Base de dados : MEDLINE
Pesquisa : A08.186.211.132.810.428.600.650.562.500 [Categoria DeCS]
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  1 / 12 MEDLINE  
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[PMID]:28574391
[Au] Autor:Gorgiladze T; Nozadze I; Abzianidze E; Tsagareli M
[Ad] Endereço:1Tbilisi State Medical University; 2Beritashvili Center for Experimental Biomedicine, Tbilisi Georgia.
[Ti] Título:NON-STEROIDAL ANTI-INFLAMMATORY DRUGS'S ANTINOCICEPTION MEDIATED BY THE OPIOID MECHANISM IN THE NUCLEUS RAPHE MAGNUS.
[So] Source:Georgian Med News;(265):99-104, 2017 Apr.
[Is] ISSN:1512-0112
[Cp] País de publicação:Georgia (Republic)
[La] Idioma:eng
[Ab] Resumo:It has been established that the midbrain periaqueductal gray matter (PAG) and rostral ventro-medial medulla (RVM) are involved in the descending pain control system. The latter involves the midline nucleus raphe magnus (NRM) and adjacent reticular formation. These brain structures are is one of important parts of CNS circuit that controls nociceptive transmission at the level of spinal cord. Here we report that microinjection of commonly used non-steroidal anti-inflammatory drugs (NSAIDs), diclofenac, ketorolac, metamizol, and xefocam into the NRM produces strong antinociception which is mediated by the opioid mechanism. The experiments were carried out on experimental and control (saline) white albino male rats. Animals were implanted with a guide cannula in the NRM and tested for antinociception following microinjection of NSAIDs into the NRM in the tail flick (TF) and hot plate (HP) tests. The analysis of variance (ANOVA) with post-hoc Tukey-Kramer multiple comparison tests were used for statistical evaluation. The obtained data show that microinjection of these NSAIDs into the NRM produced antinociception as revealed by a latency increase in the tail-flick (TF) and hot plate (HP) latencies compared to the saline control microinjected into the same nucleus. Furthermore, we definitely showed that pre-treatment with opioid antagonist naloxone in the NRM diminishes NSAID-induced antinociception expressing in significant decrease in TF and HP latencies (P<0.001). The present findings support the concept that antinociceptive effects of NSAIDs are mediated via an endogenous opioid system possibly involving the descending pain modulatory circuit.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/farmacologia
Naloxona/farmacologia
Antagonistas de Entorpecentes/farmacologia
Nociceptividade/efeitos dos fármacos
Núcleo Magno da Rafe/efeitos dos fármacos
Peptídeos Opioides/metabolismo
[Mh] Termos MeSH secundário: Animais
Diclofenaco/farmacologia
Dipirona/farmacologia
Cetorolaco/farmacologia
Masculino
Microinjeções
Núcleo Magno da Rafe/fisiologia
Piroxicam/análogos & derivados
Piroxicam/farmacologia
Ratos
Tempo de Reação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Narcotic Antagonists); 0 (Opioid Peptides); 13T4O6VMAM (Piroxicam); 144O8QL0L1 (Diclofenac); 36B82AMQ7N (Naloxone); 6429L0L52Y (Dipyrone); ER09126G7A (lornoxicam); YZI5105V0L (Ketorolac)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171110
[Lr] Data última revisão:
171110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170603
[St] Status:MEDLINE


  2 / 12 MEDLINE  
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[PMID]:27646288
[Au] Autor:Tao W; Zhou W; Wang Y; Sun T; Wang H; Zhang Z; Jin Y
[Ad] Endereço:Key Laboratory of Brain Function and Disease of Chinese Academy of Science and Collaborative Innovation Center of Chemistry for Life Sciences, Department of Biophysics and Neurobiology, University of Science and Technology of China, Hefei, Anhui 230027, China.
[Ti] Título:Histone deacetylase inhibitor-induced emergence of synaptic δ-opioid receptors and behavioral antinociception in persistent neuropathic pain.
