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  1 / 3655 MEDLINE  
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[PMID]:29324345
[Au] Autor:Xu M; Wang Y; Yang F; Wu C; Wang Z; Ye B; Jiang X; Zhao Q; Li J; Liu Y; Zhang J; Tian G; He Y; Shen J; Jiang H
[Ad] Endereço:CAS Key Laboratory for Receptor Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 555 Zuchongzhi Road, Shanghai 201203, China; University of Chinese Academy of Sciences, No. 19A Yuquan Road, Beijing 100049, China.
[Ti] Título:Synthesis and biological evaluation of a series of multi-target N-substituted cyclic imide derivatives with potential antipsychotic effect.
[So] Source:Eur J Med Chem;145:74-85, 2018 Feb 10.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:In the present study, a series of multi-target N-substituted cyclic imide derivatives which possessed potent dopamine D , serotonin 5-HT and 5-HT receptors properties were synthesized and evaluated as potential antipsychotics. Among these compounds, (3aR,4R,7S,7aS)-2-(4-(4-(benzo[b]thiophen-4-yl)piperazin-1-yl)butyl)-3a,4,7,7a-tetrahydro-1H-4,7-methanoisoindole-1,3(2H)-dione hydrochloride (3d) held a promising pharmacological profile. 3d not only showed potent and balanced in vitro activities on D /5-HT /5-HT receptors, but also endowed with low to moderate activities on 5-HT , H , α , M receptors and hERG channel, suggesting a low liability to induce side effects such as weight gain, orthostatic hypotension and QT prolongation. In animal behavioral studies, 3d reduced phencyclidine-induced hyperlocomotion with a high threshold for catalepsy induction. Compound 3d was selected as a potential antipsychotic candidate for further development.
[Mh] Termos MeSH primário: Antipsicóticos/farmacologia
Catalepsia/tratamento farmacológico
Imidas/farmacologia
[Mh] Termos MeSH secundário: Animais
Antipsicóticos/síntese química
Antipsicóticos/química
Catalepsia/induzido quimicamente
Relação Dose-Resposta a Droga
Seres Humanos
Imidas/síntese química
Imidas/química
Locomoção/efeitos dos fármacos
Masculino
Camundongos
Camundongos Endogâmicos ICR
Estrutura Molecular
Fenciclidina
Ratos
Ratos Sprague-Dawley
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antipsychotic Agents); 0 (Imides); J1DOI7UV76 (Phencyclidine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE


  2 / 3655 MEDLINE  
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[PMID]:29253020
[Au] Autor:Arime Y; Akiyama K
[Ad] Endereço:Department of Biological Psychiatry and Neuroscience, Dokkyo Medical University School of Medicine, Mibu, Tochigi, Japan.
[Ti] Título:Abnormal neural activation patterns underlying working memory impairment in chronic phencyclidine-treated mice.
[So] Source:PLoS One;12(12):e0189287, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Working memory impairment is a hallmark feature of schizophrenia and is thought be caused by dysfunctions in the prefrontal cortex (PFC) and associated brain regions. However, the neural circuit anomalies underlying this impairment are poorly understood. The aim of this study is to assess working memory performance in the chronic phencyclidine (PCP) mouse model of schizophrenia, and to identify the neural substrates of working memory. To address this issue, we conducted the following experiments for mice after withdrawal from chronic administration (14 days) of either saline or PCP (10 mg/kg): (1) a discrete paired-trial variable-delay task in T-maze to assess working memory, and (2) brain-wide c-Fos mapping to identify activated brain regions relevant to this task performance either 90 min or 0 min after the completion of the task, with each time point examined under working memory effort and basal conditions. Correct responses in the test phase of the task were significantly reduced across delays (5, 15, and 30 s) in chronic PCP-treated mice compared with chronic saline-treated controls, suggesting delay-independent impairments in working memory in the PCP group. In layer 2-3 of the prelimbic cortex, the number of working memory effort-elicited c-Fos+ cells was significantly higher in the chronic PCP group than in the chronic saline group. The main effect of working memory effort relative to basal conditions was to induce significantly increased c-Fos+ cells in the other layers of prelimbic cortex and the anterior cingulate and infralimbic cortex regardless of the different chronic regimens. Conversely, this working memory effort had a negative effect (fewer c-Fos+ cells) in the ventral hippocampus. These results shed light on some putative neural networks relevant to working memory impairments in mice chronically treated with PCP, and emphasize the importance of the layer 2-3 of the prelimbic cortex of the PFC.
