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[PMID]:28749090
[Au] Autor:Yoon HS; Hattori K; Ogawa S; Sasayama D; Ota M; Teraishi T; Kunugi H
[Ad] Endereço:Department of Mental Disorder Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan.
[Ti] Título:Relationships of Cerebrospinal Fluid Monoamine Metabolite Levels With Clinical Variables in Major Depressive Disorder.
[So] Source:J Clin Psychiatry;78(8):e947-e956, 2017 Sep/Oct.
[Is] ISSN:1555-2101
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Many studies have investigated cerebrospinal fluid (CSF) monoamine metabolite levels in depressive disorders. However, their clinical significance is still unclear. We tried to determine whether CSF monoamine metabolite levels could be a state-dependent marker for major depressive disorder (MDD) based on analyses stratified by clinical variables in a relatively large sample. METHODS: Subjects were 75 patients with MDD according to DSM-IV criteria and 87 healthy controls, matched for age, sex, and ethnicity (Japanese). They were recruited between May 2010 and November 2013. We measured homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA), and 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG) in CSF samples by high-performance liquid chromatography. We analyzed the relationships of the metabolite levels with age, sex, diagnosis, psychotropic medication use, and depression severity. RESULTS: There was a weak positive correlation between age and 5-HIAA levels in controls (ρ = 0.26, P < .016) and a similar trend in patients, while sex was unrelated to any metabolite. All monoamine metabolites in moderately to severely depressed patients (17-item Hamilton Depression Rating Scale score > 12) were significantly lower than those in controls (P < .0005 for all 3 metabolites). We found that antidepressants decreased the levels of 5-HIAA (ρ = -0.39, P < .001) and MHPG (ρ = -0.49, P < .0001) and that antipsychotics increased levels of HVA (ρ = 0.24, P < .05). There was a strong correlation between HVA and 5-HIAA levels (controls: ρ = 0.79, P = .000001; MDD: ρ = 0.66, P = .000001). HVA levels (ρ = -0.43, P < .001) and 5-HIAA levels (ρ = -0.23, P < .05), but not MHPG levels (ρ = -0.18, P > .1), were related to depression severity. CONCLUSIONS: CSF 5-HIAA and HVA levels could be state-dependent markers in MDD patients. Since 5-HIAA levels greatly decrease with the use of antidepressants, HVA levels might be more useful in the clinical setting.
[Mh] Termos MeSH primário: Transtorno Depressivo Maior
Ácido Homovanílico/líquido cefalorraquidiano
Indóis/líquido cefalorraquidiano
Metoxi-Hidroxifenilglicol/líquido cefalorraquidiano
Psicotrópicos/uso terapêutico
[Mh] Termos MeSH secundário: Adulto
Fatores Etários
Biomarcadores/líquido cefalorraquidiano
Líquido Cefalorraquidiano/efeitos dos fármacos
Líquido Cefalorraquidiano/metabolismo
Cromatografia Líquida/métodos
Transtorno Depressivo Maior/líquido cefalorraquidiano
Transtorno Depressivo Maior/diagnóstico
Transtorno Depressivo Maior/tratamento farmacológico
Transtorno Depressivo Maior/psicologia
Manual Diagnóstico e Estatístico de Transtornos Mentais
Feminino
Seres Humanos
Japão
Masculino
Meia-Idade
Escalas de Graduação Psiquiátrica
Estatística como Assunto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Indoles); 0 (Psychotropic Drugs); 534-82-7 (Methoxyhydroxyphenylglycol); 5SW11R7M7M (indole-3-lactic acid); X77S6GMS36 (Homovanillic Acid)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE


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[PMID]:28772121
[Au] Autor:Thomson SR; Seo SS; Barnes SA; Louros SR; Muscas M; Dando O; Kirby C; Wyllie DJA; Hardingham GE; Kind PC; Osterweil EK
[Ad] Endereço:Centre for Integrative Physiology/Patrick Wild Centre, University of Edinburgh, Hugh Robson Building, George Square, Edinburgh, EH8 9XD, UK; Simons Initiative for the Developing Brain, University of Edinburgh, Hugh Robson Building, George Square, Edinburgh, EH8 9XD, UK.
[Ti] Título:Cell-Type-Specific Translation Profiling Reveals a Novel Strategy for Treating Fragile X Syndrome.
