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[PMID]:28326933
[Au] Autor:Wang CT; Mao CJ; Zhang XQ; Zhang CY; Lv DJ; Yang YP; Xia KL; Liu JY; Wang F; Hu LF; Xu GY; Liu CF
[Ad] Endereço:1 Department of Neurology and Suzhou Clinical Research Center of Neurological Disease, The Second Affiliated Hospital of Soochow University, Suzhou, China.
[Ti] Título:Attenuation of hyperalgesia responses via the modulation of 5-hydroxytryptamine signalings in the rostral ventromedial medulla and spinal cord in a 6-hydroxydopamine-induced rat model of Parkinson's disease.
[So] Source:Mol Pain;13:1744806917691525, 2017 Jan.
[Is] ISSN:1744-8069
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background Although pain is one of the most distressing non-motor symptoms among patients with Parkinson's disease, the underlying mechanisms of pain in Parkinson's disease remain elusive. The aim of the present study was to investigate the role of serotonin (5-hydroxytryptamine) in the rostral ventromedial medulla (RVM) and spinal cord in pain sensory abnormalities in a 6-hydroxydopamine-treated rat model of Parkinson's disease. Methods The rotarod test was used to evaluate motor function. The radiant heat test and von Frey test were conducted to evaluate thermal and mechanical pain thresholds, respectively. Immunofluorescence was used to examine 5-hydroxytryptamine neurons and fibers in the rostral ventromedial medulla and spinal cord. High-performance liquid chromatography was used to determine 5-hydroxytryptamine and 5-hydroxyindoleacetic acid levels. Results The duration of running time on the rotarod test was significantly reduced in 6-hydroxydopamine-treated rats. Nociceptive thresholds of both mechanical and heat pain were reduced compared to sham-treated rats. In addition to the degeneration of cell bodies and fibers in the substantia nigra pars compacta, the number of rostral ventromedial medulla 5-hydroxytryptamine neurons and 5-hydroxytryptamine fibers in the spinal dorsal horn was dramatically decreased. 5-Hydroxytryptamine concentrations in both the rostral ventromedial medulla and spinal cord were reduced. Furthermore, the administration of citalopram significantly attenuated pain hypersensitivity. Interestingly, Intra-rostral ventromedial medulla (intra-RVM) microinjection of 5,7-dihydroxytryptamine partially reversed pain hypersensitivity of 6-hydroxydopamine-treated rats. Conclusions These results suggest that the decreased 5-hydroxytryptamine contents in the rostral ventromedial medulla and spinal dorsal horn may be involved in hyperalgesia in the 6-hydroxydopamine-induced rat model of Parkinson's disease.
[Mh] Termos MeSH primário: Hiperalgesia/tratamento farmacológico
Hiperalgesia/etiologia
Bulbo/metabolismo
Doença de Parkinson/complicações
Serotonina/metabolismo
Transdução de Sinais/fisiologia
Medula Espinal/metabolismo
[Mh] Termos MeSH secundário: 5,7-Di-Hidroxitriptamina/uso terapêutico
Animais
Modelos Animais de Doenças
Indóis/metabolismo
Masculino
Bulbo/efeitos dos fármacos
Oxidopamina/toxicidade
Doença de Parkinson/etiologia
Doença de Parkinson/patologia
Ratos
Ratos Sprague-Dawley
Receptores Opioides mu/metabolismo
Serotoninérgicos/farmacologia
Inibidores da Captação de Serotonina/farmacologia
Medula Espinal/efeitos dos fármacos
Simpatolíticos/toxicidade
Tirosina 3-Mono-Oxigenase/metabolismo
Ácido gama-Aminobutírico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Indoles); 0 (Receptors, Opioid, mu); 0 (Serotonin Agents); 0 (Serotonin Uptake Inhibitors); 0 (Sympatholytics); 31363-74-3 (5,7-Dihydroxytryptamine); 333DO1RDJY (Serotonin); 56-12-2 (gamma-Aminobutyric Acid); 5SW11R7M7M (indole-3-lactic acid); 8HW4YBZ748 (Oxidopamine); EC 1.14.16.2 (Tyrosine 3-Monooxygenase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170323
[St] Status:MEDLINE
[do] DOI:10.1177/1744806917691525


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[PMID]:27805543
[Au] Autor:Todurga ZG; Gunduz O; Karadag CH; Ulugol A
[Ad] Endereço:Department of Medical Pharmacology, Faculty of Medicine,Trakya University,22030-Edirne,Turkey.