[Mh] Termos MeSH primário: Transtornos da Memória/fisiopatologia
Memória de Curto Prazo/fisiologia
Neurônios/fisiologia
[Mh] Termos MeSH secundário: Animais
Encéfalo/metabolismo
Masculino
Aprendizagem em Labirinto
Camundongos Endogâmicos C57BL
Fenciclidina
Proteínas Proto-Oncogênicas c-fos/metabolismo
Cloreto de Sódio
Análise e Desempenho de Tarefas
Tirosina 3-Mono-Oxigenase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Proto-Oncogene Proteins c-fos); 451W47IQ8X (Sodium Chloride); EC 1.14.16.2 (Tyrosine 3-Monooxygenase); J1DOI7UV76 (Phencyclidine)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171219
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189287


  3 / 3655 MEDLINE  
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[PMID]:28389140
[Au] Autor:Freeman E; Lin J; Chow S; Davis C; Li M
[Ad] Endereço:Department of Psychology, University of Nebraska-Lincoln, Lincoln, NE 68588-0308, USA. Electronic address: efreeman7@unl.edu.
[Ti] Título:Sex differences in aripiprazole sensitization from adolescence to adulthood.
[So] Source:Pharmacol Biochem Behav;156:39-47, 2017 May.
[Is] ISSN:1873-5177
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The present study investigated the potential sex differences in repeated aripiprazole (ARI) treatment-induced behavioral sensitization from adolescence to adulthood, and to determine whether ARI sensitization can be transferred to olanzapine (OLZ) and/or clozapine (CLZ) using the conditioned avoidance response (CAR) and phencyclidine-induced (PCP) hyperlocomotion tests of antipsychotic activity. Male and female Sprague-Dawley adolescence rats (P46) were first treated with ARI (10mg/kg) for 5 consecutive days (P46-50) and tested for avoidance response and ARI-induced inhibition of PCP-induced hyperlocomotion. After they became adults (>P68), rats were challenged with ARI (1.5mg/kg, sc) (P70), OLZ (0.5mg/kg, sc; P73), CLZ (5mg/kg, sc; P76) and again with ARI (1.5mg/kg, sc; P84) and tested for avoidance response and ARI-induced inhibition of PCP-induced hyperlocomotion again. During the drug treatment period in adolescence, repeated ARI treatment suppressed avoidance response, inhibited the PCP-induced hyperlocomotion, and these effects were progressively increased across the 5-day period in both males and females, confirming the induction of ARI sensitization. On the challenge days, rats previously treated with ARI in adolescence also had significantly lower avoidance and lower PCP-induced hyperlocomotion than the previous vehicle rats, confirming the expression of ARI sensitization and its persistence into adulthood. More importantly, female rats made significantly more avoidances than males in both ARI and vehicle groups, indicating higher sensitivity to the acute and long-term effects of ARI. Further, on the OLZ and CLZ challenge days, prior ARI treatment seemed to increase sensitivity to OLZ exposure, however, this increase was not significant. Similarly, rats also showed an ARI sensitization to OLZ and CLZ on challenge days. Collectively, results from this experiment demonstrated a sex difference in response to ARI and enhanced inhibition of PCP-induced hyperlocomotion in animals that were pretreated with ARI as compared to controls.