[So] Source:Neuron;95(3):550-563.e5, 2017 Aug 02.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Excessive mRNA translation downstream of group I metabotropic glutamate receptors (mGlu ) is a core pathophysiology of fragile X syndrome (FX); however, the differentially translating mRNAs that contribute to altered neural function are not known. We used translating ribosome affinity purification (TRAP) and RNA-seq to identify mistranslating mRNAs in CA1 pyramidal neurons of the FX mouse model (Fmr1 ) hippocampus, which exhibit exaggerated mGlu -induced long-term synaptic depression (LTD). In these neurons, we find that the Chrm4 transcript encoding muscarinic acetylcholine receptor 4 (M ) is excessively translated, and synthesis of M downstream of mGlu activation is mimicked and occluded. Surprisingly, enhancement rather than inhibition of M activity normalizes core phenotypes in the Fmr1 , including excessive protein synthesis, exaggerated mGluR-LTD, and audiogenic seizures. These results suggest that not all excessively translated mRNAs in the Fmr1 brain are detrimental, and some may be candidates for enhancement to correct pathological changes in the FX brain.
[Mh] Termos MeSH primário: Proteína do X Frágil de Retardo Mental/metabolismo
Síndrome do Cromossomo X Frágil/tratamento farmacológico
Hipocampo/citologia
Depressão Sináptica de Longo Prazo/fisiologia
Neurônios/citologia
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Proteína do X Frágil de Retardo Mental/genética
Síndrome do Cromossomo X Frágil/genética
Síndrome do Cromossomo X Frágil/metabolismo
Metoxi-Hidroxifenilglicol/farmacologia
Camundongos Transgênicos
Biossíntese de Proteínas/efeitos dos fármacos
Receptores de Glutamato Metabotrópico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Metabotropic Glutamate); 139135-51-6 (Fragile X Mental Retardation Protein); 534-82-7 (Methoxyhydroxyphenylglycol)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170914
[Lr] Data última revisão:
170914
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170804
[St] Status:MEDLINE


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[PMID]:28422818
[Au] Autor:Gao SH; Shen LL; Wen HZ; Zhao YD; Ruan HZ
[Ad] Endereço:From the Department of Neurobiology, College of Basic Medical Science, Chongqing Key Laboratory of Neurobiology, Third Military Medical University, Chongqing, China (S.-H.G., H.-Z.W., Y.-D.Z., H.-Z.R.); and Department of Neurology, Daping Hospital, Third Military Medical University, Chongqing, China (L.-L.S.).
[Ti] Título:Inhibition of Metabotropic Glutamate Receptor Subtype 1 Alters the Excitability of the Commissural Pyramidal Neuron in the Rat Anterior Cingulate Cortex after Chronic Constriction Injury to the Sciatic Nerve.
[So] Source:Anesthesiology;127(3):515-533, 2017 Sep.
[Is] ISSN:1528-1175
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Inhibition of the metabotropic glutamate receptor subtype 1 in the anterior cingulate cortex has an analgesic effect during sustained nociceptive hypersensitivity. However, the specific changes in different subtypes of anterior cingulate cortex layer 5 pyramidal neurons, as well as the distinct effect of metabotropic glutamate receptor subtype 1 inhibition on different neuronal subtypes, have not been well studied. METHODS: Retrograde labeling combined with immunofluorescence, whole cell clamp recording, and behavioral tests combined with RNA interference were performed in a rat model of chronic constriction injury to the sciatic nerve. RESULTS: Commissural layer 5 pyramidal neurons (projecting to the contralateral cortex) existed in the anterior cingulate cortex. The voltage-gated potassium channel subunit 2-mediated current in these neurons were substantially reduced after chronic constriction injury (current densities at +30 mV for the sham, and chronic constriction injury neurons were [mean ± SD] 10.22 ± 3.42 pA/pF vs. 5.58 ± 2.71 pA/pF, respectively; n = 11; P < 0.01), which increased the spike width and fast afterhyperpolarization potential, resulting in hyperexcitability. Inhibition of metabotropic glutamate receptor subtype 1 alleviated the down-regulation of voltage-gated potassium channel subunit 2 currents (current density increased by 8.11 ± 3.22 pA/pF; n = 7; P < 0.01). Furthermore, knockdown of voltage-gated potassium channel subunit 2 current in the commissural neurons attenuated the analgesic effect of metabotropic glutamate receptor subtype 1 inhibition (n = 6 rats; P < 0.05). CONCLUSIONS: The effect of metabotropic glutamate receptor subtype 1 inhibition on commissural anterior cingulate cortex layer 5 pyramidal neurons is likely different with the modification of previously studied hyperpolarization-activated/cyclic nucleotide-gated channel-dependent neurons but relies on the alteration of voltage-gated potassium channel subunit 2 currents. These results will contribute to a better understanding of the therapeutic role of metabotropic glutamate receptor subtype 1 in chronic pain.