[Ti] Título:Descending serotonergic and noradrenergic systems do not regulate the antipruritic effects of cannabinoids.
[So] Source:Acta Neuropsychiatr;28(6):321-326, 2016 Dec.
[Is] ISSN:1601-5215
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: For centuries, cannabinoids have been known to be effective in pain states. Itch and pain are two sensations sharing a lot in common. OBJECTIVE: The goal of this research was to observe whether the cannabinoid agonist WIN 55,212-2 reduces serotonin-induced scratching behaviour and whether neurotoxic destruction of descending serotonergic and noradrenergic pathways mediate the antipruritic effect of WIN 55,212-2. Material and methods Scratching behaviour was induced by intradermal injection of serotonin (50 µg/50 µl/mouse) to Balb/c mice. The neurotoxins 5,7-dihydroxytryptamine (5,7-DHT, 50 µg/mouse) and 6-hydroxydopamine (6-OHDA, 20 µg/mouse) are applied intrathecally to deplete serotonin and noradrenaline in the spinal cord. WIN 55,212-2 (1, 3, 10 mg/kg, i.p.) dose-dependently attenuated serotonin-induced scratches. Neurotoxic destruction of neither the serotonergic nor the noradrenergic systems by 5,7-DHT and 6-OHDA, respectively, had any effect on the antipruritic action of WIN 55,212-2. CONCLUSION: Our findings indicate that cannabinoids dose-dependently reduce serotonin-induced scratching behaviour and neurotoxic destruction of descending inhibitory pathways does not mediate this antipruritic effect.
[Mh] Termos MeSH primário: Antipruriginosos/administração & dosagem
Benzoxazinas/administração & dosagem
Agonistas de Receptores de Canabinoides/administração & dosagem
Morfolinas/administração & dosagem
Naftalenos/administração & dosagem
Norepinefrina/fisiologia
Prurido/fisiopatologia
Serotonina/fisiologia
[Mh] Termos MeSH secundário: 5,7-Di-Hidroxitriptamina/administração & dosagem
Animais
Relação Dose-Resposta a Droga
Camundongos
Camundongos Endogâmicos BALB C
Vias Neurais/efeitos dos fármacos
Vias Neurais/fisiopatologia
Oxidopamina/administração & dosagem
Prurido/induzido quimicamente
Serotonina/administração & dosagem
Medula Espinal/efeitos dos fármacos
Medula Espinal/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antipruritics); 0 (Benzoxazines); 0 (Cannabinoid Receptor Agonists); 0 (Morpholines); 0 (Naphthalenes); 31363-74-3 (5,7-Dihydroxytryptamine); 333DO1RDJY (Serotonin); 5H31GI9502 (Win 55212-2); 8HW4YBZ748 (Oxidopamine); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170117
[Lr] Data última revisão:
170117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161103
[St] Status:MEDLINE


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[PMID]:27729269
[Au] Autor:Lucena F; Foletto V; Mascarin LZ; Tonussi CR
[Ad] Endereço:Department of Pharmacology, Federal University of Santa Catarina, Florianópolis, SC 88040-900, Brazil.
[Ti] Título:Analgesic and anti-edematogenic effects of oral trypsin were abolished after subdiaphragmatic vagotomy and spinal monoaminergic inhibition in rats.