[Mh] Termos MeSH primário: Fatores Etários
Antipsicóticos/farmacologia
Aripiprazol/farmacologia
Fatores Sexuais
[Mh] Termos MeSH secundário: Animais
Aprendizagem da Esquiva/efeitos dos fármacos
Feminino
Locomoção/efeitos dos fármacos
Masculino
Fenciclidina/farmacologia
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antipsychotic Agents); 82VFR53I78 (Aripiprazole); J1DOI7UV76 (Phencyclidine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170409
[St] Status:MEDLINE


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[PMID]:28353244
[Au] Autor:Ma D; Guest PC
[Ad] Endereço:Department of neurosciences, University of Cambridge, Clifford Allbutt building, Hills road, Cambridge, CB2 0AH, UK.
[Ti] Título:Generation of the Acute Phencyclidine Rat Model for Proteomic Studies of Schizophrenia.
[So] Source:Adv Exp Med Biol;974:257-261, 2017.
[Is] ISSN:0065-2598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Administration of the non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist phencyclidine (PCP) to rodents has been used as the gold standard preclinical model for schizophrenia. PCP treatment induces hyperlocomotion and stereotypic behaviour, which resemble the positive symptoms of schizophrenia. In addition, proteomic studies have identified changes in proteins associated with energy metabolism and neurotransmission which are typical hallmarks of the disease. This chapter presents a protocol for the generation of this model, behavioural assessment and preparation of key bio-samples to provide the raw materials for proteomic analyses.
[Mh] Termos MeSH primário: Modelos Animais de Doenças
Hormônios/análise
Imunoensaio/métodos
Proteínas do Tecido Nervoso/análise
Fenciclidina/toxicidade
Proteômica/métodos
Esquizofrenia/induzido quimicamente
[Mh] Termos MeSH secundário: Doença Aguda
Animais
Química Encefálica
Inflamação
Locomoção
Masculino
Ratos
Ratos Sprague-Dawley
Esquizofrenia/metabolismo
Soro
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hormones); 0 (Nerve Tissue Proteins); J1DOI7UV76 (Phencyclidine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170330
[St] Status:MEDLINE
[do] DOI:10.1007/978-3-319-52479-5_23


  5 / 3655 MEDLINE  
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[PMID]:28342897
[Au] Autor:Paasonen J; Salo RA; Ihalainen J; Leikas JV; Savolainen K; Lehtonen M; Forsberg MM; Gröhn O
[Ad] Endereço:A.I.V. Institute for Molecular Sciences, Department of Neurobiology, University of Eastern Finland, P.O. Box 1627, FI-70211, Kuopio, Finland.
[Ti] Título:Dose-response effect of acute phencyclidine on functional connectivity and dopamine levels, and their association with schizophrenia-like symptom classes in rat.
[So] Source:Neuropharmacology;119:15-25, 2017 Jun.
[Is] ISSN:1873-7064
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Current drug treatments for schizophrenia (SCZ) can alleviate positive symptoms, but have little effect on the negative symptoms and cognitive deficits that are difficult to translate into preclinical models for drug development. Therefore, we aimed to determine the dose-response effects of acute phencyclidine (PCP, 1.0-5.0 mg/kg) on rat brain connectivity and detect markers for different SCZ-like symptoms. Pharmacological functional magnetic resonance imaging (phMRI) and microdialysis were used to investigate PCP-induced effects on functional connectivity (FC) and dopamine levels, respectively. Next, we evaluated the association between PCP-induced changes in imaging parameters and behavior. PCP at doses of 3.0-5.0 mg/kg induced fMRI signal changes in several brain regions associated with SCZ. Additionally, the FC was globally disturbed, dopamine levels increased, and locomotor activity increased, reflecting the manifestation of SCZ-like positive symptoms. A distinct pattern in the measures was observed at lower PCP doses (1.0-2.0 mg/kg); PCP induced fMRI signal changes in the fronto-cortical regions, and increased dopamine levels in the medial prefrontal cortex. In addition to the dysconnectivity of these regions, the hippocampal FC was disrupted. These observations are consistent with the induction of SCZ-like cognitive deficits and negative symptoms, which were observed as impaired novel object recognition and decreased social interaction. No indicators for positive symptoms were observed at lower PCP doses. We conclude that acute PCP induces SCZ-like symptom classes in a dose-dependent manner; PCP doses of 1.0-2.0 mg/kg are more suitable for modeling SCZ-like negative symptoms and cognitive deficits, while SCZ-like positive symptoms dominate at doses of 3.0-5.0 mg/kg.