[Mh] Termos MeSH primário: Giro do Cíngulo/fisiopatologia
Células Piramidais/fisiologia
Receptores de Glutamato Metabotrópico/agonistas
Nervo Isquiático/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Comportamento Animal/fisiologia
Western Blotting
Doença Crônica
Constrição Patológica
Modelos Animais de Doenças
Regulação para Baixo/fisiologia
Imunofluorescência
Masculino
Metoxi-Hidroxifenilglicol/análogos & derivados
Neuralgia
Técnicas de Patch-Clamp
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Metabotropic Glutamate); 534-82-7 (Methoxyhydroxyphenylglycol); CF5G2G268A (dihydroxyphenylethylene glycol)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170901
[Lr] Data última revisão:
170901
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170420
[St] Status:MEDLINE
[do] DOI:10.1097/ALN.0000000000001654


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[PMID]:28272307
[Au] Autor:Hori H; Yoshimura R; Katsuki A; Atake K; Igata R; Konishi Y; Beppu H; Tominaga H
[Ad] Endereço:Department of Psychiatry, University of Occupational and Environmental Health, Iseigaoka, Yahatanishi-ku, Kitakyushu, Fukuoka 8078555, Japan. hori-h@med.uoeh-u.ac.jp.
[Ti] Título:Blood Biomarkers Predict the Cognitive Effects of Aripiprazole in Patients with Acute Schizophrenia.
[So] Source:Int J Mol Sci;18(3), 2017 Mar 06.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Aripiprazole has been reported to exert variable effects on cognitive function in patients with schizophrenia. Therefore, in the present study, we evaluated biological markers, clinical data, and psychiatric symptoms in order to identify factors that influence cognitive function in patients with schizophrenia undergoing aripiprazole treatment. We evaluated cognitive function in 51 patients with schizophrenia using Brief Assessment of Cognition in Schizophrenia (BACS), as well as background information, psychiatric symptoms, plasma catecholamine metabolites-homovanillic acid (HVA), 3-methoxy-4-hydroxyphenylglycol (MHPG)-, and serum brain-derived neurotrophic factor (BDNF). Multivariate analyses were performed in order to identify factors independently associated with cognitive function. Brain-derived neurotrophic factor levels, number of hospitalizations, and MHPG levels were associated with verbal memory and learning. Total hospitalization period and MHPG levels were associated with working memory. Age at first hospitalization and education were associated with motor speed. The number of hospital admissions, Positive and Negative Syndrome Scale negative subscale scores (PANSS-N), MHPG levels, BDNF levels, and Drug-Induced Extrapyramidal Symptoms Scale (DIEPSS) scores were associated with verbal fluency. Homovanillic acid and MHPG levels, duration of illness, and PANSS-N scores were associated with attention and processing speed. Brain-derived neurotrophic factor and MHPG levels were associated with executive function. These results suggest that treatment of psychiatric symptoms and cognitive dysfunction may be improved in patients treated with aripiprazole by controlling for these contributing factors.