[So] Source:Life Sci;166:60-65, 2016 Dec 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Rheumatoid arthritis brings great burdens to the patients. In addition to the highly expensive treatment, they are commonly associated with severe side effects. In such context, the research for safe and affordable treatments is needed. MAIN METHODS: Arthritis was induced by CFA (0.5mg/mL) in female wistar rats. Trypsin was given p.o. (2.95mg/kg; 2mL) 24h after the intra-articular CFA injection. Articular incapacitation was measured daily by counting the paw elevation time (PET; s) during 1-min periods of stimulated walk, throughout the 7-days after intra-articular CFA injection. Articular diameter (AD) was accessed just after each PET measurement, taken the difference between naïve and diseased knee-joint diameter (cm). KEY FINDINGS: The present study showed that orally administered trypsin was able to reduce nociception and edema, effects that could be observed throughout the evaluation period. These effect, however, were not observed in animals underwent subdiaphragmatic vagotomy, suggesting a vagal mediation for trypsin effects. Likewise, these effects were blocked in rats which received intrathecal injection of the neurotoxins 5,7-dihydroxytryptamine or 6-hydroxydopamine, suggesting the involvement of spinal amines from axon terminals. SIGNIFICANCE: The present study proposes that oral trypsin may cause vagal activation, followed by the activation of descending inhibitory pathways and such mechanism may lead to a novel approach for the treatment of arthritis.
[Mh] Termos MeSH primário: Analgésicos/uso terapêutico
Artrite Experimental/tratamento farmacológico
Artrite Reumatoide/tratamento farmacológico
Edema/tratamento farmacológico
Nociceptividade/efeitos dos fármacos
Tripsina/uso terapêutico
[Mh] Termos MeSH secundário: 5,7-Di-Hidroxitriptamina/administração & dosagem
5,7-Di-Hidroxitriptamina/farmacologia
Administração Oral
Adrenérgicos/administração & dosagem
Adrenérgicos/farmacologia
Analgésicos/administração & dosagem
Analgésicos/farmacologia
Animais
Artrite Experimental/complicações
Artrite Reumatoide/complicações
Edema/complicações
Feminino
Injeções Espinhais
Oxidopamina/administração & dosagem
Oxidopamina/farmacologia
Ratos Wistar
Serotoninérgicos/administração & dosagem
Serotoninérgicos/farmacologia
Tripsina/administração & dosagem
Tripsina/farmacologia
Vagotomia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic Agents); 0 (Analgesics); 0 (Serotonin Agents); 31363-74-3 (5,7-Dihydroxytryptamine); 8HW4YBZ748 (Oxidopamine); EC 3.4.21.4 (Trypsin)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170206
[Lr] Data última revisão:
170206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161013
[St] Status:MEDLINE


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[PMID]:27137992
[Au] Autor:Rysz M; Bromek E; Haduch A; Liskova B; Wójcikowski J; Daniel WA
[Ad] Endereço:Institute of Pharmacology, Polish Academy of Sciences, Smetna 12, 31-343 Kraków, Poland.
[Ti] Título:The reverse role of the hypothalamic paraventricular (PVN) and arcuate (ARC) nuclei in the central serotonergic regulation of the liver cytochrome P450 isoform CYP2C11.
[So] Source:Biochem Pharmacol;112:82-9, 2016 Jul 15.
[Is] ISSN:1873-2968
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Our recent work showed that the brain serotonergic system negatively regulated liver cytochrome P450. The aim of our present research was to study the effect of damage to the serotonergic innervation of the paraventricular (PVN) or arcuate nuclei (ARC) of the hypothalamus on the neuroendocrine regulation of cytochrome P450 (CYP). Male rats received bilateral injections of the serotonergic neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) into the PVN or ARC. One week after the injection brain neurotransmitters, serum hormones (growth hormone, testosterone, corticosterone, thyroid hormones), pituitary somatostatin and liver cytochrome P450 expression and activity were measured. Lesion of the serotonergic innervation of the PVN decreased serotonin level in the hypothalamic area containing the PVN, causing an increase in growth hormone and testosterone concentrations in the blood and, subsequently, an increase in the expression (mRNA and protein level) and activity of isoform CYP2C11 in the liver. In contrast, damage to the serotonergic innervation of the ARC, which caused a decrease in serotonin level in the hypothalamic area containing the ARC, reduced the concentration of growth hormone and the expression and activity of CYP2C11. In conclusion, the obtained results show a reverse effect of the serotonergic innervation of the hypothalamic paraventricular (a negative effect) and arcuate nuclei (a positive effect) on growth hormone secretion and growth hormone-dependent CYP2C11 expression. They also suggest that CYP2C11 expression may be changed by drugs acting via the serotonergic system, their effect depending on their mechanism of action, route of administration (intracerebral, peripheral) and distribution pattern within the hypothalamus.
