ライフサイエンスコーパス: dizocilpine

1 were less pronounced than those produced by dizocilpine.

2 toaffinity labeling of the AChR using (125)I-dizocilpine.

3 via in vivo blockade of NMDA receptors with dizocilpine.

4 bers immediately after bilateral infusion of dizocilpine (0, 0.25, 1.25, and 6.25 microgram/0.5 micro

5 of the noncompetitive NMDA channel blocker, dizocilpine (0.01 mg/kg, s.c. given 20 min prior to the

6 tion of FR115427 (0.1-3 mg/kg i.v.; n = 20), dizocilpine (0.03-0.3 mg/kg; n = 15), CGS19755 (1-30 mg/

7 A higher dose of dizocilpine (0.1 mg/kg s.c.) completely blocked the trem

8 mg/kg i.v.; n=18) or RSR13 (150 mg/kg i.v. )+dizocilpine (0.25 mg/kg i.v.; n=15).

9 ubjected to 75 min of MCAO after being given dizocilpine (0.25 mg/kg i.v.; n=18) or RSR13 (150 mg/kg

10 he non-competitive NMDA receptor antagonist, dizocilpine (0.25 mg/kg), has previously been shown to b

11 not blocked by concomitant administration of dizocilpine (0.25 mg/kg).

12 Dizocilpine (0.3 mg/kg) induced similar PPI deficits in

13 Dizocilpine (0.5 mg/kg i.v.) caused a 90% reduction in m

14 The NMDA receptor antagonist, dizocilpine (0.63 mg/kg day) blocked AMPH-induced neurod

15 The NMDA receptor antagonist dizocilpine (100 nmol infused into the cerebral ventricl

16 NMDA receptor binding was examined using [3H]dizocilpine ([3H]MK-801).

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

18 aspartate (NMDA) receptor antagonist MK-801 (dizocilpine) (5-250 microM) produced significant increas

19 7-sulfamoyl-benzo(F)quinoxaline) and MK-801 (dizocilpine, (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]c

20 forebrain was completely reversed following dizocilpine administration.

21 Chronic dizocilpine alone did not affect high-affinity nicotinic

22 -28 mm3 vs. 81+/-60 mm3, p<0.05) compared to dizocilpine alone, respectively.

23 They complement our earlier findings that dizocilpine also attenuates drinking and c-fos expressio

24 Morphine and dizocilpine also impaired reversal learning but only at

25 CPP, CGP40116 and dizocilpine also prevented the appearance of cerebellar

26 Dizocilpine also suppressed c-fos expression induced by

27 by cyclothiazide persists in the presence of dizocilpine (an antagonist of N-methyl-D-aspartate-selec

28 mpetitive inhibitors cocaine and MK-801 [(+)-dizocilpine, an anticonvulsant] indicated they bind to a

29 nolone, and by the NMDA receptor antagonists dizocilpine and (R)-CPP.

30 d locomotor response to the psychostimulants dizocilpine and amphetamine, and with robust alterations

31 e effects were only marginally attenuated by dizocilpine and APV.

32 gnaling by glutamate was blocked by EGTA and dizocilpine and by silencing expression of the NMDA-R NR

33 evident, a plot of the regional f values for dizocilpine and FR115427 revealed a strong overall relat

34 cal differences in the metabolic profiles of dizocilpine and FR115427 were evident, a plot of the reg

35 affected only in the hippocampus, where both dizocilpine and nicotine significantly increased binding

36 an N-methyl-D-aspartate receptor antagonist (dizocilpine), and an opiate agonist (morphine) were stud

37 e receptor by the anticonvulsant MK-801 [(+)-dizocilpine] and the abused drug cocaine led to an inhib

38 uptive and the startle-increasing effects of dizocilpine are mediated by different central sites.

