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

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

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

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

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

23 -801 microinjection (vehicle, 34.2 +/- 3.4%; MK-801, -2.5 +/- 2.8%), with minimal change in HPR.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

51 2 kHz but increased them at 20 kHz, and (-)-MK-801 was ineffective.

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

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

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

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

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

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

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

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

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

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

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

63 ort-term treatment with the NMDAR antagonist MK-801, suggesting that they arise from acute effects of

64 ent induced by injection of NMDAR antagonist MK-801.

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 We administered the NMDA receptor antagonist MK-801 and the GABA(A) receptor antagonist bicuculline m

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

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

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

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

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

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

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

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

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

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

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

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

83 etreatment with the NMDA receptor antagonist MK-801.

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

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

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

87 neuroserpin or 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 vented by treatment with an NMDA-antagonist, MK-801.

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

97 6, and a selective NMDA receptor antagonist, MK-801, inhibit the dephosphorylation of DAPK after in v

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

99 Moreover, NMDA receptor antagonists MK-801 and memantine prevented seizure-related SD and ap

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

133 19 cells that was substantially inhibited by MK-801.

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

135 in place preference, are not phenocopied by MK-801, suggesting a developmental origin.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

158 otion or prepulse inhibition but facilitated MK-801-induced hyperlocomotion.

159 G(q) but not G(i) coupled DREADD facilitated MK-801-induced hyperlocomotion.

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

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

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

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

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

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

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

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

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

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

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

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

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

173 ng reduced the level of freezing response in MK-801-treated rats to control levels.

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 anomalous recovery following "irreversible" MK-801 block.

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

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

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

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

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

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

186 At the behavioral level, MK-801 exposure during adolescence did not disrupt the a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

256 ocker applied through the recording pipette (MK-801).

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

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

259 4 cAMP phosphodiesterase inhibitor, reverses MK-801-induced impairments in latent inhibition.

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

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

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

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

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

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

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

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

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

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

270 cordings from PFC brain slices revealed that MK-801 exposure during adolescence preferentially reduce

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

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

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

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

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

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

277 Here we assessed whether exposure to MK-801 during adolescence in male rats triggers a state

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

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

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

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

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