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1 s, cannabis, cocaine, fentanyl, opiates, and phencyclidine.
2  and reversed deficits induced by subchronic phencyclidine.
3 recisely-dosed administration of ketamine or phencyclidine.
4 gonist-enhanced photolabeling inhibitable by phencyclidine.
5 ugs of abuse, such as cocaine, morphine, and phencyclidine.
6 ine but was enhanced 10-fold by proadifen or phencyclidine.
7 e also blocked the PPI-disruptive effects of phencyclidine.
8 ncluding amphetamine, morphine, nicotine and phencyclidine.
9  receptor by a high-affinity AChR inhibitor, phencyclidine.
10 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
11  blockers MK 801 (0.01, 0.1 and 1 mg/kg) and phencyclidine (4 mg/kg) elevated AADC activity in both t
12 NMDAR, reverted the memory deficit caused by phencyclidine (a non-competitive antagonist of NMDAR), a
13 to study the lesions induced in rat brain by phencyclidine (alone or when augmented with pilocarpine)
14 antagonists dizocilpine maleate (MK-801) and phencyclidine also increase cell death in this structure
15 r recent use of marijuana, cocaine, opiates, phencyclidine, amphetamines, and methadone.
16 geted glutamatergic neurotransmission, since phencyclidine, an N-methyl-D-aspartate (NMDA) receptor a
17 rized noncompetitive antagonists such as the phencyclidine analogue [piperidyl-3,4-(3)H(N)]-N-[1-(2-t
18 nally produced from a mouse immunized with a phencyclidine analogue hapten 5-[N-(1'phenylcyclohexyl)a
19 at quinacrine can inhibit the binding of [3H]phencyclidine and [3H]ethidium in a manner fully consist
20 th classes of RNA molecules are displaced by phencyclidine and cocaine from their binding site on the
21 ial sensitivity to the open channel blockers phencyclidine and dizolcipine (MK-801).
22 ingle locus of the acetylcholine receptor as phencyclidine and ethidium.
23                          The psychotomimetic phencyclidine and its potent congener dizocilpine are no
24 o THC's effect in rats and the psychotropics phencyclidine and ketamine in zebrafish was established.
25 partate (NMDA) receptor antagonists, such as phencyclidine and ketamine, have been used to study the
26 hyl-D-aspartic acid (NMDA) receptor, such as phencyclidine and ketamine, produce an acute psychotic s
27                            We find that both phencyclidine and methamphetamine, despite differing in
28                                              Phencyclidine and other antagonists of the N-methyl-D-as
29                                         PCP (phencyclidine) and ketamine are noncompetitive blockers
30 buse that induce psychotic behavior, such as phencyclidine, and drugs with wide therapeutic utility,
31 ously detected amphetamine, methamphetamine, phencyclidine, and opiates in saliva.
32 inhibited by the channel blockers QX-222 and phencyclidine, and potentiated by the alpha7nAChR specif
33  therapeutic mechanisms because ketamine and phencyclidine are known to induce psychotic-like symptom
34        Some investigators have reported that phencyclidine at higher doses or by more prolonged treat
35 nding of the noncompetitive antagonist [(3)H]phencyclidine, azietomidate and etomidate bind with 10-f
36 C6C channel binding by the inhibition of [3H]phencyclidine binding and by equilibrium measurements of
37 he AChR as demonstrated by inhibition of [3H]phencyclidine binding; apparent KD values ranged from 50
38 acting brain proteins forming a low affinity phencyclidine-binding entity in a synaptic membrane comp
39  distinct from the glutamate-, glycine-, and phencyclidine-binding sites and is probably mechanistica
40 ,d]cyclohepten-5,10-imine (MK-801)-sensitive phencyclidine-binding sites.
41                                We found that phencyclidine can kill a relatively large number of neur
42                         Repeated exposure to phencyclidine caused a reduction in both basal and evoke
43 The addition of a low dose of pilocarpine to phencyclidine caused the widespread pattern of damage to
44 ists (trimethaphan, hexamethonium, procaine, phencyclidine, cocaine, or clonidine), and the peptides
45 ), or psychotomimetic effects (specifically, phencyclidine discriminative stimulus effects).