39 imetic phencyclidine and its potent congener dizocilpine are noncompetitive antagonists of the NMDA r

40 ion of the antagonists of the NMDAR complex (dizocilpine), as well as NR2A (PEAQX) and NR2B (Ro 25-69

41 The combination of nicotine and dizocilpine attenuated the effects of each with diminish

42 ly, the data indicate that the high-affinity dizocilpine binding site is not located in the lumen of

43 a noncompetitive manner, the location of the dizocilpine binding site(s) has yet to be clearly establ

44 produce a polyamine-like enhancement of [3H]dizocilpine binding to NMDA receptors is consistent with

45 n constant (K(d)) and stoichiometry of [(3)H]dizocilpine binding; 2) the displacement of dizocilpine

46 Here we show that phenobarbital and dizocilpine can block measures of METH neurotoxicity by

47 In addition, dizocilpine, CPP and CGP40116 were able to partially pre

48 had any effect on animal behavior except for dizocilpine, CPP, CGP40116 and (+/-)HA-966 which resulte

49 Phenobarbital and dizocilpine did not block depletions by altering the hyp

50 competitive inhibitors (NCIs) and conversely dizocilpine displacement of fluorescent and radiolabeled

51 Phenobarbital or dizocilpine during METH exposure blocked the depletions

52 hyl-d-aspartate receptor antagonist (NMDAR), dizocilpine (DZP), and a muscarinic cholinergic receptor

53 In contrast, chronic nicotine and dizocilpine had a mutually potentiating effect of increa

54 This dose od dizocilpine had no effect on acquisition of conditioned

55 Dizocilpine had no effect on motor behavior when given a

56 Dizocilpine had no inhibitory effects on feeding after 2

57 Inhibition of NMDA receptors with dizocilpine hydrogen maleate (1 microm) prevented both O

58 Blockade of NMDARs with dizocilpine hydrogen maleate (MK-801, 20 microM) had a n

59 ced by the specific NMDA receptor antagonist dizocilpine hydrogen maleate (MK801).

60 As indexed by MK801 (dizocilpine hydrogen maleate), an open channel blocker,

61 When slices received dizocilpine immediately after decapitation, TUNEL-positi

62 7 was approximately 30-fold less potent than dizocilpine in this regard.

63 of inhibition of the receptor by MK-801 [(+)-dizocilpine] in the microsecond-to-millisecond time regi

64 ic drugs haloperidol and clozapine prevented dizocilpine-induced effects on miR-219.

65 c acid, hydrochloride] blocked inhibition of dizocilpine-induced hyperlocomotion mediated by overexpr

66 ity binding in the cerebellum and diminished dizocilpine-induced increased nicotinic low-affinity bin

67 eus accumbens antagonized d-amphetamine- and dizocilpine-induced PPI disruption, hyperlocomotion, and

68 Startle reactivity was increased by dizocilpine infusion into amygdala, dorsal hippocampus,

69 n contrast, no change in PPI was produced by dizocilpine infusion into nucleus accumbens, ventral hip

70 brain slices to the NMDA receptor antagonist dizocilpine maleate (MK-801) and measuring MK-801-induce

71 The NMDA receptor antagonists dizocilpine maleate (MK-801) and phencyclidine also incr

72 ted exposure to the NMDA receptor antagonist dizocilpine maleate (MK-801) during periadolescence [fro

73 Treatment with the NMDA receptor antagonist dizocilpine maleate (MK-801) for 24 h before birth also

74 inhibition in vivo, because intraperitoneal dizocilpine maleate (MK-801) injection in young adult ra

75 effect of intrathecal NMDA-receptor blocker dizocilpine maleate (MK-801) on the peripheral immune re

76 Four experiments examined the effect of dizocilpine maleate (MK-801), a noncompetitive N-methyl-

77 y-6-nitro-7-sulfamoylbenzo(f)quinoxaline and dizocilpine maleate (MK-801), also suppressed calcium os

78 e present study compared amnestic effects of dizocilpine maleate (MK-801), an NMDA receptor antagonis

79 the noncompetitive NMDA receptor antagonist, dizocilpine maleate (MK-801), on spatial working memory

80 ceptors using the non-competitive antagonist dizocilpine maleate (MK801) arrested the developmental d

81 Postnatal injection of dizocilpine maleate (MK801), a specific NMDA antagonist,

82 locked with NMDA antagonists [AP5 and MK801 (dizocilpine maleate)] indicating glutamate signaling is

83 that the blockade of harmaline's actions by dizocilpine may be occurring at NMDA channels within the

84 clidine (1.0, 2.0, and 3.0 mg/kg, i.p.), and dizocilpine (MK-801) (0.0125, 0.05, and 0.1 mg/kg, i.p.)