[So] Source:Neuroscience;339:54-63, 2016 Dec 17.
[Is] ISSN:1873-7544
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The efficacy of opioids in patients with chronic neuropathic pain remains controversial. Although activation of δ-opioid receptors (DORs) in the brainstem reduces inflammation-induced persistent hyperalgesia, it is not effective under persistent neuropathic pain conditions and these clinical problems remain largely unknown. In this study, by using a chronic constriction injury (CCI) of the sciatic nerve in rats, we found that in the brainstem nucleus raphe magnus (NRM), DORs emerged on the surface membrane of central synaptic terminals on day 3 after CCI surgery and disappeared on day 14. Histone deacetylase (HDAC) inhibitors microinjected into the NRM in vivo increased the level of synaptosomal DOR protein and NRM infusion of DOR agonists producing an antinociceptive effect in a nerve growth factor (NGF) signaling-dependent manner. In vitro, in CCI rat slices incubated with HDAC inhibitors, DOR agonists significantly inhibited EPSCs. This effect was blocked by tyrosine receptor kinase A antagonists. Chromatin immunoprecipitation analysis revealed that NRM infusion of HDAC inhibitors in CCI rats increased the level of histone H4 acetylation at Ngf gene promoter regions. NGF was infused into the NRM or incubated CCI rat slices drove DORs to the surface membrane of synaptic terminals. Taken together, epigenetic upregulation of NGF activity by HDAC inhibitors in the NRM promotes the trafficking of DORs to pain-modulating neuronal synapses under neuropathic pain conditions, leading to δ-opioid analgesia. These findings indicate that therapeutic use of DOR agonists combined with HDAC inhibitors might be effective in chronic neuropathic pain managements.
[Mh] Termos MeSH primário: Analgésicos/farmacologia
Dor Crônica/tratamento farmacológico
Inibidores de Histona Desacetilases/farmacologia
Neuralgia/tratamento farmacológico
Receptores Opioides delta/metabolismo
Sinapses/metabolismo
[Mh] Termos MeSH secundário: Animais
Membrana Celular/efeitos dos fármacos
Membrana Celular/metabolismo
Dor Crônica/metabolismo
Modelos Animais de Doenças
Epigênese Genética
Histonas/metabolismo
Ácidos Hidroxâmicos/metabolismo
Masculino
Neuralgia/metabolismo
Núcleo Magno da Rafe/efeitos dos fármacos
Núcleo Magno da Rafe/metabolismo
Ratos Wistar
Receptores Opioides delta/agonistas
Nervo Isquiático/fisiopatologia
Sinapses/efeitos dos fármacos
Fatores de Tempo
Técnicas de Cultura de Tecidos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Analgesics); 0 (Histone Deacetylase Inhibitors); 0 (Histones); 0 (Hydroxamic Acids); 0 (Receptors, Opioid, delta); 3X2S926L3Z (trichostatin A)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161105
[St] Status:MEDLINE


  3 / 12 MEDLINE  
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[PMID]:26438555
[Au] Autor:Pei P; Liu L; Zhao L; Cui Y; Qu Z; Wang L
[Ad] Endereço:Acupuncture and Moxibustion Department, Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing, PR China.
[Ti] Título:Effect of electroacupuncture pretreatment at GB20 on behaviour and the descending pain modulatory system in a rat model of migraine.
[So] Source:Acupunct Med;34(2):127-35, 2016 Apr.