[Mh] Termos MeSH primário: Encéfalo
Dopamina/metabolismo
Alucinógenos/toxicidade
Fenciclidina/toxicidade
Esquizofrenia/induzido quimicamente
Esquizofrenia/patologia
[Mh] Termos MeSH secundário: Animais
Encéfalo/diagnóstico por imagem
Encéfalo/metabolismo
Encéfalo/patologia
Mapeamento Encefálico
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Processamento de Imagem Assistida por Computador
Relações Interpessoais
Locomoção/efeitos dos fármacos
Imagem por Ressonância Magnética
Masculino
Microdiálise
Oxigênio/sangue
Ratos
Ratos Wistar
Recognição (Psicologia)/efeitos dos fármacos
Esquizofrenia/diagnóstico por imagem
Psicologia do Esquizofrênico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hallucinogens); J1DOI7UV76 (Phencyclidine); S88TT14065 (Oxygen); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170831
[Lr] Data última revisão:
170831
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170327
[St] Status:MEDLINE


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[PMID]:28167638
[Au] Autor:Maple AM; Call T; Kimmel PC; Hammer RP
[Ad] Endereço:Department of Basic Medical Sciences (A.M.M., P.C.K., R.P.H.), and Departments of Pharmacology and Psychiatry (R.P.H.), University of Arizona College of Medicine, Phoenix; and Department of Psychology (A.M.M., P.C.K., R.P.H.) and Interdisciplinary Graduate Program in Neuroscience (T.C., R.P.H.), Ari
[Ti] Título:Effects of Repeated Ropinirole Treatment on Phencyclidine-Induced Hyperlocomotion, Prepulse Inhibition Deficits, and Social Avoidance in Rats.
[So] Source:J Pharmacol Exp Ther;361(1):109-114, 2017 Apr.
[Is] ISSN:1521-0103
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Phencyclidine (PCP), a noncompetitive N-methyl d-aspartate (NMDA) receptor antagonist, provides the most complete pharmacologic model of schizophrenia in humans and animals. Acute PCP causes hyperlocomotion, disrupts prepulse inhibition (PPI), and increases social avoidance in rats. We have previously shown that repeated treatment with the dopamine (DA) D -like receptor agonists, quinpirole or ropinirole, prevents agonist-induced PPI disruption. In the present study, we examined whether repeated ropinirole treatment similarly attenuates the effects of PCP in a more complete model of schizophrenia symptoms and examined the effect of repeated D -like agonist treatment on locomotion, PPI, and social interaction after acute PCP challenge. The acute effect of PCP (3.0 or 6.0 mg/kg) on locomotor activity was examined to establish a minimum effective dose. Thereafter, the effect of PCP challenge (3.0 mg/kg) on locomotor activity, PPI, and social interaction was assessed in adult male rats before or 7-10 days after termination of repeated daily treatment with ropinirole (0.1 mg/kg) or saline vehicle (0.1 ml/kg) for 28 days. Repeated ropinirole treatment attenuates PCP-induced hyperlocomotion, PPI deficits, and social avoidance. These findings suggest that repeated ropinirole treatment might affect a final common pathway that is vulnerable to both PCP- and dopamine agonist-induced behavioral disruption, thereby providing an alternative approach to block the effects of PCP.