[Mh] Termos MeSH primário: 5,7-Di-Hidroxitriptamina/farmacologia
Núcleo Arqueado do Hipotálamo/efeitos dos fármacos
Hidrocarboneto de Aril Hidroxilases/genética
Família 2 do Citocromo P450/genética
Fígado/efeitos dos fármacos
Núcleo Hipotalâmico Paraventricular/efeitos dos fármacos
Serotonina/metabolismo
Esteroide 16-alfa-Hidroxilase/genética
[Mh] Termos MeSH secundário: Animais
Núcleo Arqueado do Hipotálamo/metabolismo
Masculino
Núcleo Hipotalâmico Paraventricular/metabolismo
Hormônios Hipofisários/sangue
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Pituitary Hormones); 31363-74-3 (5,7-Dihydroxytryptamine); 333DO1RDJY (Serotonin); EC 1.14.14.1 (Aryl Hydrocarbon Hydroxylases); EC 1.14.14.1 (CYP2C11 protein, rat); EC 1.14.14.1 (Cytochrome P450 Family 2); EC 1.14.14.1 (Steroid 16-alpha-Hydroxylase)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170523
[Lr] Data última revisão:
170523
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160504
[St] Status:MEDLINE


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[PMID]:26821292
[Au] Autor:Tran L; Keele NB
[Ad] Endereço:Institute for Biomedical Studies, Baylor University, Waco, TX, USA.
[Ti] Título:CaMKIIα knockdown decreases anxiety in the open field and low serotonin-induced upregulation of GluA1 in the basolateral amygdala.
[So] Source:Behav Brain Res;303:152-9, 2016 Apr 15.
[Is] ISSN:1872-7549
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Hyperactivation of the amygdala is implicated in anxiety and mood disorders, but the precise underlying mechanisms are unclear. We previously reported that depletion of serotonin (5-hydroxytryptamine, 5-HT) in the basolateral nucleus of the amygdala (BLA) using the serotonergic neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) potentiated learned fear and increased glutamate receptor (Glu) expression in BLA. Here we investigated the hypothesis that CaMKII facilitates anxiety-like behavior and increased Glu/AMPA receptor subunit A1 (GluA1) expression following depletion of 5-HT in the BLA. Infusion of 5,7-DHT into the BLA resulted in anxiety-like behavior in the open field test (OFT) and increased the phosphorylation of CaMKIIα (Thr-286) in the BLA. Knockdown of the CaMKIIα subunit using adeno-associated virus (AAV)-delivered shRNAi concomitantly attenuated anxiety-like behavior in the OFT and decreased GluA1 expression in the BLA. Our results suggest that the CaMKII signaling plays a key role in low 5-HT-induced anxiety and mood disturbances, potentially through regulation of GluA1 expression in the BLA.
[Mh] Termos MeSH primário: Ansiedade/metabolismo
Complexo Nuclear Basolateral da Amígdala/metabolismo
Quinase da Proteína Quinase Dependente de Cálcio-Calmodulina/metabolismo
Receptores de AMPA/metabolismo
Serotonina/metabolismo
[Mh] Termos MeSH secundário: 5,7-Di-Hidroxitriptamina/administração & dosagem
Animais
Ansiedade/induzido quimicamente
Masculino
Fosforilação
Ratos
Ratos Sprague-Dawley
Receptores de AMPA/genética
Serotoninérgicos/administração & dosagem
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Receptors, AMPA); 0 (Serotonin Agents); 0 (glutamate receptor ionotropic, AMPA 1); 31363-74-3 (5,7-Dihydroxytryptamine); 333DO1RDJY (Serotonin); EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinase Kinase)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170415
[Lr] Data última revisão:
170415
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160129
[St] Status:MEDLINE


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[PMID]:26476009
[Au] Autor:Johnson PL; Molosh A; Fitz SD; Arendt D; Deehan GA; Federici LM; Bernabe C; Engleman EA; Rodd ZA; Lowry CA; Shekhar A
[Ad] Endereço:Department of Anatomy & Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA; Department of Psychiatry, Institute of Psychiatric Research, Indiana University School of Medicine, Indianapolis, IN, USA; Stark Neurosciences Research Institute, Indiana University School of Medi
[Ti] Título:Pharmacological depletion of serotonin in the basolateral amygdala complex reduces anxiety and disrupts fear conditioning.