[Is] ISSN:1759-9873
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: While electroacupuncture (EA) pretreatment has been found to ameliorate migraine-like symptoms, the underlying mechanisms remain poorly understood. Emerging evidence suggests that the brainstem descending pain modulatory system, comprising the periaqueductal grey (PAG), raphe magnus nucleus (RMg), and trigeminal nucleus caudalis (TNC), may be involved in migraine pathophysiology. We hypothesised that EA would ameliorate migraine-like symptoms via modulation of this descending system. METHODS: We used a conscious rat model of migraine induced by repeated electrical stimulation of the dura. Forty male Sprague-Dawley rats were randomly assigned to one of four groups: an EA group, which received EA at GB20 following dural stimulation; a sham acupuncture (SA) group, which received manual acupuncture at a non-acupuncture point following dural stimulation; a Model group, which received dural stimulation but no acupuncture; and a Control group, which received neither dural stimulation nor acupuncture (electrode implantation only). HomeCageScan was used to measure effects on behaviour, and immunofluorescence staining was used to examine neural activation (c-Fos immunoreactivity) in the PAG, RMg, and TNC. RESULTS: Compared to the Model group, rats in the EA group showed a significant increase in exploratory, locomotor and eating/drinking behaviour (p<0.01) and a significant decrease in freezing-like resting and grooming behaviour (p<0.05). There was a significant increase in the mean number of c-Fos neurons in the PAG, RMg, and TNC in Model versus Control groups (p<0.001); however, this was significantly attenuated by EA treatment (p<0.001). There were no significant differences between the SA and Model groups in behaviour or c-Fos immunoreactivity. CONCLUSIONS: EA pretreatment ameliorates behavioural changes in a rat model of recurrent migraine, possibly via modulation of the brainstem descending pathways.
[Mh] Termos MeSH primário: Pontos de Acupuntura
Eletroacupuntura
Transtornos de Enxaqueca/terapia
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Ingestão de Alimentos
Seres Humanos
Locomoção
Masculino
Transtornos de Enxaqueca/fisiopatologia
Núcleo Magno da Rafe/fisiopatologia
Substância Cinzenta Periaquedutal/fisiopatologia
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151007
[St] Status:MEDLINE
[do] DOI:10.1136/acupmed-2015-010840


  4 / 12 MEDLINE  
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[PMID]:25953142
[Au] Autor:Insola A; Padua L; Mazzone P; Valeriani M
[Ad] Endereço:Unità Operativa di Neurofisiopatologia, CTO, Via S. Nemesio 21, 00145 Rome, Italy. Electronic address: angelo.insola@virgilio.it.
[Ti] Título:Low- and high-frequency subcortical SEP amplitude reduction during pure passive movement.
[So] Source:Clin Neurophysiol;126(12):2366-75, 2015 Dec.
[Is] ISSN:1872-8952
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: To investigate the effect of pure passive movement on both cortical and subcortical somatosensory evoked potentials (SEPs). METHODS: Median nerve SEPs were recorded in 8 patients suffering from Parkinson's disease (PD) and two patients with essential tremor. PD patients underwent electrode implantation in the subthalamic (STN) nucleus (3 patients) and pedunculopontine (PPTg) nucleus (5 patients), while 2 patients with essential tremor were implanted in the ventral intermediate nucleus (VIM) of the thalamus. In anesthetized patients, SEPs were recorded at rest and during a passive movement of the thumb of the stimulated wrist from the intracranial electrode contacts and from the scalp. Also the high-frequency oscillations (HFOs) were analyzed. RESULTS: Amplitudes of both deep and scalp components were decreased during passive movement, but the reduction was higher at cortical than subcortical level. Also the HFOs were reduced by movement. CONCLUSION: The different amount of the movement-related decrease suggests that the cortical SEP gating is not only the result of a subcortical somatosensory volley attenuation, but a further mechanism acting at cortical level should be considered. SIGNIFICANCE: Our results are important for understanding the physiological mechanism of the sensory-motor interaction during passive movement.
[Mh] Termos MeSH primário: Eletrodos Implantados
Potenciais Somatossensoriais Evocados/fisiologia
Movimento/fisiologia
Núcleo Magno da Rafe/fisiologia
Núcleo Subtalâmico/fisiologia
[Mh] Termos MeSH secundário: Idoso
Feminino
Seres Humanos
Masculino
Nervo Mediano/fisiologia
Meia-Idade
Doença de Parkinson/diagnóstico
Doença de Parkinson/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1603
[Cu] Atualização por classe:151121
[Lr] Data última revisão:
151121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150509
[St] Status:MEDLINE


  5 / 12 MEDLINE  
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[PMID]:25936842
[Au] Autor:Hauck M
[Ad] Endereço:Department of Neurology, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany; Department of Neurophysiology, University Medical Center Hamburg-Eppendorf, Germany.