[Mh] Termos MeSH primário: Aprendizagem da Esquiva/efeitos dos fármacos
Hipercinese/induzido quimicamente
Hipercinese/tratamento farmacológico
Indóis/administração & dosagem
Fenciclidina/toxicidade
Inibição Pré-Pulso/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Aprendizagem da Esquiva/fisiologia
Agonistas de Dopamina/administração & dosagem
Hipercinese/psicologia
Masculino
Inibição Pré-Pulso/fisiologia
Ratos
Ratos Sprague-Dawley
Receptores de N-Metil-D-Aspartato/antagonistas & inibidores
Receptores de N-Metil-D-Aspartato/fisiologia
Esquizofrenia/induzido quimicamente
Comportamento Social
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dopamine Agonists); 0 (Indoles); 0 (Receptors, N-Methyl-D-Aspartate); 030PYR8953 (ropinirole); J1DOI7UV76 (Phencyclidine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170605
[Lr] Data última revisão:
170605
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170208
[St] Status:MEDLINE
[do] DOI:10.1124/jpet.116.238634


  7 / 3655 MEDLINE  
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[PMID]:28158698
[Au] Autor:Zidkova M; Hlozek T; Balik M; Kopecky O; Tesinsky P; Svanda J; Balikova MA
[Ad] Endereço:Institute Forensic Medicine and Toxicology, First Faculty of Medicine, Charles University and General University Hospital, Ke Karlovu 2, Prague 2, Prague.
[Ti] Título:Two Cases of Non-fatal Intoxication with a Novel Street Hallucinogen: 3-Methoxy-Phencyclidine.
[So] Source:J Anal Toxicol;41(4):350-354, 2017 May 01.
[Is] ISSN:1945-2403
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:3-Methoxy-phencyclidine (3-MeO-PCP) is a structural derivative of the dissociative hallucinogen phencyclidine (PCP). Although PCP toxicity is well documented, little is known about this new psychoactive substance despite being available on the black market even in central Europe. The objective of this case report is to present clinical and laboratory data of analytically confirmed non-fatal intoxication of two subjects with 3-MeO-PCP. A preliminary assessment of potential metabolites excreted into urine was enabled using the liquid chromatography high resolution mass spectrometric method.
[Mh] Termos MeSH primário: Alucinógenos/toxicidade
Fenciclidina/análogos & derivados
Drogas Ilícitas/toxicidade
[Mh] Termos MeSH secundário: Cromatografia Líquida
Europa (Continente)
Alucinógenos/urina
Seres Humanos
Fenciclidina/toxicidade
Fenciclidina/urina
Drogas Ilícitas/urina
Detecção do Abuso de Substâncias
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hallucinogens); 0 (Street Drugs); 0 (methoxydine); J1DOI7UV76 (Phencyclidine)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170726
[Lr] Data última revisão:
170726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170204
[St] Status:MEDLINE
[do] DOI:10.1093/jat/bkx009


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[PMID]:28121123
[Au] Autor:Yavas E; Young AM
[Ad] Endereço:Department of Neuroscience, Psychology and Behaviour, University of Leicester , Lancaster Road, Leicester LE1 9HN, United Kingdom.
[Ti] Título:N-Methyl-d-aspartate Modulation of Nucleus Accumbens Dopamine Release by Metabotropic Glutamate Receptors: Fast Cyclic Voltammetry Studies in Rat Brain Slices in Vitro.
[So] Source:ACS Chem Neurosci;8(2):320-328, 2017 Feb 15.
[Is] ISSN:1948-7193
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The N-methyl-d-aspartate (NMDA) receptor antagonist, phencyclidine, induces behavioral changes in rodents mimicking symptoms of schizophrenia, possibly mediated through dysregulation of glutamatergic control of mesolimbic dopamine release. We tested the hypothesis that NMDA receptor activation modulates accumbens dopamine release, and that phencyclidine pretreatment altered this modulation. NMDA caused a receptor-specific, dose-dependent decrease in electrically stimulated dopamine release in nucleus accumbens brain slices. This decrease was unaffected by picrotoxin, making it unlikely to be mediated through GABAergic neurones, but was decreased by the metabotropic glutamate receptor antagonist, (RS)-α-methyl-4-sulfonophenylglycine, indicating that NMDA activates mechanisms controlled by these receptors to decrease stimulated dopamine release. The effect of NMDA was unchanged by in vivo pretreatment with phencyclidine (twice daily for 5 days), with a washout period of at least 7 days before experimentation, which supports the hypothesis that there is no enduring direct effect of PCP at NMDA receptors after this pretreatment procedure. We propose that NMDA depression of accumbal dopamine release is mediated by metabotropic glutamate receptors located pre- or perisynaptically, and suggest that NMDA evoked increased extrasynaptic spillover of glutamate is sufficient to activate these receptors that, in turn, inhibit dopamine release. Furthermore, we suggest that enduring functional changes brought about by subchronic phencyclidine pretreatment, modeling deficits in schizophrenia, are downstream effects consequent on chronic blockade of NMDA receptors, rather than direct effects on NMDA receptors themselves.