46     Surprisingly, another psychotropic drug, phencyclidine, displayed a selective D2R/beta-arrestin p
47  data demonstrate that a single injection of phencyclidine enhances amphetamine-induced behaviors 24
48 c properties, both (+)-11 and (-)-12 blocked phencyclidine-evoked ambulations in a dose-dependent man
49 ilability in rats and effectively suppresses phencyclidine-evoked locomotor activity at doses that do
50                                              Phencyclidine has attracted the attention of neuroscient
51 binding of the noncompetitive antagonist [3H]phencyclidine (IC50 = 9 microM) than of [3H]histrionicot
52 inity in the nAChR desensitized state ([(3)H]phencyclidine; IC50 = 4 muM) than in the resting state (
53 data suggest that repeated administration of phencyclidine in monkeys may be useful for studying psyc
54     However, the response to haloperidol and phencyclidine indicates that normal D2R signaling homeos
55  of epilepsy, Parkinson's disease, pain, and phencyclidine-induced cognitive deficits.
56  Systemic oxytocin administration attenuated phencyclidine-induced hyperactivity and increased pro-so
57 ect on temperature, significantly attenuated phencyclidine-induced hyperactivity and increased social
58  occupancy in mice and effectively inhibited phencyclidine-induced hyperlocomotion.
59 s GluN2D knockout mice were not resistant to phencyclidine-induced hyperlocomotion.
60  knockout mice showed reduced sensitivity to phencyclidine-induced hyperlocomotion.
61 nt models for anxiety but did not potentiate phencyclidine-induced hyperlocomotor activity.
62 roved spatial working memory and reversal of phencyclidine-induced learning and memory deficits.
63                     Strikingly, cocaine- and phencyclidine-induced psychomotor activities were enhanc
64                           The main action of phencyclidine is as a non-competitive antagonist of the
65 mpetitive NMDA receptor antagonists, such as phencyclidine, ketamine and MK801, produce psychosis in
66 partate (NMDA) receptor antagonists, such as phencyclidine, ketamine, and dizocipline (MK-801).
67 at NMDAR channel blockers, including MK-801, phencyclidine, ketamine, and the Alzheimer's disease dru
68 ne derivatives to probe the structure of the phencyclidine locus in either the resting or desensitize
69 that the delayed effects of a single dose of phencyclidine may produce a schizophrenia-like state in
70 d with an animal model of schizophrenia, the phencyclidine model.
71      The effects of the psychotomimetic drug phencyclidine on the neurochemistry and function of the
72 ission, attenuated the disruptive effects of phencyclidine on working memory, stereotypy, locomotion,
73 c end of the channel is fully inhibitable by phencyclidine or proadifen, whereas neither drug inhibit
74 s exposed in utero to opiates, amphetamines, phencyclidine, or maternal human immunodeficiency virus
75 grees C); (ii) CrV-induced inhibition of the phencyclidine (PCP) analogue [(3)H]thienylcyclohexylpipe
76                                        Three phencyclidine (PCP) analogues possessing a highly rigid
77 nd TID bind to the same site, the amine NCAs phencyclidine (PCP) and histrionicotoxin (HTX), which ar
78          The behavioral syndrome produced by phencyclidine (PCP) and its analog ketamine represents a
79 ls elicited by the NMDA-receptor antagonists phencyclidine (PCP) and ketamine.
80 ylamide (LSD) and dissociative drugs such as phencyclidine (PCP) and the symptoms, neurochemical abno
81 ber of structurally diverse compounds at the phencyclidine (PCP) binding site in postmortem human fro
82 ned and prepared to interact either with the phencyclidine (PCP) binding site of the N-methyl-d-aspar
83  range of relative selectivity for sigma and phencyclidine (PCP) binding sites on N-methyl-D-aspartat
84       Exposure to methamphetamine (METH) and phencyclidine (PCP) during early development is thought
85  The noncompetitive NMDA receptor antagonist phencyclidine (PCP) has psychotomimetic properties in hu
86                                              Phencyclidine (PCP) has recently been shown to induce ap
87  examined the microsomal brain metabolism of phencyclidine (PCP) in male and female Sprague-Dawley ra
88 ling of the rat frontal cortex after chronic phencyclidine (PCP) intervention, which induces SCZ-like
89                                              Phencyclidine (PCP) is a compound that results in abnorm
90   Electrophysiological studies indicate that phencyclidine (PCP) markedly disrupts neuronal activity
91  of schizophrenia endophenotypes, namely the phencyclidine (PCP) mouse model and the A(2A)R knockout
92 esensitized state, we examined the effect of phencyclidine (PCP) on [(125)I]TID photolabeling.