[Ti] Título:Intracranial SEPs recordings - The new way to go?
[So] Source:Clin Neurophysiol;126(12):2251-2, 2015 Dec.
[Is] ISSN:1872-8952
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Mh] Termos MeSH primário: Eletrodos Implantados
Potenciais Somatossensoriais Evocados/fisiologia
Movimento/fisiologia
Núcleo Magno da Rafe/fisiologia
Núcleo Subtalâmico/fisiologia
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Masculino
[Pt] Tipo de publicação:COMMENT; EDITORIAL
[Em] Mês de entrada:1603
[Cu] Atualização por classe:151121
[Lr] Data última revisão:
151121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150505
[St] Status:MEDLINE


  6 / 12 MEDLINE  
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[PMID]:25933550
[Au] Autor:Condés-Lara M; Martínez-Lorenzana G; Rubio-Beltrán E; Rodríguez-Jiménez J; Rojas-Piloni G; González-Hernández A
[Ad] Endereço:Departamento de Neurobiología del Desarrollo y Neurofisiología, Instituto de Neurobiología, Universidad Nacional Autónoma de México, Campus UNAM-Juriquilla, México.
[Ti] Título:Hypothalamic paraventricular nucleus stimulation enhances c-Fos expression in spinal and supraspinal structures related to pain modulation.
[So] Source:Neurosci Res;98:59-63, 2015 Sep.
[Is] ISSN:1872-8111
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:The hypothalamic paraventricular nuclei (PVN) inhibits spinal nociception. Furthermore, projections from the PVN to other structures related to pain modulation exist, but a functional interaction has not yet been fully demonstrated. As an initial approach, we show here that PVN electric stimulation with the same parameters used to induce analgesia in rats enhances c-Fos expression not only in the dorsal horn of the spinal cord but also in the nucleus raphe magnus, locus coeruleus and the periaqueductal gray area. These results suggest that a functional interaction between these structures could occur, possibly to assure a mechanism of endogenous analgesia.
[Mh] Termos MeSH primário: Locus Cerúleo/metabolismo
Núcleo Magno da Rafe/metabolismo
Dor/metabolismo
Núcleo Hipotalâmico Paraventricular/fisiologia
Substância Cinzenta Periaquedutal/metabolismo
Proteínas Proto-Oncogênicas c-fos/metabolismo
Medula Espinal/metabolismo
[Mh] Termos MeSH secundário: Animais
Estimulação Elétrica
Masculino
Ratos Wistar
Corno Dorsal da Medula Espinal/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Proto-Oncogene Proteins c-fos)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:150803
[Lr] Data última revisão:
150803
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150503
[St] Status:MEDLINE


  7 / 12 MEDLINE  
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[PMID]:25852071
[Au] Autor:Tao W; Chen Q; Wang L; Zhou W; Wang Y; Zhang Z
[Ad] Endereço:Chinese Academy of Sciences Key Laboratory of Brain Function and Disease, Department of Neurobiology and Biophysics, University of Science and Technology of China, Hefei, Anhui, China.
[Ti] Título:Brainstem brain-derived neurotrophic factor signaling is required for histone deacetylase inhibitor-induced pain relief.
[So] Source:Mol Pharmacol;87(6):1035-41, 2015 Jun.
