ライフサイエンスコーパス: phencyclidine

1 gonist-enhanced photolabeling inhibitable by phencyclidine.

2 ugs of abuse, such as cocaine, morphine, and phencyclidine.

3 ine but was enhanced 10-fold by proadifen or phencyclidine.

4 e also blocked the PPI-disruptive effects of phencyclidine.

5 ncluding amphetamine, morphine, nicotine and phencyclidine.

6 receptor by a high-affinity AChR inhibitor, phencyclidine.

7 hetamine (0.125, 0.25, and 0.5 mg/kg, i.p.), phencyclidine (1.0, 2.0, and 3.0 mg/kg, i.p.), and dizoc

8 blockers MK 801 (0.01, 0.1 and 1 mg/kg) and phencyclidine (4 mg/kg) elevated AADC activity in both t

9 to study the lesions induced in rat brain by phencyclidine (alone or when augmented with pilocarpine)

10 antagonists dizocilpine maleate (MK-801) and phencyclidine also increase cell death in this structure

11 r recent use of marijuana, cocaine, opiates, phencyclidine, amphetamines, and methadone.

12 geted glutamatergic neurotransmission, since phencyclidine, an N-methyl-D-aspartate (NMDA) receptor a

13 rized noncompetitive antagonists such as the phencyclidine analogue [piperidyl-3,4-(3)H(N)]-N-[1-(2-t

14 nally produced from a mouse immunized with a phencyclidine analogue hapten 5-[N-(1'phenylcyclohexyl)a

15 at quinacrine can inhibit the binding of [3H]phencyclidine and [3H]ethidium in a manner fully consist

16 th classes of RNA molecules are displaced by phencyclidine and cocaine from their binding site on the

17 ial sensitivity to the open channel blockers phencyclidine and dizolcipine (MK-801).

18 ingle locus of the acetylcholine receptor as phencyclidine and ethidium.

19 The psychotomimetic phencyclidine and its potent congener dizocilpine are no

20 partate (NMDA) receptor antagonists, such as phencyclidine and ketamine, have been used to study the

21 hyl-D-aspartic acid (NMDA) receptor, such as phencyclidine and ketamine, produce an acute psychotic s

22 Phencyclidine and other antagonists of the N-methyl-D-as

23 PCP (phencyclidine) and ketamine are noncompetitive blockers

24 buse that induce psychotic behavior, such as phencyclidine, and drugs with wide therapeutic utility,

25 ously detected amphetamine, methamphetamine, phencyclidine, and opiates in saliva.

26 inhibited by the channel blockers QX-222 and phencyclidine, and potentiated by the alpha7nAChR specif

27 therapeutic mechanisms because ketamine and phencyclidine are known to induce psychotic-like symptom

28 Some investigators have reported that phencyclidine at higher doses or by more prolonged treat

29 nding of the noncompetitive antagonist [(3)H]phencyclidine, azietomidate and etomidate bind with 10-f

30 C6C channel binding by the inhibition of [3H]phencyclidine binding and by equilibrium measurements of

31 he AChR as demonstrated by inhibition of [3H]phencyclidine binding; apparent KD values ranged from 50

32 acting brain proteins forming a low affinity phencyclidine-binding entity in a synaptic membrane comp

33 distinct from the glutamate-, glycine-, and phencyclidine-binding sites and is probably mechanistica

34 ,d]cyclohepten-5,10-imine (MK-801)-sensitive phencyclidine-binding sites.

35 We found that phencyclidine can kill a relatively large number of neur

36 Repeated exposure to phencyclidine caused a reduction in both basal and evoke

37 The addition of a low dose of pilocarpine to phencyclidine caused the widespread pattern of damage to

38 ists (trimethaphan, hexamethonium, procaine, phencyclidine, cocaine, or clonidine), and the peptides

39 ), or psychotomimetic effects (specifically, phencyclidine discriminative stimulus effects).

40 Surprisingly, another psychotropic drug, phencyclidine, displayed a selective D2R/beta-arrestin p

41 data demonstrate that a single injection of phencyclidine enhances amphetamine-induced behaviors 24

42 c properties, both (+)-11 and (-)-12 blocked phencyclidine-evoked ambulations in a dose-dependent man

43 ilability in rats and effectively suppresses phencyclidine-evoked locomotor activity at doses that do

44 Phencyclidine has attracted the attention of neuroscient

45 binding of the noncompetitive antagonist [3H]phencyclidine (IC50 = 9 microM) than of [3H]histrionicot

46 inity in the nAChR desensitized state ([(3)H]phencyclidine; IC50 = 4 muM) than in the resting state (

47 data suggest that repeated administration of phencyclidine in monkeys may be useful for studying psyc

48 However, the response to haloperidol and phencyclidine indicates that normal D2R signaling homeos

49 of epilepsy, Parkinson's disease, pain, and phencyclidine-induced cognitive deficits.

50 nt models for anxiety but did not potentiate phencyclidine-induced hyperlocomotor activity.

51 roved spatial working memory and reversal of phencyclidine-induced learning and memory deficits.

52 Strikingly, cocaine- and phencyclidine-induced psychomotor activities were enhanc

53 The main action of phencyclidine is as a non-competitive antagonist of the

54 mpetitive NMDA receptor antagonists, such as phencyclidine, ketamine and MK801, produce psychosis in

55 partate (NMDA) receptor antagonists, such as phencyclidine, ketamine, and dizocipline (MK-801).

56 ne derivatives to probe the structure of the phencyclidine locus in either the resting or desensitize

57 that the delayed effects of a single dose of phencyclidine may produce a schizophrenia-like state in

58 d with an animal model of schizophrenia, the phencyclidine model.