93                                              Phencyclidine (PCP) suppression of PPI in animals has be
94 atial knowledge, we used the psychotomimetic phencyclidine (PCP) to disrupt cognitive behavior and as
95 esis that using the NMDA receptor antagonist phencyclidine (PCP) to disrupt postnatal glutamatergic t
96                  We used the psychotomimetic phencyclidine (PCP) to investigate the relationships amo
97  of NPS-MS to identify a novel derivative of phencyclidine (PCP) within an unknown powder seized in D
98                                              Phencyclidine (PCP), a drug of abuse, has psychomimetic
99 letely lost after repeated administration of phencyclidine (PCP), a mouse model of schizophrenia.
100                                              Phencyclidine (PCP), a non-competitive antagonist of the
101  the N-methyl-D-aspartate (NMDA) antagonist, phencyclidine (PCP), alters striatal function, we sought
102 ment induced by subchronic administration of phencyclidine (PCP), an NMDAR noncompetitive antagonist.
103 izophrenia emerged from the observation that phencyclidine (PCP), an open channel antagonist of the N
104 he N-methyl-D-aspartate receptor antagonist, phencyclidine (PCP), induces enduring deficits in novel
105 gue of the cationic noncompetitive inhibitor phencyclidine (PCP), was used to characterize the cembra
106 on, the effects of the NMDA channel blocker, phencyclidine (PCP), were tested.
107                      Likewise, FPPQ inhibits phencyclidine (PCP)-induced hyperactivity and displays p
108 clozapine-mediated suppression of MK-801 and phencyclidine (PCP)-induced hyperlocomotion is betaarres
109 stigate the effects of mGlu(3) activation on phencyclidine (PCP)-induced impairments in thalamo-accum
110  tested in vivo and compared with MK-801 for phencyclidine (PCP)-like motor stimulation, antinocicept
111 +4alpha-amine (NEFA), a structural analog of phencyclidine (PCP).
112  presence and absence of the NMDA antagonist phencyclidine (PCP).
113  of SZ, generated by neonatal treatment with phencyclidine (PCP).
114 wal induced by sub-chronic administration of phencyclidine (PCP).
115 tamate receptor, such as the psychotomimetic phencyclidine (PCP).
116  prenatal blockade of the NMDA receptor with phencyclidine (PCP).
117 e, behavioral and neuroanatomical effects of phencyclidine (PCP).
118 ta-subunits was inhibited by the presence of phencyclidine (PCP).
119 eeks' treatment in rats treated with saline, phencyclidine (PCP, 15 mg/kg/d by osmotic minipump), or
120 A) receptor antagonists such as ketamine and phencyclidine precipitate psychotic symptoms in schizoph
121 , the effect of conotoxin on the affinity of phencyclidine, proadifen, and ethidium.
122 clear that chronic intermittent low doses of phencyclidine produce a pattern of metabolic and neuroch
123 .g., ketamine, MK-801, dextromethorphan, and phencyclidine) produce analgesia but do not induce compl
124                    Chronic administration of phencyclidine produced a selective impairment of extradi
125                  We found that in subchronic phencyclidine (scPCP)-treated mice, an animal model that
126  by two tetrahydroisoquinolines that bind to phencyclidine sites in neuronal membranes.
127 se have allowed assessment of the ability of phencyclidine to produce equivalent changes in the roden
128 M, whereas it inhibited the binding of [(3)H]phencyclidine to the Torpedo nAChR ion channel in the re
129 itive antagonists [(3)H]tetracaine and [(3)H]phencyclidine to Torpedo nAChR-rich membranes (IC(50) va
130 r UNC9994 on schizophrenia-like behaviors in phencyclidine-treated or NR1-knockdown hypoglutamatergic
131 ecreased dopamine utilization remained after phencyclidine treatment was stopped, an indication that
132 xcitatory pathways is the mechanism by which phencyclidine triggers widespread neuronal degeneration;
133                         Monkeys treated with phencyclidine twice a day for 14 days displayed performa
134 , phenethylamines, piperazines, ketamine and phencyclidine-type substances, tryptamines).
135 ith 1-(1-phenylcyclohexyl)piperidine (PCP or phencyclidine) was determined at 2.2-A resolution.
136  pH and ionic strength on the binding of [3H]phencyclidine were determined.

 
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