rise in cell Ca(2+) that was blocked by MK-801, by the ATPase apyrase, by the P2Y(1) receptor an

129 diated evoked EPSCs (eEPSCs) were blocked by MK-801, they showed no evidence of recovery when the irr

130 dependent block of NMDA receptor currents by MK-801 [(5S,10R)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a

131 NMDA-mEPSCs) were substantially decreased by MK-801 within 2 min in a use-dependent manner.

132 e blockade of NMDA receptor (NMDAR) EPSCs by MK-801 [(5R,10S)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a

133 The influx was inhibited by MK-801, a specific pore blocker of N-Methyl-D-aspartic a

134 19 cells that was substantially inhibited by MK-801.

135 anical activation of NMDAR and inhibition by MK-801.

136 ly 7-fold, which was completely prevented by MK-801.

137 as attenuated (30% and 60%, respectively) by MK-801 pretreatment.

138 iscrimination learning, impairment of SDA by MK-801 likely reflects disruption of spatial working mem

139 and partially sensitive to pore block by (+)MK-801, (-)MK-801, ketamine, memantine, amantadine, and

140 cochlea was significantly attenuated by (+)-MK-801 and PD 174494 in the organ of Corti and modiolar

141 hat the pH-dependent block of NR1/NR2A by (-)MK-801 but not (+)MK-801 reflects an increase in the MK-

142 ber or function, because 3-NP did not change MK-801 [(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cycloh

143 glutamate, NMDA, or KA; glutamate and CNQX, MK-801, or AP-7; ACh, nicotine or muscarine; ACh and alp

144 n that blockade of NMDAR by non-competitive (MK-801) and competitive (AP5) antagonists increase food

145 In contrast, MK-801 application at rest for 10 min did not significan

146 In controls, MK-801 did not alter the increase in norepinephrine or g

147 In parietal cortex, MK-801 produced significantly less disinhibition.

148 This revealed distal MK-801-sensitive synaptic inputs that predict the format

149 Dizocilpine (MK-801), a non-competitive NMDA antagonist, at 1-45 micr

150 th the NMDA receptor antagonist dizocilpine (MK-801) 30 min before unilateral visual cortex ablation.

151 strong NMDA receptor antagonist dizocilpine (MK-801) for 28 days starting at 8 weeks of age reduced 2

152 of the NMDA receptor antagonist dizocilpine (MK-801).

153 glutamate receptor antagonist, dizocilpine (MK-801).

154 otine base/kg/day for 28 days), dizocilpine (MK-801) (0.3 mg/kg/day for 28 days), an NMDA receptor an

155 For dizocilpine (MK-801), the differential potency of MK-801 stereoisomer

156 vity), agonist-dependent [(3)H] dizocilpine (MK-801) binding to NMDA receptors in cortical homogenate

157 s blocked by the NMDA antagonist dizocilpine(MK-801) and by a membrane-permeable scavenger of ROS.

158 as phencyclidine, ketamine, and dizocipline (MK-801).

159 ow that Gfa2-A2AR KO mice exhibited enhanced MK-801 psychomotor response and decreased working memory

160 e features of schizophrenia, namely enhanced MK-801 psychomotor response (positive symptoms) and decr

161 litation seen 3 h after training, and giving MK-801 before the second peppermint training trial elimi

162 D males with the exception of increased (3)H-MK-801 binding in cortex.

163 dition, PD female rats showed increased (3)H-MK-801 binding in the striatum and hippocampus, but not

164 We also measured [(3)H]CGP39653 and [(3)H]MK-801 binding site expression in the hippocampus in sch

165 Agonist-dependent [(3)H]MK-801 binding was decreased in PFC but not parietal cor

166 nding site density were (3)[H]kainate, (3)[H]MK-801, and (3)[H]AMPA, respectively.

167 in phrenic amplitude at 60 min post-hypoxia; MK-801, -0.5 +/- 4.1%, means +/- S.E.M.), with little ch

168 dro-5H-dibenzo [a,b] cyclohepten-5,10-imine (MK-801) or (D) 2-amino-5-phosphopenoic acid (AP-5) at .5

169 hydro-5H-dibenzo[a,d]cyclohepten-5,10-imine (MK-801)-sensitive phencyclidine-binding sites.

170 schizophrenia showed that SAR218645 improved MK-801-induced episodic memory deficits in rats and atte

171 say and did not promote reversal learning in MK-801-treated mice.