[So] Source:Pharmacol Biochem Behav;138:174-9, 2015 Nov.
[Is] ISSN:1873-5177
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The basolateral and lateral amygdala nuclei complex (BLC) is implicated in a number of emotional responses including conditioned fear and social anxiety. Based on previous studies demonstrating that enhanced serotonin release in the BLC leads to increased anxiety and fear responses, we hypothesized that pharmacologically depleting serotonin in the BLC using 5,7-dihydroxytryptamine (5,7-DHT) injections would lead to diminished anxiety and disrupted fear conditioning. To test this hypothesis, 5,7-DHT(a serotonin-depleting agent) was bilaterally injected into the BLC. Desipramine (a norepinephrine reuptake inhibitor) was systemically administered to prevent non-selective effects on norepinephrine. After 5days, 5-7-DHT-treated rats showed increases in the duration of social interaction (SI) time, suggestive of reduced anxiety-like behavior. We then used a cue-induced fear conditioning protocol with shock as the unconditioned stimulus and tone as the conditioned stimulus for rats pretreated with bilateral 5,7-DHT, or vehicle, injections into the BLC. Compared to vehicle-treated rats, 5,7-DHT rats had reduced acquisition of fear during conditioning (measured by freezing time during tone), also had reduced fear retrieval/recall on subsequent testing days. Ex vivo analyses revealed that 5,7-DHT reduced local 5-HT concentrations in the BLC by ~40% without altering local norepinephrine or dopamine concentrations. These data provide additional support for 5-HT playing a critical role in modulating anxiety-like behavior and fear-associated memories through its actions within the BLC.
[Mh] Termos MeSH primário: Tonsila do Cerebelo/metabolismo
Ansiedade/tratamento farmacológico
Ansiedade/psicologia
Condicionamento (Psicologia)/efeitos dos fármacos
Medo/efeitos dos fármacos
Medo/psicologia
Antagonistas da Serotonina/farmacologia
Serotonina/metabolismo
[Mh] Termos MeSH secundário: 5,7-Di-Hidroxitriptamina/farmacologia
Inibidores da Captação Adrenérgica/farmacologia
Tonsila do Cerebelo/efeitos dos fármacos
Animais
Sinais (Psicologia)
Desipramina/farmacologia
Eletrochoque
Relações Interpessoais
Masculino
Microinjeções
Ratos
Ratos Wistar
Serotoninérgicos/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Adrenergic Uptake Inhibitors); 0 (Serotonin Agents); 0 (Serotonin Antagonists); 31363-74-3 (5,7-Dihydroxytryptamine); 333DO1RDJY (Serotonin); TG537D343B (Desipramine)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:161101
[Lr] Data última revisão:
161101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151018
[St] Status:MEDLINE


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[PMID]:26467129
[Au] Autor:Muchacki R; Szkilnik R; Malinowska-Borowska J; Zelazko A; Lewkowicz L; Nowak PG
[Ad] Endereço:Beskid Oncology Center, John Paul II City Hospital in Bielsko-Biala, Poland.
[Ti] Título:Impairment in Pain Perception in Adult Rats Lesioned as Neonates with 5.7-Dihydroxytryptamine.
[So] Source:Adv Clin Exp Med;24(3):419-27, 2015 May-Jun.