[Mh] Termos MeSH primário: Antipsicóticos/efeitos adversos
Aripiprazol/efeitos adversos
Fator Neurotrófico Derivado do Encéfalo/sangue
Cognição/efeitos dos fármacos
Ácido Homovanílico/sangue
Metoxi-Hidroxifenilglicol/sangue
Esquizofrenia/sangue
[Mh] Termos MeSH secundário: Adulto
Antipsicóticos/uso terapêutico
Aripiprazol/uso terapêutico
Biomarcadores/sangue
Função Executiva/efeitos dos fármacos
Feminino
Seres Humanos
Masculino
Memória de Curto Prazo/efeitos dos fármacos
Meia-Idade
Esquizofrenia/tratamento farmacológico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antipsychotic Agents); 0 (Biomarkers); 0 (Brain-Derived Neurotrophic Factor); 534-82-7 (Methoxyhydroxyphenylglycol); 82VFR53I78 (Aripiprazole); X77S6GMS36 (Homovanillic Acid)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170425
[Lr] Data última revisão:
170425
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170309
[St] Status:MEDLINE


  5 / 3209 MEDLINE  
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[PMID]:28266711
[Au] Autor:Vergouts M; Doyen PJ; Peeters M; Opsomer R; Michiels T; Hermans E
[Ad] Endereço:Group of Neuropharmacology, Institute of Neuroscience, Université catholique de Louvain, Avenue Hippocrate B1.54.10, Brussels, Belgium.
[Ti] Título:PKC epsilon-dependent calcium oscillations associated with metabotropic glutamate receptor 5 prevent agonist-mediated receptor desensitization in astrocytes.
[So] Source:J Neurochem;141(3):387-399, 2017 May.
[Is] ISSN:1471-4159
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A critical role has been assigned to protein kinase C (PKC)ε in the control of intracellular calcium oscillations triggered upon activation of type 5 metabotropic glutamate receptor (mGluR5) in cultured astrocytes. Nevertheless, the physiological significance of this particular signalling profile in the response of astrocytes to glutamate remains largely unknown. Considering that kinases are frequently involved in the regulation of G protein-coupled receptors, we have examined a putative link between the nature of the calcium signals and the response regulation upon repeated exposures of astrocytes to the agonist (S)-3,5-dihydroxyphenylglycine. We show that upon repeated mGluR5 activations, a robust desensitization was observed in astrocytes grown in culture conditions favouring the peak-plateau-type response. At variance, in cell cultures where calcium oscillations were predominating, the response was fully preserved even during repeated challenges with the agonist. Pharmacological inhibition of PKCε or genetic suppression of this isoform using shRNA was found to convert an oscillatory calcium profile to a sustained calcium mobilization and this latter profile was subject to desensitization upon repetitive mGluR5 activation. Our results suggest a yet undocumented scheme in which the activity of PKCε contributes to preserve the receptor sensitivity upon repeated or sustained activations. Cover Image for this issue: doi: 10.1111/jnc.13797.
[Mh] Termos MeSH primário: Astrócitos/metabolismo
Sinalização do Cálcio/efeitos dos fármacos
Proteína Quinase C-épsilon/metabolismo
Receptor de Glutamato Metabotrópico 5/agonistas
Receptor de Glutamato Metabotrópico 5/metabolismo
[Mh] Termos MeSH secundário: Alcanos/farmacologia
Animais
Astrócitos/efeitos dos fármacos
Ciclopropanos/farmacologia
Proteína Glial Fibrilar Ácida/metabolismo
Imuno-Histoquímica
Lentivirus/genética
Metoxi-Hidroxifenilglicol/análogos & derivados
Metoxi-Hidroxifenilglicol/farmacologia
Cultura Primária de Células
Ratos
Ratos Sprague-Dawley
Transdução Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alkanes); 0 (Cyclopropanes); 0 (FR236924); 0 (Glial Fibrillary Acidic Protein); 0 (Grm5 protein, rat); 0 (Receptor, Metabotropic Glutamate 5); 534-82-7 (Methoxyhydroxyphenylglycol); CF5G2G268A (dihydroxyphenylethylene glycol); EC 2.7.11.13 (Protein Kinase C-epsilon)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170502
[Lr] Data última revisão:
170502
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170308
[St] Status:MEDLINE
[do] DOI:10.1111/jnc.14007


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[PMID]:27940130
[Au] Autor:Akiyama T; Hayashi Y; Hanaoka Y; Shibata T; Akiyama M; Nakamura K; Tsuyusaki Y; Kubota M; Yoshinaga H; Kobayashi K
[Ad] Endereço:Department of Child Neurology, Okayama University Hospital, Okayama, Japan. Electronic address: takiyama@okayama-u.ac.jp.
[Ti] Título:Simultaneous measurement of monoamine metabolites and 5-methyltetrahydrofolate in the cerebrospinal fluid of children.
[So] Source:Clin Chim Acta;465:5-10, 2017 Feb.