[Mh] Termos MeSH primário: Dopamina/metabolismo
Agonistas de Aminoácidos Excitatórios/farmacologia
N-Metilaspartato/farmacologia
Núcleo Accumbens/efeitos dos fármacos
Núcleo Accumbens/metabolismo
Receptores de Glutamato Metabotrópico/metabolismo
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Di-Hidro-beta-Eritroidina/farmacologia
Relação Dose-Resposta a Droga
Estimulação Elétrica
Técnicas Eletroquímicas
Antagonistas de Aminoácidos Excitatórios/farmacologia
Feminino
Antagonistas GABAérgicos/farmacologia
Técnicas In Vitro
Antagonistas Nicotínicos/farmacologia
Fenciclidina/farmacologia
Picrotoxina/farmacologia
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Excitatory Amino Acid Agonists); 0 (Excitatory Amino Acid Antagonists); 0 (GABA Antagonists); 0 (Nicotinic Antagonists); 0 (Receptors, Metabotropic Glutamate); 124-87-8 (Picrotoxin); 23255-54-1 (Dihydro-beta-Erythroidine); 6384-92-5 (N-Methylaspartate); J1DOI7UV76 (Phencyclidine); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170126
[St] Status:MEDLINE
[do] DOI:10.1021/acschemneuro.6b00397


  9 / 3655 MEDLINE  
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[PMID]:28031399
[Au] Autor:Dauth S; Maoz BM; Sheehy SP; Hemphill MA; Murty T; Macedonia MK; Greer AM; Budnik B; Parker KK
[Ad] Endereço:Disease Biophysics Group, Wyss Institute for Biologically Inspired Engineering, John A. Paulson School of Engineering and Applied Sciences, Harvard University, Cambridge, Massachusetts; and.
[Ti] Título:Neurons derived from different brain regions are inherently different in vitro: a novel multiregional brain-on-a-chip.
[So] Source:J Neurophysiol;117(3):1320-1341, 2017 Mar 01.
[Is] ISSN:1522-1598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Brain in vitro models are critically important to developing our understanding of basic nervous system cellular physiology, potential neurotoxic effects of chemicals, and specific cellular mechanisms of many disease states. In this study, we sought to address key shortcomings of current brain in vitro models: the scarcity of comparative data for cells originating from distinct brain regions and the lack of multiregional brain in vitro models. We demonstrated that rat neurons from different brain regions exhibit unique profiles regarding their cell composition, protein expression, metabolism, and electrical activity in vitro. In vivo, the brain is unique in its structural and functional organization, and the interactions and communication between different brain areas are essential components of proper brain function. This fact and the observation that neurons from different areas of the brain exhibit unique behaviors in vitro underline the importance of establishing multiregional brain in vitro models. Therefore, we here developed a multiregional brain-on-a-chip and observed a reduction of overall firing activity, as well as altered amounts of astrocytes and specific neuronal cell types compared with separately cultured neurons. Furthermore, this multiregional model was used to study the effects of phencyclidine, a drug known to induce schizophrenia-like symptoms in vivo, on individual brain areas separately while monitoring downstream effects on interconnected regions. Overall, this work provides a comparison of cells from different brain regions in vitro and introduces a multiregional brain-on-a-chip that enables the development of unique disease models incorporating essential in vivo features. Due to the scarcity of comparative data for cells from different brain regions in vitro, we demonstrated that neurons isolated from distinct brain areas exhibit unique behaviors in vitro. Moreover, in vivo proper brain function is dependent on the connection and communication of several brain regions, underlining the importance of developing multiregional brain in vitro models. We introduced a novel brain-on-a-chip model, implementing essential in vivo features, such as different brain areas and their functional connections.