[Is] ISSN:1521-0111
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Our previous study demonstrated that persistent pain can epigenetically suppress the transcription of Gad2 [encoding glutamic acid decarboxylase 65 (GAD65)] and consequently impair the inhibitory function of GABAergic synapses in central pain-modulating neurons. This contributes to the development of persistent pain sensitization. Histone deacetylase (HDAC) inhibitors increased GAD65 activity considerably, restored GABA synaptic function, and rendered sensitized pain behavior less pronounced. However, the molecular mechanisms by which HDAC regulates GABAergic transmission through GAD65 under pain conditions are unknown. This work showed that HDAC inhibitor-induced increases in colocalization of GAD65 and synaptic protein synapsin I on the presynaptic axon terminals of the nucleus raphe magnus (NRM) were blocked by a TrkB receptor antagonist K252a [(9S,10R,12R)-2,3,9,10,11,12-hexahydro-10-hydroxy-9-methyl-1-oxo-9,12-epoxy-1H-diindolo[1,2,3-fg:3',2',1'-kl]pyrrolo[3,4-i][1,6]benzodiazocine-10-carboxylic acid methyl ester], indicating that BDNF-TrkB signaling may be required in GAD65 modulation of GABA synaptic function. At the brain-derived neurotrophic factor (BDNF) promoter, HDAC inhibitors induced significant increases in H3 hyperacetylation, consistent with the increase in BDNF mRNA and total proteins. Although exogenous BDNF facilitated GABA miniature inhibitory postsynaptic currents and GAD65 accumulation in NRM neuronal synapses in normal rats, it failed to do so in animals subjected to persistent inflammation. In addition, blockade of the TrkB receptor with K252a has no effect on miniature inhibitory postsynaptic currents and synaptic GAD65 accumulation under normal conditions. In addition, the analgesic effects of HDAC inhibitors on behavior were blocked by NRM infusion of K252a. These findings suggest that BDNF-TrkB signaling is required for drugs that reverse the epigenetic effects of chronic pain at the gene level, such as HDAC inhibitors.
[Mh] Termos MeSH primário: Analgésicos/farmacologia
Fator Neurotrófico Derivado do Encéfalo/metabolismo
Inibidores de Histona Desacetilases/farmacologia
Núcleo Magno da Rafe/efeitos dos fármacos
Dor/metabolismo
[Mh] Termos MeSH secundário: Analgésicos/uso terapêutico
Animais
Fator Neurotrófico Derivado do Encéfalo/genética
Carbazóis/farmacologia
Glutamato Descarboxilase/metabolismo
Inibidores de Histona Desacetilases/uso terapêutico
Ácidos Hidroxâmicos/farmacologia
Alcaloides de Indol/farmacologia
Inflamação/metabolismo
Masculino
Núcleo Magno da Rafe/metabolismo
Dor/tratamento farmacológico
Dor/fisiopatologia
Regiões Promotoras Genéticas
Ratos Wistar
Receptor trkB/antagonistas & inibidores
Receptor trkB/metabolismo
Transdução de Sinais
Sinapses/metabolismo
Sinapsinas/metabolismo
Ácido gama-Aminobutírico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Analgesics); 0 (Brain-Derived Neurotrophic Factor); 0 (Carbazoles); 0 (Histone Deacetylase Inhibitors); 0 (Hydroxamic Acids); 0 (Indole Alkaloids); 0 (Synapsins); 3X2S926L3Z (trichostatin A); 56-12-2 (gamma-Aminobutyric Acid); 58IFB293JI (vorinostat); 97161-97-2 (staurosporine aglycone); EC 2.7.10.1 (Receptor, trkB); EC 4.1.1.15 (Glutamate Decarboxylase); EC 4.1.1.15 (glutamate decarboxylase 2)
[Em] Mês de entrada:1507
[Cu] Atualização por classe:150508
[Lr] Data última revisão:
150508
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150409
[St] Status:MEDLINE
[do] DOI:10.1124/mol.115.098186


  8 / 12 MEDLINE  
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[PMID]:25701840
[Au] Autor:Zhu B; Chen Y; Zhang H; Liu X; Guo SW
[Ad] Endereço:Department of Obstetrics and Gynecology, The People's Hospital, Wenzhou, China.
[Ti] Título:Resveratrol Reduces Myometrial Infiltration, Uterine Hyperactivity, and Stress Levels and Alleviates Generalized Hyperalgesia in Mice With Induced Adenomyosis.