172 a and dendritic length of SNB motoneurons in MK-801-treated, intact males were below those of normal

173 lity and its regulation of BLA plasticity in MK-801-treated rats.

174 in prepulse inhibition tasks, and increased MK-801-induced anxiety-like behaviors.

175 and osmotic minipumps continuously infusing MK-801, a noncompetitive NMDA receptor antagonist, or sa

176 than twofold, with NMDA receptor inhibitors MK-801 and d-AP5 preventing this release.

177 ciceptive sensitization using the inhibitors MK-801 and AP5 (NMDAR), and ivabradine and ZD7288 (HCN).

178 With intracellular MK-801 [(+)-5-methyl-10,11-dihydro-5H-dibenzo [a,d]-cycl

179 ated) but not on post-SNL day 2; intrathecal MK-801 reversed SNL-pain at both times.

180 anomalous recovery following "irreversible" MK-801 block.

181 tagonist (+)-MK-801, its inactive isomer (-)-MK-801, the selective NR1/2B NMDA receptor antagonist PD

182 D-aspartate (NMDA) receptor (e.g., ketamine, MK-801, dextromethorphan, and phencyclidine) produce ana

183 Repeated administration of 0.1 mg/kg MK-801 with ethanol potentiated, whereas 0.25 mg/kg atte

184 T-maze after ip administration of 0.06 mg/kg MK-801, 0.1 mg/kg MK-801, or saline on postnatal days (P

185 ministration of 0.06 mg/kg MK-801, 0.1 mg/kg MK-801, or saline on postnatal days (P) P23 and P33 (Exp

186 sensitization between ethanol and 0.25 mg/kg MK-801.

187 By loading MK-801 into pre- or postsynaptic neurons during paired r

188 MDA receptor antagonist dizocilpine maleate (MK-801) and measuring MK-801-induced disinhibition in ar

189 DA receptor antagonists dizocilpine maleate (MK-801) and phencyclidine also increase cell death in th

190 MDA receptor antagonist dizocilpine maleate (MK-801) during periadolescence [from postnatal day 35 (P

191 MDA receptor antagonist dizocilpine maleate (MK-801) for 24 h before birth also caused an increase in

192 examined the effect of dizocilpine maleate (MK-801), a noncompetitive N-methyl-Daspartate (NMDA) rec

193 benzo(f)quinoxaline and dizocilpine maleate (MK-801), also suppressed calcium oscillations, revealing

194 DA receptor antagonist, dizocilpine maleate (MK-801), on spatial working memory during development.

195 a,d)cyclohepten-5,10-imine hydrogen maleate (MK-801) prevented cell death, although the non-NMDA rece

196 a,d]cyclohepten-5,10-imine hydrogen maleate (MK-801).

197 of NMDARs with dizocilpine hydrogen maleate (MK-801, 20 microM) had a negligible effect on respirator

198 a,d]cyclohepten-5,10-imine hydrogen maleate (MK-801; hydrogen maleate) on 24-h ischemia-induced CRH c

199 ibenzo [a,d] cyclohepten-5,10-imine maleate (MK-801) and by the antagonists of NR2B receptor ifenprod

200 -dibenzo[a,d]cyclohepten-5,10-imine maleate (MK-801) to investigate the effects of enhancing and bloc

201 -dibenzo[a,d]cyclohepten-5,10-imine maleate (MK-801), a noncompetitive NMDA receptor antagonist, indi

202 ibenzo [a,d] cyclohepten-5,10-imine maleate (MK-801), a well characterized use-dependent blocker of N

203 dibenzo [a,d]cyclohepten-5,10-imine maleate (MK-801)] or non-NMDA [CNQX or 4-(8-methyl-9H-1,3-dioxolo

204 less only in rats pretreated with masseteric MK-801.

205 t dizocilpine maleate (MK-801) and measuring MK-801-induced disinhibition in areas of higher and lowe

206 cation channels that are resistant to Mg2+, MK-801, memantine and competitive antagonists.

207 control animals underwent stimulation minus MK-801, and a non-stimulated control animal underwent su

208 Moreover, MK-801 inhibits NMDAR-mediated activation of p38-MAPK an

209 Morphine, MK-801 and acetylsalicylic acid (ASA) were active system

210 o 19.87 +/- 3.03% with cotreatment of 250 nM MK-801.