[Mh] Termos MeSH primário: Encéfalo/anatomia & histologia
Encéfalo/citologia
Neurônios/classificação
Neurônios/fisiologia
[Mh] Termos MeSH secundário: Potenciais de Ação/fisiologia
Análise de Variância
Animais
Animais Recém-Nascidos
Astrócitos/metabolismo
Células Cultivadas
Cromatografia Líquida de Alta Pressão
Feminino
Expressão Gênica/fisiologia
Glutamato Descarboxilase/metabolismo
Alucinógenos/farmacologia
Masculino
Proteínas do Tecido Nervoso/metabolismo
Neurônios/efeitos dos fármacos
Consumo de Oxigênio
Fenciclidina/farmacologia
Análise de Componente Principal
Mapas de Interação de Proteínas
Ratos
Ratos Sprague-Dawley
Espectrometria de Massas em Tandem
Proteína Vesicular 1 de Transporte de Glutamato/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hallucinogens); 0 (Nerve Tissue Proteins); 0 (Slc17a7 protein, rat); 0 (Vesicular Glutamate Transport Protein 1); EC 4.1.1.15 (Glutamate Decarboxylase); J1DOI7UV76 (Phencyclidine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161230
[St] Status:MEDLINE
[do] DOI:10.1152/jn.00575.2016


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[PMID]:27986516
[Au] Autor:Knox LT; Jing Y; Bawazier-Edgecombe J; Collie ND; Zhang H; Liu P
[Ad] Endereço:Department of Anatomy, School of Biomedical Sciences, University of Otago, Dunedin, New Zealand; Brain Health Research Centre, University of Otago, Dunedin, New Zealand.
[Ti] Título:Effects of withdrawal from repeated phencyclidine administration on behavioural function and brain arginine metabolism in rats.
[So] Source:Pharmacol Biochem Behav;153:45-59, 2017 Feb.
[Is] ISSN:1873-5177
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Phencyclidine (PCP) induces behavioural changes in humans and laboratory animals that resemble positive and negative symptoms, and cognitive impairments in schizophrenia. It has been shown repeated treatment of PCP leading to persistent symptoms even after the drug discontinuation, and there is a growing body of evidence implicating altered arginine metabolism in the pathogenesis of schizophrenia. The present study investigated the effects of withdrawal from repeated daily injection of PCP (2mg/kg) for 12 consecutive days on animals'behavioural performance and arginine metabolism in the hippocampus and prefrontal cortex in male young adult rats. Repeated PCP treatment reduced spontaneous alternations in the Y-maze and exploratory and locomotor activities in the open field under the condition of a washout period of 24h, but not 4days. Interestingly, the PCP treated rats also displayed spatial working memory deficits when tested 8-10days after withdrawal from PCP and showed altered levels of arginase activities and eight out of ten l-arginine metabolites in neurochemical- and region-specific manner. Cluster analyses showed altered relationships among l-arginine and its three main metabolites as a function of withdrawal from repeated PCP treatment in a duration-specific manner. Multiple regression analysis revealed significant neurochemical-behavioural correlations. Collectively, the results suggest both the residual and long-term effects of withdrawal from repeated PCP treatment on behavioural function and brain arginine metabolism. These findings demonstrate, for the first time, the influence of the withdrawal duration on animals' behaviour and brain arginine metabolism.
[Mh] Termos MeSH primário: Arginina/metabolismo
Comportamento Animal/efeitos dos fármacos
Encéfalo/metabolismo
Fenciclidina/farmacologia
[Mh] Termos MeSH secundário: Aminoácidos/metabolismo
Animais
Poliaminas Biogênicas/análise
Peso Corporal/efeitos dos fármacos
Análise por Conglomerados
Masculino
Aprendizagem em Labirinto/efeitos dos fármacos
Atividade Motora/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acids); 0 (Biogenic Polyamines); 94ZLA3W45F (Arginine); J1DOI7UV76 (Phencyclidine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170825
[Lr] Data última revisão:
170825
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161218
[St] Status:MEDLINE



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