[Is] ISSN:1873-3492
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: We describe a new method for simultaneous measurement of monoamine metabolites (3-O-methyldopa [3-OMD], 3-methoxy-4-hydroxyphenylethyleneglycol [MHPG], 5-hydroxyindoleacetic acid [5-HIAA], and homovanillic acid [HVA]) and 5-methyltetrahydrofolate (5-MTHF) and its use on cerebrospinal fluid (CSF) samples from pediatric patients. METHODS: Monoamine metabolites and 5-MTHF were measured by high-performance liquid chromatography with fluorescence detection. CSF samples were prospectively collected from children according to a standardized collection protocol in which the first 1-ml fraction was used for analysis. RESULTS: Monoamine metabolites and 5-MTHF were separated within 10min. They showed linearity from the limit of detection to 1024nmol/l. The limit of quantification of each metabolite was sufficiently low for the CSF sample assay. In 42 CSF samples after excluding cases with possibly altered neurotransmitter profiles, the concentrations of 3-OMD, MHPG, 5-HIAA, HVA, and 5-MTHF showed significant age dependence and their ranges were comparable with the reference values in the literature. The metabolite profiles of aromatic l-amino acid decarboxylase deficiency, Segawa disease, and folate receptor α defect by this method were compatible with those in the literature. CONCLUSIONS: This method is a simple means of measuring CSF monoamine metabolites and 5-MTHF, and is especially useful for laboratories not equipped with electrochemical detectors.
[Mh] Termos MeSH primário: Di-Hidroxifenilalanina/análogos & derivados
Ácido Homovanílico/líquido cefalorraquidiano
Ácido Hidroxi-Indolacético/líquido cefalorraquidiano
Metoxi-Hidroxifenilglicol/líquido cefalorraquidiano
Tetra-Hidrofolatos/líquido cefalorraquidiano
[Mh] Termos MeSH secundário: Descarboxilases de Aminoácido-L-Aromático/líquido cefalorraquidiano
Descarboxilases de Aminoácido-L-Aromático/deficiência
Cromatografia Líquida de Alta Pressão/métodos
Di-Hidroxifenilalanina/líquido cefalorraquidiano
Distúrbios Distônicos/líquido cefalorraquidiano
Fluorescência
Receptor 1 de Folato/líquido cefalorraquidiano
Receptor 1 de Folato/deficiência
Receptor 1 de Folato/genética
Seres Humanos
Limite de Detecção
Distrofias Neuroaxonais/líquido cefalorraquidiano
Valores de Referência
Reprodutibilidade dos Testes
Tirosina/análogos & derivados
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (FOLR1 protein, human); 0 (Folate Receptor 1); 0 (Tetrahydrofolates); 42HK56048U (Tyrosine); 534-82-7 (Methoxyhydroxyphenylglycol); 54-16-0 (Hydroxyindoleacetic Acid); 63-84-3 (Dihydroxyphenylalanine); EC 4.1.1.28 (Aromatic-L-Amino-Acid Decarboxylases); EC 4.1.1.28 (DDC protein, human); TYK22LML8F (5-methyltetrahydrofolate); V3O7J20DWN (3-methoxytyrosine); X77S6GMS36 (Homovanillic Acid)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161213
[St] Status:MEDLINE


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[PMID]:27908790
[Au] Autor:Li J; Chen H; Wu S; Cheng Y; Li Q; Wang J; Zhu G
[Ad] Endereço:Key Laboratory of Xin'an Medicine, Ministry of Education, Anhui University of Chinese Medicine, Hefei 230038, China.
[Ti] Título:MPP inhibits mGluR1/5-mediated long-term depression in mouse hippocampus by calpain activation.
[So] Source:Eur J Pharmacol;795:22-27, 2017 Jan 15.