85 mg of the nicotine base/kg/day for 28 days), dizocilpine (MK-801) (0.3 mg/kg/day for 28 days), an NMD

86 pretreated with the NMDA receptor antagonist dizocilpine (MK-801) 30 min before unilateral visual cor

87 f the N-methyl-D-aspartate (NMDA) antagonist dizocilpine (MK-801) and the non-NMDA antagonists 2,3-di

88 immunoreactivity), agonist-dependent [(3)H] dizocilpine (MK-801) binding to NMDA receptors in cortic

89 ent with the strong NMDA receptor antagonist dizocilpine (MK-801) for 28 days starting at 8 weeks of

90 In both, the glutamate antagonist dizocilpine (MK-801) reduced the swelling.

91 ve, non-competitive NMDA receptor antagonist dizocilpine (MK-801) was compared with glutamate and gly

92 A dose-response curve for dizocilpine (MK-801) was then constructed in conscious n

93 Dizocilpine (MK-801), a non-competitive NMDA antagonist,

94 ects of prior versus delayed applications of dizocilpine (MK-801), a noncompetitive NMDA antagonist,

95 the noncompetitive NMDA receptor antagonist dizocilpine (MK-801), at the appropriate doses, would al

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

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

98 and with the glutamate receptor antagonist, dizocilpine (MK-801).

99 ned sections from rats injected acutely with dizocilpine (MK-801; 1.5-5 mg/kg, i.p.) were analysed to

100 When treatment with dizocilpine (MK-801; 10 microM), a non-competitive NMDA

101 Although the dissociative anesthetic dizocilpine [(+)-MK-801] inhibits nicotinic acetylcholin

102 ls, which was blocked by the NMDA antagonist dizocilpine(MK-801) and by a membrane-permeable scavenge

103 ydro-5H-dibenzo[a,d]cyclohepten-5, 10-imine (dizocilpine; MK-801), a noncompetitive NMDA channel bloc

104 ly, exposure to the NMDA receptor antagonist dizocilpine (MK801 20 microM) and the polyamine site ant

105 he non-competitive NMDA receptor antagonist, dizocilpine (MK801) and of the competitive NMDA receptor

106 timulatory effects of the psychomimetic drug dizocilpine (MK801).

107 s attenuated by the NMDA receptor antagonist dizocilpine (MK801).

108 ride, D2), glutamate (CPP, competitive NMDA; dizocilpine, non-competitive NMDA; NBQX, AMPA) and GABA

109 at suppression of c-fos expression following dizocilpine occurred in the NMDA R1 receptor containing

110 thienylcyclohexylpiperidine was inhibited by dizocilpine on desensitized AChRs.

111 Thus, to characterize the binding site for dizocilpine on the AChR we examined 1) the dissociation

112 ximately 140 microM) binding sites exist for dizocilpine on the desensitized and resting AChR, respec

113 e patterns produced by CGS19755 and that for dizocilpine or FR115427 was poor (r = 0.28 and 0.5 respe

114 Here we show that pharmacological (dizocilpine) or genetic (NR1 hypomorphism) disruption of

115 phosphonopentanoic acid] and noncompetitive (dizocilpine, or MK-801 [(5S,10R)-(+)-5-methyl-10,11-dihy

116 Dizocilpine pre-treatment blocked NMDA-induced necrosis

117 glutamate antagonists, CPP and CGP40116 and dizocilpine prevented the L-CPA-induced locomotor dysfun

118 Dizocilpine produced characteristic alterations in 1CGU

119 ]dizocilpine binding; 2) the displacement of dizocilpine radioligand binding by noncompetitive inhibi

120 RSR13+dizocilpine resulted in smaller cortical infarct volume

121 Dizocilpine significantly decreased PPI after infusion i

122 Chronic dizocilpine significantly increased low-affinity nicotin

123 -7-sulfonamide in combination with 10 microM dizocilpine to block alpha-amino-3-hydroxy-5-methyl-4-is

124 osplenial, piriform and entorhinal cortex of dizocilpine-treated rats whereas these areas appeared re

125 The chronic dose of dizocilpine used was behaviorally active causing a drama

126 Photoaffinity labeling of the AChR by (125)I-dizocilpine was primarily restricted to the alpha1 subun

127 hich was broadly similar to that elicited by dizocilpine with increases in 1CGU in the pontine nuclei

128 pam, the present experiment examined whether dizocilpine would block the development of tolerance to