[Is] ISSN:1899-5276
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Whereas some studies have demonstrated the essential role of 5-hydroxytryptamine (5-HT) in tramadol and acetaminophen analgesia, other research has presented conflicting results. To dispel doubts, some aspects of the involvement of 5-HT in the antinociceptive properties of these drugs remain to be clarified. OBJECTIVES: The aim of this study was to determine whether the serotoninergic system dysfunction produced by neonatal 5-HT lesion in rats may affect the antinociceptive effects of tramadol and acetaminophen administered in adulthood. MATERIAL AND METHODS: Three days after birth, the control rats were pretreated with desipramine HCl (20 mg/kg i.p.) 30 min before intraventricular saline--vehicle injection. A separate group received 5.7-DHT; 2×35 µg in each lateral ventricle. At the age of 8 weeks, 5-HT and 5-hydroxyidoleaceticacid (5-HIAA) concentrations were determined in the thalamus and spinal cord by an HPLC/ED method. The antinociceptive effects of tramadol (20 mg/kg i.p.) or acetaminophen (100 mg/kg i.p.) were evaluated by a battery of tests. RESULTS: 5.7-DHT lesioning was associated with a reduction in 5-HT and 5-HIAA content of the thalamus (>85% and >90%) and spinal cord (>58% and 70%). Neonatal 5.7-DHT treatment produced a significant reduction in the antinociceptive effect of tramadol in the hot plate, tail-immersion, paw withdrawal and writhing tests. In the formalin hind paw test, the results were ambiguous. 5-HT lesion was also associated with a decrease in the analgesic effect of acetaminophen in the hot plate and writhing tests. A similar relationship wasn't found in the other assessments conducted with the use of acetaminophen. CONCLUSIONS: The present study provides evidence that (1) an intact serotoninergic system is required for the adequate antinociceptive action of tramadol, and (2) the serotoninergic system exerts a negligible influence on acetaminophen-induced analgesia in rats. We hypothesize that similar abnormalities in nociception may occur in patients with 5-HT dysfunction (e.g. depression), so these results should be complied in analgesic dosage adjustment.
[Mh] Termos MeSH primário: 5,7-Di-Hidroxitriptamina/toxicidade
Acetaminofen/farmacologia
Analgésicos não Entorpecentes/farmacologia
Analgésicos Opioides/farmacologia
Percepção da Dor/efeitos dos fármacos
Dor/prevenção & controle
Medula Espinal/efeitos dos fármacos
Tálamo/efeitos dos fármacos
Tramadol/farmacologia
[Mh] Termos MeSH secundário: Fatores Etários
Animais
Animais Recém-Nascidos
Modelos Animais de Doenças
Ácido Hidroxi-Indolacético/metabolismo
Masculino
Dor/etiologia
Dor/metabolismo
Dor/fisiopatologia
Dor/psicologia
Medição da Dor
Ratos Wistar
Neurônios Serotoninérgicos/efeitos dos fármacos
Neurônios Serotoninérgicos/metabolismo
Serotonina/metabolismo
Medula Espinal/metabolismo
Medula Espinal/fisiopatologia
Tálamo/metabolismo
Tálamo/fisiopatologia
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Analgesics, Non-Narcotic); 0 (Analgesics, Opioid); 31363-74-3 (5,7-Dihydroxytryptamine); 333DO1RDJY (Serotonin); 362O9ITL9D (Acetaminophen); 39J1LGJ30J (Tramadol); 54-16-0 (Hydroxyindoleacetic Acid)
[Em] Mês de entrada:1511
[Cu] Atualização por classe:151015
[Lr] Data última revisão:
151015
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151016
[St] Status:MEDLINE
[do] DOI:10.17219/acem/23362


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[PMID]:26354844
[Au] Autor:Magnusson J; Cummings KJ
[Ad] Endereço:Department of Biomedical Sciences, College of Veterinary Medicine, University of Missouri, Columbia, Missouri.
[Ti] Título:Plasticity in breathing and arterial blood pressure following acute intermittent hypercapnic hypoxia in infant rat pups with a partial loss of 5-HT neurons.
[So] Source:Am J Physiol Regul Integr Comp Physiol;309(10):R1273-84, 2015 Nov 15.