[Is] ISSN:1879-0712
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Neurotoxins are harmful to nervous system and cause either neuronal cell death or impairment of synaptic activity, which contributes to Parkinson's disease or other neuronal disorders. Hippocampal synaptic plasticity was proposed as a cellular model for memory processing. In this study, we reported a novel effect of neurotoxin, 1-methyl-4-phenylpyridinium (MPP ), on metabotropic glutamate receptor 1/5 agonist, 3,5-dihydroxyphenylglycine (DHPG)-induced hippocampal synaptic plasticity, and MPP incubation blocked DHPG-induced hippocampal long-term depression (LTD) in Schaffer collateral-CA1 synapses. Our further findings indicated that, this blockage was reversed by pre-application of calpain inhibitor III, but not by cathepsin inhibitors. Biochemical analysis showed that MPP treatment stimulated calpain activation, displayed by spectrin breakdown. Interestingly, the level and activity of protein tyrosine phosphatase 1B (PTP1B) were reduced after MPP incubation and the decrease of PTP1B was prohibited by calpain inhibitor III. In addition, PTP1B inhibitor also blocked DHPG-induced LTD, mimicking the effect of MPP . In summary, our data implicated that MPP activated calpain-dependent PTP1B degradation, which subsequently impaired hippocampal LTD. This novel effect of MPP might partially explain the impairment of memory processing in the pathogenesis of PD.
[Mh] Termos MeSH primário: 1-Metil-4-fenilpiridínio/toxicidade
Calpaína/metabolismo
Hipocampo/efeitos dos fármacos
Hipocampo/fisiologia
Depressão Sináptica de Longo Prazo/efeitos dos fármacos
Receptor de Glutamato Metabotrópico 5/metabolismo
Receptores de Glutamato Metabotrópico/metabolismo
[Mh] Termos MeSH secundário: Animais
Ativação Enzimática/efeitos dos fármacos
Masculino
Metoxi-Hidroxifenilglicol/análogos & derivados
Metoxi-Hidroxifenilglicol/farmacologia
Camundongos
Proteína Tirosina Fosfatase não Receptora Tipo 1/metabolismo
Receptor de Glutamato Metabotrópico 5/agonistas
Receptores de Glutamato Metabotrópico/agonistas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptor, Metabotropic Glutamate 5); 0 (Receptors, Metabotropic Glutamate); 0 (metabotropic glutamate receptor type 1); 534-82-7 (Methoxyhydroxyphenylglycol); CF5G2G268A (dihydroxyphenylethylene glycol); EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 1); EC 3.1.3.48 (Ptpn1 protein, mouse); EC 3.4.22.- (Calpain); R865A5OY8J (1-Methyl-4-phenylpyridinium)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170508
[Lr] Data última revisão:
170508
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161203
[St] Status:MEDLINE


  8 / 3209 MEDLINE  
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[PMID]:27884589
[Au] Autor:Machado TR; Alves GJ; Quinteiro-Filho WM; Palermo-Neto J
[Ad] Endereço:Neuroimmunomodulation Research Group, School of Veterinary Medicine and Animal Science, University of São Paulo, São Paulo, Brazil; Department of Pathology, School of Veterinary Medicine, Universidade de São Paulo, São Paulo, SP, Brazil.
[Ti] Título:Cohabitation with an Ehrlich tumor-bearing cagemate induces immune but not behavioral changes in male mice.
[So] Source:Physiol Behav;169:82-89, 2017 Feb 01.
[Is] ISSN:1873-507X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cohabitation with Ehrlich ascitic tumor-injected conspecifics induces behavioral, neurochemical, endocrine and immune changes indicative of stress and immune impairment in female mice. The present work analyzed the effects of similar cohabitation in Swiss and Balb/C male mice. At least 12 pairs of male mice were divided into a control group and an experimental group. On experimental day 1 (ED1), one animal within each experimental pair was inoculated with 5×10 Ehrlich tumor cells intraperitoneally (i.p.); the other animal was kept undisturbed and was referred to as the CSP (companion of a sick partner). One male mouse of each control pair was treated i.p. with 0.9% NaCl (1mL/kg); the other animal (the CHP, companion of a healthy partner) was kept undisturbed. Cohabitation with a sick partner for 11days did not induce any behavioral, hypothalamic noradrenergic, corticosterone or adrenal weight changes in the Swiss CSP male mice compared to those of the Swiss CHP group. However, impairments in neutrophil phagocytosis and oxidative burst as well as increased levels of catecholamines were observed in Swiss and Balb/C CSP mice relative to CHP male animals of the same strains on ED11 and ED14, respectively. Moreover, after a challenge with 5×10 Ehrlich tumor cells on ED11 of cohabitation, the number and concentration of tumor cells found in the ascitic fluid were higher in the Swiss CSP male mice than in the CHP mice. These data suggest that the immune changes observed in Swiss and Balb/C male CSP mice after cohabitation with a sick cagemate might, ultimately, depend on the changes induced by catecholamines, as previously reported for CSP female mice. However, contrary to that reported in Swiss CSP female mice, changes in behavioral and hypothalamic noradrenaline activity were not found in the Swiss CSP male mice analyzed in this work. This fact suggests that male and female CSP mice might use similar immune but different CNS strategies against the threats posed by the tumor-bearing animals.