59 The effects of the psychotomimetic drug phencyclidine on the neurochemistry and function of the

60 ission, attenuated the disruptive effects of phencyclidine on working memory, stereotypy, locomotion,

61 c end of the channel is fully inhibitable by phencyclidine or proadifen, whereas neither drug inhibit

62 s exposed in utero to opiates, amphetamines, phencyclidine, or maternal human immunodeficiency virus

63 grees C); (ii) CrV-induced inhibition of the phencyclidine (PCP) analogue [(3)H]thienylcyclohexylpipe

64 Three phencyclidine (PCP) analogues possessing a highly rigid

65 nd TID bind to the same site, the amine NCAs phencyclidine (PCP) and histrionicotoxin (HTX), which ar

66 The behavioral syndrome produced by phencyclidine (PCP) and its analog ketamine represents a

67 ylamide (LSD) and dissociative drugs such as phencyclidine (PCP) and the symptoms, neurochemical abno

68 ber of structurally diverse compounds at the phencyclidine (PCP) binding site in postmortem human fro

69 ned and prepared to interact either with the phencyclidine (PCP) binding site of the N-methyl-d-aspar

70 range of relative selectivity for sigma and phencyclidine (PCP) binding sites on N-methyl-D-aspartat

71 Exposure to methamphetamine (METH) and phencyclidine (PCP) during early development is thought

72 The noncompetitive NMDA receptor antagonist phencyclidine (PCP) has psychotomimetic properties in hu

73 Phencyclidine (PCP) has recently been shown to induce ap

74 examined the microsomal brain metabolism of phencyclidine (PCP) in male and female Sprague-Dawley ra

75 ling of the rat frontal cortex after chronic phencyclidine (PCP) intervention, which induces SCZ-like

76 Phencyclidine (PCP) is a compound that results in abnorm

77 Electrophysiological studies indicate that phencyclidine (PCP) markedly disrupts neuronal activity

78 esensitized state, we examined the effect of phencyclidine (PCP) on [(125)I]TID photolabeling.

79 Phencyclidine (PCP) suppression of PPI in animals has be

80 atial knowledge, we used the psychotomimetic phencyclidine (PCP) to disrupt cognitive behavior and as

81 We used the psychotomimetic phencyclidine (PCP) to investigate the relationships amo

82 letely lost after repeated administration of phencyclidine (PCP), a mouse model of schizophrenia.

83 Phencyclidine (PCP), a non-competitive antagonist of the

84 the N-methyl-D-aspartate (NMDA) antagonist, phencyclidine (PCP), alters striatal function, we sought

85 ment induced by subchronic administration of phencyclidine (PCP), an NMDAR noncompetitive antagonist.

86 izophrenia emerged from the observation that phencyclidine (PCP), an open channel antagonist of the N

87 he N-methyl-D-aspartate receptor antagonist, phencyclidine (PCP), induces enduring deficits in novel

88 gue of the cationic noncompetitive inhibitor phencyclidine (PCP), was used to characterize the cembra

89 on, the effects of the NMDA channel blocker, phencyclidine (PCP), were tested.

90 clozapine-mediated suppression of MK-801 and phencyclidine (PCP)-induced hyperlocomotion is betaarres

91 tested in vivo and compared with MK-801 for phencyclidine (PCP)-like motor stimulation, antinocicept

92 presence and absence of the NMDA antagonist phencyclidine (PCP).

93 of SZ, generated by neonatal treatment with phencyclidine (PCP).

94 wal induced by sub-chronic administration of phencyclidine (PCP).

95 tamate receptor, such as the psychotomimetic phencyclidine (PCP).

96 prenatal blockade of the NMDA receptor with phencyclidine (PCP).

97 e, behavioral and neuroanatomical effects of phencyclidine (PCP).

98 ta-subunits was inhibited by the presence of phencyclidine (PCP).

99 +4alpha-amine (NEFA), a structural analog of phencyclidine (PCP).

100 eeks' treatment in rats treated with saline, phencyclidine (PCP, 15 mg/kg/d by osmotic minipump), or

101 A) receptor antagonists such as ketamine and phencyclidine precipitate psychotic symptoms in schizoph

102 , the effect of conotoxin on the affinity of phencyclidine, proadifen, and ethidium.

103 clear that chronic intermittent low doses of phencyclidine produce a pattern of metabolic and neuroch

104 .g., ketamine, MK-801, dextromethorphan, and phencyclidine) produce analgesia but do not induce compl

105 Chronic administration of phencyclidine produced a selective impairment of extradi

106 by two tetrahydroisoquinolines that bind to phencyclidine sites in neuronal membranes.

107 se have allowed assessment of the ability of phencyclidine to produce equivalent changes in the roden

108 M, whereas it inhibited the binding of [(3)H]phencyclidine to the Torpedo nAChR ion channel in the re

109 itive antagonists [(3)H]tetracaine and [(3)H]phencyclidine to Torpedo nAChR-rich membranes (IC(50) va

110 r UNC9994 on schizophrenia-like behaviors in phencyclidine-treated or NR1-knockdown hypoglutamatergic

111 ecreased dopamine utilization remained after phencyclidine treatment was stopped, an indication that

112 xcitatory pathways is the mechanism by which phencyclidine triggers widespread neuronal degeneration;

113 Monkeys treated with phencyclidine twice a day for 14 days displayed performa

114 , phenethylamines, piperazines, ketamine and phencyclidine-type substances, tryptamines).

115 ith 1-(1-phenylcyclohexyl)piperidine (PCP or phencyclidine) was determined at 2.2-A resolution.

116 pH and ionic strength on the binding of [3H]phencyclidine were determined.