[So] Source:Reprod Sci;22(11):1336-49, 2015 Nov.
[Is] ISSN:1933-7205
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In this study, we sought to determine whether resveratrol (RSV), a nonhormonal compound, would suppress the myometrial infiltration, improve pain behavior, lower stress level, improve the expression of some proteins known to be involved in adenomyosis, and reduce uterine contractility in a mice model of adenomyosis. Adenomyosis was induced in 28 female ICR mice neonatally dosed with tamoxifen, while another 12 (group C) were dosed with solvent only, serving as a blank control. Starting from 4 weeks after birth, hotplate test was administrated to all mice every 4 weeks. At the 16th week, all mice with induced adenomyosis were randomly divided into 3 groups: low-dose RSV (2 mg/kg), high-dose RSV (3 mg/kg), and untreated. Group C received no treatment. After 3 weeks of treatment, they were hotplate tested again, their uterine horns and brains were harvested, and a blood sample was taken to measure the plasma corticosterone (CORT) level by enzyme-linked immunosorbent assay. The left uterine horn was used for immunohistochemistry analysis. The brain stem nucleus raphe magnus (NRM) sections were subjected to immunofluorescence staining for glutamic acid decarboxylase isoform 65 (GAD65). The depth of myometrial infiltration and uterine contractility was evaluated. We found that RSV is well tolerated and that it dose dependently suppressed myometrial infiltration, improved generalized hyperalgesia, reduced uterine contractility and lowered plasma CORT levels, and improved the expression of some proteins known to be involved in adenomyosis. It also elevated the number of GAD65-expressing neurons in the brain stem NRM, possibly boosting the GABAergic inhibition of pain due to adenomyosis. Therefore, RSV appears to be a promising compound for treating adenomyosis.
[Mh] Termos MeSH primário: Adenomiose/tratamento farmacológico
Hiperalgesia/tratamento farmacológico
Miométrio/efeitos dos fármacos
Estilbenos/farmacologia
Contração Uterina/efeitos dos fármacos
Útero/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adenomiose/induzido quimicamente
Adenomiose/metabolismo
Adenomiose/patologia
Adenomiose/fisiopatologia
Adenomiose/psicologia
Animais
Animais Recém-Nascidos
Comportamento Animal/efeitos dos fármacos
Análise por Conglomerados
Corticosterona/sangue
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Feminino
Glutamato Descarboxilase/metabolismo
Hiperalgesia/induzido quimicamente
Hiperalgesia/metabolismo
Hiperalgesia/fisiopatologia
Hiperalgesia/psicologia
Camundongos Endogâmicos ICR
Miométrio/metabolismo
Miométrio/patologia
Núcleo Magno da Rafe/efeitos dos fármacos
Núcleo Magno da Rafe/enzimologia
Limiar da Dor/efeitos dos fármacos
Fenótipo
Tempo de Reação
Tamoxifeno
Fatores de Tempo
Útero/metabolismo
Útero/patologia
Útero/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Stilbenes); 094ZI81Y45 (Tamoxifen); EC 4.1.1.15 (Glutamate Decarboxylase); EC 4.1.1.15 (glutamate decarboxylase 2); Q369O8926L (resveratrol); W980KJ009P (Corticosterone)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150222
[St] Status:MEDLINE
[do] DOI:10.1177/1933719115572479


  9 / 12 MEDLINE  
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[PMID]:25975144
[Au] Autor:Sinyakova NA; Kulikova EA; Kulikov AV
[Ti] Título:[Serotonin and dopamine brain metabolism in mice with different predisposition to catalepsy].
[So] Source:Zh Vyssh Nerv Deiat Im I P Pavlova;64(6):686-92, 2014 Nov-Dec.