[Is] ISSN:1522-1490
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The role of serotonin (5-HT) neurons in cardiovascular responses to acute intermittent hypoxia (AIH) has not been studied in the neonatal period. We hypothesized that a partial loss of 5-HT neurons would reduce arterial blood pressure (BP) at rest, increase the fall in BP during hypoxia, and reduce the long-term facilitation of breathing (vLTF) and BP following AIH. We exposed 2-wk-old, 5,7-dihydroxytryptamine-treated and controls to AIH (10% O2; n = 13 control, 14 treated), acute intermittent hypercapnia (5% CO2; n = 12 and 11), or acute intermittent hypercapnic hypoxia (AIHH; 10% O2, 5% CO2; n = 15 and 17). We gave five 5-min challenges of AIH and acute intermittent hypercapnia, and twenty ∼20-s challenges of AIHH to mimic sleep apnea. Systolic BP (sBP), diastolic BP, mean arterial pressure, heart rate (HR), ventilation (V̇e), and metabolic rate (V̇o2) were continuously monitored. 5,7-Dihydroxytryptamine induced an ∼35% loss of 5-HT neurons from the medullary raphe. Compared with controls, pups deficient in 5-HT neurons had reduced resting sBP (∼6 mmHg), mean arterial pressure (∼5 mmHg), and HR (56 beats/min), and experienced a reduced drop in BP during hypoxia. AIHH induced vLTF in both groups, reflected in increased V̇e and V̇e/V̇o2, and decreased arterial Pco2. The sBP of pups deficient in 5-HT neurons, but not controls, was increased 1 h following AIHH. Our data suggest that a relatively small loss of 5-HT neurons compromises resting BP and HR, but has no influence on ventilatory plasticity induced by AIHH. AIHH may be useful for reversing cardiorespiratory defects related to partial 5-HT system dysfunction.
[Mh] Termos MeSH primário: Pressão Sanguínea/fisiologia
Hipercapnia/metabolismo
Hipóxia/patologia
Fenômenos Fisiológicos Respiratórios
Neurônios Serotoninérgicos/fisiologia
Serotonina/metabolismo
[Mh] Termos MeSH secundário: 5,7-Di-Hidroxitriptamina/farmacologia
Animais
Animais Recém-Nascidos
Feminino
Frequência Cardíaca
Masculino
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
31363-74-3 (5,7-Dihydroxytryptamine); 333DO1RDJY (Serotonin)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:161126
[Lr] Data última revisão:
161126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150911
[St] Status:MEDLINE
[do] DOI:10.1152/ajpregu.00241.2015


  9 / 1268 MEDLINE  
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[PMID]:26073764
[Au] Autor:Vasudeva RK; Hobby AR; Kirby LG
[Ad] Endereço:Temple University School of Medicine, Center for Substance Abuse Research, 3500 North Broad St., Philadelphia, PA 19140, USA. Electronic address: tue49457@temple.edu.
[Ti] Título:Ethanol consumption in the Sprague-Dawley rat increases sensitivity of the dorsal raphe nucleus to 5,7-dihydroxytryptamine.
[So] Source:Behav Brain Res;295:35-44, 2015 Dec 15.
[Is] ISSN:1872-7549
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Alcoholism afflicts 1 in 13 US adults, and comorbidity with depression is common. Levels of serotonin (5-HT) metabolites in alcoholic or depressed humans and rat strains are lower compared to healthy counterparts. Rats bred for ethanol (EtOH) preference are common in EtOH studies, however out-bred strains better model the range of EtOH consumption in humans. We examined voluntary EtOH consumption in out-bred Sprague-Dawley (SD) rats placed in the 20% EtOH intermittent access drinking paradigm (IA). Acquisition of 20% EtOH consumption (g EtOH/kg/24h) was assessed during the first 6-8 weeks of IA. Rats naturally separated into two groups (Drinkers or Non-drinkers) based on EtOH intake above or below 0.5 g/kg/24h prior to treatment intervention. We examined the effect of central 5-HT depletion on EtOH consumption by infusing 5,7-dihyroxytryptamine (5,7-DHT; i.c.v., 200-300 µg) or vehicle and measured EtOH consumption for 4 weeks post-operatively in IA. Compared to baseline, there was no effect of vehicle or 5,7-DHT on EtOH consumption during the post-operative period. Quantification of 5-HT depletion in the dorsal raphe nucleus (DRN) using tryptophan hydroxylase-2 (TPH2) immunohistochemistry resulted in a 76% decrease in staining with 5,7-DHT treatment. Interestingly, preservation of the ventromedial (VM) sub-regions was evident in all animals treated with 5,7-DHT, regardless of drinking behavior. In addition, Drinkers treated with 5,7-DHT had significantly more TPH2 depletion in the DRN compared to Non-drinkers. Our findings indicate that out-bred SD rats exhibit a natural EtOH consumption behavior (Drinker or Non-drinker) that is stable across time and independent of 5-HT depletion in the CNS. In addition, rats that regularly consumed >0.5 g EtOH/kg had greater sensitivity to 5,7-DHT in the DRN, indicating an interaction between EtOH and sensitivity of DRN 5-HT cells to neurotoxic substances. This may contribute to the dysfunctionality of the 5-HT system in alcoholic humans and lead to a better understanding of current pharmacological treatments for this addiction.