[Mh] Termos MeSH primário: Carcinoma de Ehrlich/imunologia
Carcinoma de Ehrlich/psicologia
Comportamento Social
[Mh] Termos MeSH secundário: Glândulas Suprarrenais/patologia
Animais
Catecolaminas/sangue
Corticosterona/sangue
Comportamento Exploratório/fisiologia
Citometria de Fluxo
Abrigo para Animais
Hipotálamo/metabolismo
Masculino
Metoxi-Hidroxifenilglicol/metabolismo
Camundongos
Camundongos Endogâmicos BALB C
Transplante de Neoplasias
Neutrófilos/patologia
Norepinefrina/metabolismo
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Catecholamines); 534-82-7 (Methoxyhydroxyphenylglycol); W980KJ009P (Corticosterone); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170628
[Lr] Data última revisão:
170628
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161126
[St] Status:MEDLINE


  9 / 3209 MEDLINE  
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[PMID]:27567940
[Au] Autor:Sheng N; Yang J; Silm K; Edwards RH; Nicoll RA
[Ad] Endereço:Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, United States.
[Ti] Título:A slow excitatory postsynaptic current mediated by a novel metabotropic glutamate receptor in CA1 pyramidal neurons.
[So] Source:Neuropharmacology;115:4-9, 2017 Mar 15.
[Is] ISSN:1873-7064
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Slow excitatory postsynaptic currents (EPSCs) mediated by metabotropic glutamate receptors (mGlu receptors) have been reported in several neuronal subtypes, but their presence in hippocampal pyramidal neurons remains elusive. Here we find that in CA1 pyramidal neurons a slow EPSC is induced by repetitive stimulation while ionotropic glutamate receptors and glutamate-uptake are blocked whereas it is absent in the VGLUT1 knockout mouse in which presynaptic glutamate is lost, suggesting the slow EPSC is mediated by glutamate activating mGlu receptors. However, it is not inhibited by known mGlu receptor antagonists. These findings suggest that this slow EPSC is mediated by a novel mGlu receptor, and that it may be involved in neurological diseases associated with abnormal high-concentration of extracellular glutamate. This article is part of the Special Issue entitled 'Metabotropic Glutamate Receptors, 5 years on'.
[Mh] Termos MeSH primário: Região CA1 Hipocampal/fisiologia
Potenciais Pós-Sinápticos Excitadores/fisiologia
Receptores de Glutamato Metabotrópico/fisiologia
Proteína Vesicular 1 de Transporte de Glutamato/deficiência
[Mh] Termos MeSH secundário: Animais
Benzoatos/farmacologia
Região CA1 Hipocampal/efeitos dos fármacos
Antagonistas de Aminoácidos Excitatórios/farmacologia
Potenciais Pós-Sinápticos Excitadores/efeitos dos fármacos
Feminino
Glicina/análogos & derivados
Glicina/farmacologia
Masculino
Metoxi-Hidroxifenilglicol/análogos & derivados
Metoxi-Hidroxifenilglicol/farmacologia
Camundongos
Camundongos Knockout
Técnicas de Cultura de Órgãos
Ratos
Ratos Sprague-Dawley
Receptores de Glutamato Metabotrópico/antagonistas & inibidores
Proteína Vesicular 1 de Transporte de Glutamato/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzoates); 0 (Excitatory Amino Acid Antagonists); 0 (Receptors, Metabotropic Glutamate); 0 (Slc17a7 protein, mouse); 0 (Vesicular Glutamate Transport Protein 1); 146669-29-6 (alpha-methyl-4-carboxyphenylglycine); 534-82-7 (Methoxyhydroxyphenylglycol); CF5G2G268A (dihydroxyphenylethylene glycol); TE7660XO1C (Glycine)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170707
[Lr] Data última revisão:
170707
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160829
[St] Status:MEDLINE


  10 / 3209 MEDLINE  
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[PMID]:27461371
[Au] Autor:Aubrey KR; Drew GM; Jeong HJ; Lau BK; Vaughan CW
[Ad] Endereço:Pain Management Research Institute, Kolling Institute of Medical Research, Northern Clinical School, The University of Sydney and Royal North Shore Hospital, St. Leonards, New South Wales, Australia.