211 injected intrathecally with either an NMDA (MK-801) or an NK-1 (L-703,606) receptor antagonist or we

212 s of muscimol, bicuculline (136 pmol), NMDA, MK-801 (10 pmol) or vehicle.

213 nt block of NR1/NR2A by (-)MK-801 but not (+)MK-801 reflects an increase in the MK-801 association ra

214 present results indicate that the ability of MK-801 and dextromethorphan to protect against methamphe

215 mulation following blinded administration of MK-801 (4 mg/kg i.v.); control animals underwent stimula

216 he results showed that the administration of MK-801 significantly reduced (P<0.05) HIF-1alpha express

217 Intraperitoneal administration of MK-801, an N-methyl-d-aspartate (NMDA) receptor antagoni

218 n expression following the administration of MK-801, taken together with electrophysiological data, i

219 The similar behavioral competencies of MK-801-pretreated animals and those whose lesion-induced

220 co-exposure to a non-toxic concentration of MK-801 (20 microM).

221 esult of sensitization to the second dose of MK-801 (Experiment 2) and was observed when the drug was

222 eater than that produced by the same dose of MK-801 given intravenously or in the biceps muscle.

223 Both doses of MK-801 abolished acquisition of SDA performance in Exper

224 Rolipram attenuated the disruptive effect of MK-801 on latent inhibition, which suggests a role for t

225 ynaptic mechanisms, we tested the effects of MK-801 (40 microm) against miniature IPSC (mIPSC) freque

226 ates from Simulation 1 to predict effects of MK-801 on the DRL task.

227 ce but were more sensitive to the effects of MK-801.

228 onse to the locomotor stimulating effects of MK-801.

229 Spinal infusion of MK-801 (10-50 nmol/10 micro l) similarly reduced the num

230 id (NMDA) receptors by intra-CA3 infusion of MK-801, a non-competitive NMDA receptor antagonist, reve

231 reatment, the rats received one injection of MK-801 (dizocilpine 3mg/kg) or saline control.

232 Injections of MK-801 before each of these exposures inhibited the expe

233 e authors report that systemic injections of MK-801, an NMDA receptor antagonist, impaired male sexua

234 Results showed that acute microinfusion of MK-801 into the insular cortex prevented the attenuation

235 ilpine (MK-801), the differential potency of MK-801 stereoisomers determined at recombinant NMDA rece

236 at alter pH sensitivity alter the potency of MK-801, supporting the interpretation that the pH sensit

237 onal damage occurred despite the presence of MK-801 and Gd3+, whereas injury was decreased by NAS or

238 Brief stimulation in the presence of MK-801 significantly depressed evoked NMDA-eEPSCs but on

239 In the presence of MK-801, a non-competitive NMDA receptor antagonist, micr

240 subunits while maintaining the properties of MK-801 binding site blockers, exert microtubules stabili

241 he interpretation that the pH sensitivity of MK-801 binding reflects the changes at the proton sensor

242 Moreover, clozapine-mediated suppression of MK-801 and phencyclidine (PCP)-induced hyperlocomotion i

243 into a complex that was functional, based on MK-801 binding, but it is retained in the ER.

244 Notably, application of 7CK or MK-801 also converts spine enlargement resulting from a

245 amate receptor antagonists kynurenic acid or MK-801 were co-administered or not.

246 changes in haloperidol-induced catalepsy or MK-801-induced locomotion were seen following PD.

247 ic acid] and noncompetitive (dizocilpine, or MK-801 [(5S,10R)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a

248 NAc (intravenous infusion of 50 mg/kg/h) or MK-801 (0.16 mg/kg; given intraperitoneally); this step

249 Lorazepam (0.5-1.0 mg/kg) or MK-801 (0.1-0.3 mg/kg) treatment at 1 h into each of thr

250 l, mice previously treated with lorazepam or MK-801 for earlier withdrawals exhibited reduced HIC act

251 Vehicle (saline, 5 x 100 nl) or MK-801 (10 microM; 5 x 100 nl) was also microinjected in

252 s of bicuculline, but not muscimol, NMDA, or MK-801 induced phase advances.

253 Chronic treatment with either PTX or MK-801 did not affect frequency-specific oscillatory act

254 In particular, MK-801 produces an underestimation of duration when anim

255 isinhibitory state induced by periadolescent MK-801 to normal levels.