[Mh] Termos MeSH primário: 5,7-Di-Hidroxitriptamina/farmacologia
Núcleo Dorsal da Rafe/efeitos dos fármacos
Etanol/farmacologia
[Mh] Termos MeSH secundário: Consumo de Bebidas Alcoólicas/metabolismo
Animais
Núcleo Dorsal da Rafe/metabolismo
Masculino
Ratos
Ratos Sprague-Dawley
Serotonina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
31363-74-3 (5,7-Dihydroxytryptamine); 333DO1RDJY (Serotonin); 3K9958V90M (Ethanol)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:170813
[Lr] Data última revisão:
170813
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150616
[St] Status:MEDLINE


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[PMID]:26059263
[Au] Autor:Rysz M; Bromek E; Haduch A; Sadakierska-Chudy A; Daniel WA
[Ad] Endereço:Institute of Pharmacology, Polish Academy of Sciences, Kraków, Poland.
[Ti] Título:Damage to the Brain Serotonergic System Increases the Expression of Liver Cytochrome P450.
[So] Source:Drug Metab Dispos;43(9):1345-52, 2015 Sep.
[Is] ISSN:1521-009X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Genes coding for cytochrome P450 are regulated by endogenous hormones such as the growth hormone, corticosteroids, thyroid, and sex hormones. Secretion of these hormones is regulated by the respective hypothalamus-pituitary-secretory organ axes. Since the brain sends its serotonergic projections from the raphe nuclei to the hypothalamus, we have assumed that damage to these nuclei may affect the neuroendocrine regulation of cytochrome P450 expression in the liver. Thereby, 5,7-dihydroxytryptamine (5,7-DHT), a serotonergic neurotoxin, was injected into the dorsal and median raphe nuclei of male Wistar rats. Ten days after the neurotoxin injections, the brain concentrations of neurotransmitters, serum hormone, and cytokine levels, as well as the expression of cytochrome P450 in the liver were measured. Injection of 5,7-DHT decreased serotonin concentration in the brain followed by a significant rise in the levels of the growth hormone, corticosterone, and testosterone, and a drop in triiodothyronine concentration in the serum. No changes in interleukin (IL) levels (IL-2 and IL-6) were observed. Simultaneously, the activity and protein level of liver CYP1A, CYP3A1, and CYP2C11 rose (the activity of CYP2A/2B/2C6/2D was not significantly changed). Similarly, the mRNA levels of CYP1A1, CYP1A2, CYP2C11, and CYP3A1 were elevated. This is the first report demonstrating the effect of intracerebral administration of serotonergic neurotoxin on liver cytochrome P450. The obtained results indicate involvement of the brain serotonergic system in the neuroendocrine regulation of liver cytochrome P450 expression. The physiologic and pharmacological significance of the findings is discussed.
[Mh] Termos MeSH primário: 5,7-Di-Hidroxitriptamina/toxicidade
Sistema Enzimático do Citocromo P-450/metabolismo
Isoenzimas/metabolismo
Fígado/enzimologia
Serotonina/metabolismo
[Mh] Termos MeSH secundário: Animais
Encéfalo/efeitos dos fármacos
Encéfalo/metabolismo
Sistema Enzimático do Citocromo P-450/genética
Isoenzimas/genética
Masculino
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Isoenzymes); 31363-74-3 (5,7-Dihydroxytryptamine); 333DO1RDJY (Serotonin); 9035-51-2 (Cytochrome P-450 Enzyme System)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:150723
[Lr] Data última revisão:
150723
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150611
[St] Status:MEDLINE
[do] DOI:10.1124/dmd.115.064980



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