[Ti] Título:Endocannabinoids control vesicle release mode at midbrain periaqueductal grey inhibitory synapses.
[So] Source:J Physiol;595(1):165-178, 2017 Jan 01.
[Is] ISSN:1469-7793
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:KEY POINTS: The midbrain periaqueductal grey (PAG) forms part of an endogenous analgesic system which is tightly regulated by the neurotransmitter GABA. The role of endocannabinoids in regulating GABAergic control of this system was examined in rat PAG slices. Under basal conditions GABAergic neurotransmission onto PAG output neurons was multivesicular. Activation of the endocannabinoid system reduced GABAergic inhibition by reducing the probability of release and by shifting release to a univesicular mode. Blockade of endocannabinoid system unmasked a tonic control over the probability and mode of GABA release. These findings provides a mechanistic foundation for the control of the PAG analgesic system by disinhibition. ABSTRACT: The midbrain periaqueductal grey (PAG) has a crucial role in coordinating endogenous analgesic responses to physiological and psychological stressors. Endocannabinoids are thought to mediate a form of stress-induced analgesia within the PAG by relieving GABAergic inhibition of output neurons, a process known as disinhibition. This disinhibition is thought to be achieved by a presynaptic reduction in GABA release probability. We examined whether other mechanisms have a role in endocannabinoid modulation of GABAergic synaptic transmission within the rat PAG. The group I mGluR agonist DHPG ((R,S)-3,5-dihydroxyphenylglycine) inhibited evoked IPSCs and increased their paired pulse ratio in normal external Ca , and when release probability was reduced by lowering Ca . However, the effect of DHPG on the coefficient of variation and kinetics of evoked IPSCs differed between normal and low Ca . Lowering external Ca had a similar effect on evoked IPSCs to that observed for DHPG in normal external Ca . The low affinity GABA receptor antagonist TPMPA ((1,2,5,6-tetrahydropyridin-4-yl)methylphosphinic acid) inhibited evoked IPSCs to a greater extent in low than in normal Ca . Together these findings indicate that the normal mode of GABA release is multivesicular within the PAG, and that DHPG and lowering external Ca switch this to a univesicular mode. The effects of DHPG were mediated by mGlu5 receptor engagement of the retrograde endocannabinoid system. Blockade of endocannabinoid breakdown produced a similar shift in the mode of release. We conclude that endocannabinoids control both the mode and the probability of GABA release within the PAG.
[Mh] Termos MeSH primário: Endocanabinoides/fisiologia
Substância Cinzenta Periaquedutal/fisiologia
Sinapses/fisiologia
Ácido gama-Aminobutírico/fisiologia
[Mh] Termos MeSH secundário: Animais
Cálcio/fisiologia
Feminino
Antagonistas GABAérgicos/farmacologia
Técnicas In Vitro
Potenciais Pós-Sinápticos Inibidores/efeitos dos fármacos
Masculino
Metoxi-Hidroxifenilglicol/análogos & derivados
Metoxi-Hidroxifenilglicol/farmacologia
Substância Cinzenta Periaquedutal/efeitos dos fármacos
Ácidos Fosfínicos/farmacologia
Piperidinas/farmacologia
Pirazóis/farmacologia
Piridinas/farmacologia
Ratos Sprague-Dawley
Receptores de Glutamato Metabotrópico/agonistas
Receptores de Glutamato Metabotrópico/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 ((1,2,5,6-tetrahydropyridin-4-yl)methylphosphinic acid); 0 (Endocannabinoids); 0 (GABA Antagonists); 0 (Phosphinic Acids); 0 (Piperidines); 0 (Pyrazoles); 0 (Pyridines); 0 (Receptors, Metabotropic Glutamate); 3I4FA44MAI (AM 251); 534-82-7 (Methoxyhydroxyphenylglycol); 56-12-2 (gamma-Aminobutyric Acid); CF5G2G268A (dihydroxyphenylethylene glycol); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160728
[St] Status:MEDLINE
[do] DOI:10.1113/JP272292



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