256 LFP disinhibition induced by periadolescent MK-801 treatment resembles that observed in the normal P

257 tal state associated with the periadolescent MK-801 exposure.

258 Phenobarbital, MK-801, and phenytoin were administered at 1, 2, and 4 h

259 Pretreated MK-801 animals were trained first in an orientation task

260 sitivity to a glutamatergic psychostimulant (MK-801), cognitive impairments, and deficits in social r

261 4 cAMP phosphodiesterase inhibitor, reverses MK-801-induced impairments in latent inhibition.

262 g, mice were injected with MK-801, rolipram, MK-801 and rolipram, or vehicle and received 20 preexpos

263 administration of 2.5 or 5.0 microg per side MK-801 or saline on P26 (Experiment 2).

264 account for the effects produced by systemic MK-801 administration.

265 Because the same doses of systemic MK-801 have no effect on T-maze position discrimination

266 Pretreatment with systemic MK-801 (0.25 mg/kg, ip), a non-competitive N-methyl-d-as

267 ropathy, although it was less effective than MK-801.

268 tive to extracellular Ca(2+) levels and that MK-801 blocks NMDAR-dependent LTD in the hippocampus of

269 X; 0.5 microm)-treated slices and found that MK-801 did not alter mIPSC frequency or amplitude.

270 It is likely that MK-801 pretreatment acts, at least in part, by preservin

271 electrophysiological analyses revealed that MK-801 administration during periadolescence elicits an

272 Phrenic LTF was eliminated by the MK-801 injection (vehicle, 32.8 +/- 3.7% above baseline

273 Phrenic LTF was eliminated by the MK-801 microinjection (vehicle, 34.2 +/- 3.4%; MK-801, -

274 ut not (+)MK-801 reflects an increase in the MK-801 association rate even though protons reduce chann

275 ons reduce channel open probability and thus MK-801 access to its binding site.

276 The recovery could not be attributed to MK-801 unbinding or insertion of new receptors, suggesti

277 Compared to MK-801, ifenprodil, a selective NR2B antagonist, was les

278 The increased sensitivity to MK-801 exhibited by PDE11A KO mice may be explained by t

279 No age differences in sensitivity to MK-801 were found between PND 21 and 30.

280 The partial sensitivity to (+)MK-801 may reflect its ability to stimulate agonist unbi

281 brief memory reactivation session was used: MK-801 administration impaired, whereas DCS increased, f

282 Experiments using MK-801 indicated that this resulted in part from similar

283 Research using MK-801, an N-methyl-D-aspartate (NMDA) open channel bloc

284 ter the propagating response was visualized, MK-801 restored resting Ca(2+) levels.

285 In vivo, MK-801 and dextromethorphan reduce methamphetamine-induc

286 When MK-801 was administered (intraperitoneally) before both

287 Such a disinhibition was not observed when MK-801 was given during adulthood, indicating that the p

288 ne had no effect or enhanced tremor, whereas MK-801 and CCPA reduced tremor.

289 ic inhibition of NMDA receptor activity with MK-801 reduced PDE4A1 and PDE4A5 expression and activity

290 s coinjection of 120 nmol of NMDA along with MK-801 increased the cell number from 10% to 59%.

291 ound that when facilitation was blocked with MK-801 there was a rapid (approximately 30-40 min) anoma

292 ls or blocking NMDAR channel ion fluxes with MK-801 on LTD and NMDAR signaling in the mouse hippocamp

293 day before training, mice were injected with MK-801, rolipram, MK-801 and rolipram, or vehicle and re

294 Similar results were obtained with MK-801.

295 ckade was induced by combined perfusion with MK-801 and NMDA.

296 i.c.v. pretreatment with MK-801, an NMDA receptor antagonist, blunted (50%) the r

297 t systemic antagonism of NMDA receptors with MK-801 [(+)-5-methyl-10,11-dihydro-SH-dibenzo[a,d]cycloh

298 ampus were decreased in animals treated with MK-801, an NMDA receptor antagonist, or GYKI-52466, an A

299 ity was blocked by concurrent treatment with MK-801 or by two tetrahydroisoquinolines that bind to ph

300 in enriched mGlu5 KO mice and treatment with MK-801 reinstated PPI disruption in EE mGlu5 KO mice onl

301 electrically (20 Hz, 20 min) with or without MK-801 or AP-5 (50 micromol/L).