[Is] ISSN:0044-4677
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:Catalepsy usually is caused by imbalance of dopamine (DA) and serotonin (5-HT) systems of brain. The aim of our work was to verify if this imbalance plays an important role in the mechanism of hereditary catalepsy in mice. Maintenance of DA, 5-HT and their main metabolites--5-hydroxyindoleacetic acid, 3,4-dihydroxyphenylacetic acid, homovanilic acid was determined in cortex, hypothalamus, hippocampus, striatum, substantia nigra and nuclei raphes in catalepsy-resistant AKR/J mice strain and catalepsy-prone CBA/LacJ mice strain and recombinant mice AKR/J.CBA-D13Mit76 (D13) strain. The latest strain was selected by transferring of a fragment of the chromosome 13 from CBA/LacJ carrying the main gene of hereditary catalepsy to AKR/J genome. There were no interstrain differences in concentration of biogenic amines and their metabolites in all brain regions. As a result of our work the hypothesis about the important role of 5-HT and/or DA systems of brain in the mechanism of hereditary catalepsy in mice was denied.
[Mh] Termos MeSH primário: Ácido 3,4-Di-Hidroxifenilacético/metabolismo
Catalepsia/metabolismo
Dopamina/metabolismo
Ácido Homovanílico/metabolismo
Ácido Hidroxi-Indolacético/metabolismo
Serotonina/metabolismo
[Mh] Termos MeSH secundário: Animais
Catalepsia/genética
Catalepsia/fisiopatologia
Córtex Cerebral/metabolismo
Córtex Cerebral/fisiopatologia
Corpo Estriado/metabolismo
Corpo Estriado/fisiopatologia
Cruzamentos Genéticos
Predisposição Genética para Doença
Hipocampo/metabolismo
Hipocampo/fisiopatologia
Hipotálamo/metabolismo
Hipotálamo/fisiopatologia
Masculino
Camundongos Endogâmicos AKR
Camundongos Endogâmicos CBA
Núcleo Accumbens/metabolismo
Núcleo Accumbens/fisiopatologia
Núcleo Magno da Rafe/metabolismo
Núcleo Magno da Rafe/fisiopatologia
Substância Negra/metabolismo
Substância Negra/fisiopatologia
[Pt] Tipo de publicação:ENGLISH ABSTRACT; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
102-32-9 (3,4-Dihydroxyphenylacetic Acid); 333DO1RDJY (Serotonin); 54-16-0 (Hydroxyindoleacetic Acid); VTD58H1Z2X (Dopamine); X77S6GMS36 (Homovanillic Acid)
[Em] Mês de entrada:1506
[Cu] Atualização por classe:150515
[Lr] Data última revisão:
150515
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150516
[St] Status:MEDLINE


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[PMID]:25107878
[Au] Autor:Benarroch EE
[Ad] Endereço:From the Department of Neurology, Mayo Clinic, Rochester, MN. benarroch.eduardo@mayo.edu.
[Ti] Título:Medullary serotonergic system: organization, effects, and clinical correlations.
[So] Source:Neurology;83(12):1104-11, 2014 Sep 16.
[Is] ISSN:1526-632X
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Esclerose Amiotrófica Lateral/metabolismo
Bulbo/metabolismo
Espasticidade Muscular/metabolismo
Vias Neurais/metabolismo
Dor/metabolismo
Neurônios Serotoninérgicos/metabolismo
Síndrome da Serotonina/metabolismo
Traumatismos da Medula Espinal/metabolismo
[Mh] Termos MeSH secundário: Morte Súbita
Seres Humanos
Espasticidade Muscular/etiologia
Núcleo Magno da Rafe/metabolismo
Núcleo Escuro da Rafe/metabolismo
Núcleo Pálido da Rafe/metabolismo
Receptores de Serotonina/metabolismo
Respiração
Serotonina/metabolismo
Traumatismos da Medula Espinal/complicações
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Serotonin); 333DO1RDJY (Serotonin)
[Em] Mês de entrada:1412
[Cu] Atualização por classe:140916
[Lr] Data última revisão:
140916
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:140810
[St] Status:MEDLINE
[do] DOI:10.1212/WNL.0000000000000806



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