Base de dados : LILACS
Pesquisa : D27.505.519.625.240.300 [Categoria DeCS]
Referências encontradas : 13 [refinar]
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  1 / 13 LILACS  
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Baldisserotto, B
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Id: biblio-888962
Autor: Bianchini, AE; Garlet, QI; da Cunha, JA; Bandeira Junior, G; Brusque, ICM; Salbego, J; Heinzmann, BM; Baldisserotto, B.
Título: Monoterpenoids (thymol, carvacrol and S-(+)-linalool) with anesthetic activity in silver catfish (Rhamdia quelen): evaluation of acetylcholinesterase and GABAergic activity
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;50(12):e6346, 2017. tab, graf.
Idioma: en.
Resumo: This study evaluated the anesthetic potential of thymol and carvacrol, and their influence on acetylcholinesterase (AChE) activity in the muscle and brain of silver catfish (Rhamdia quelen). The AChE activity of S-(+)-linalool was also evaluated. We subsequently assessed the effects of thymol and S-(+)-linalool on the GABAergic system. Fish were exposed to thymol and carvacrol (25, 50, 75, and 100 mg/L) to evaluate time for anesthesia and recovery. Both compounds induced sedation at 25 mg/L and anesthesia with 50-100 mg/L. However, fish exposed to carvacrol presented strong muscle contractions and mortality. AChE activity was increased in the brain of fish at 50 mg/L carvacrol and 100 mg/L thymol, and decreased in the muscle at 100 mg/L carvacrol. S-(+)-linalool did not alter AChE activity. Anesthesia with thymol was reversed by exposure to picrotoxin (GABAA antagonist), similar to the positive control propofol, but was not reversed by flumazenil (antagonist of benzodiazepine binding site), as observed for the positive control diazepam. Picrotoxin did not reverse the effect of S-(+)-linalool. Thymol exposure at 50 mg/L is more suitable than carvacrol for anesthesia in silver catfish, because this concentration did not cause any mortality or interference with AChE activity. Thymol interacted with GABAA receptors, but not with the GABAA/benzodiazepine site. In contrast, S-(+)-linalool did not act in GABAA receptors in silver catfish.
Descritores: Acetilcolinesterase/metabolismo
Anestésicos/farmacologia
Peixes-Gato
Monoterpenos/farmacologia
Receptores de GABA-A/metabolismo
Timol/farmacologia
-Acetilcolinesterase/fisiologia
Adjuvantes Anestésicos/farmacologia
Análise de Variância
Anestesia/veterinária
Encéfalo/efeitos dos fármacos
Encéfalo/enzimologia
Peixes-Gato/metabolismo
Diazepam/farmacologia
Antagonistas GABAérgicos/farmacologia
Músculos/efeitos dos fármacos
Músculos/enzimologia
Óleos Voláteis/química
Picrotoxina/farmacologia
Receptores de GABA-A/fisiologia
Reprodutibilidade dos Testes
Estatísticas não Paramétricas
Fatores de Tempo
Limites: Animais
Tipo de Publ: Estudo de Avaliação
Responsável: BR1.1 - BIREME


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Id: lil-600698
Autor: Drumond, L. E; Kushmerick, C; Guidine, P. A. M; Doretto, M. C; Moraes, M. F. D; Massensini, A. R.
Título: Reduced hippocampal GABAergic function in Wistar audiogenic rats
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;44(10):1054-1059, Oct. 2011. ilus.
Idioma: en.
Resumo: Epilepsy is a neurological disorder associated with excitatory and inhibitory imbalance within the underlying neural network. This study evaluated inhibitory γ-amino-butyric acid (GABA)ergic modulation in the CA1 region of the hippocampus of male Wistar rats and Wistar audiogenic rats (aged 90 ± 3 days), a strain of inbred animals susceptible to audiogenic seizures. Field excitatory postsynaptic potentials and population spike complexes in response to Schaffer collateral fiber stimulation were recorded in hippocampal slices before and during application of picrotoxin (50 µM, 60 min), a GABA A antagonist, and the size of the population spike was quantified by measuring its amplitude and slope. In control audiogenic-resistant Wistar rats (N = 9), picrotoxin significantly increased both the amplitude of the population spike by 51 ± 19 percent and its maximum slope by 73 ± 21 percent. In contrast, in slices from Wistar audiogenic rats (N = 6), picrotoxin caused no statistically significant change in population spike amplitude (33 ± 46 percent) or slope (11 ± 29 percent). Data are reported as means ± SEM. This result indicates a functional reduction of GABAergic neurotransmission in hippocampal slices from Wistar audiogenic rats.
Descritores: Região CA1 Hipocampal/efeitos dos fármacos
Epilepsia/metabolismo
Antagonistas GABAérgicos/farmacologia
Picrotoxina/farmacologia
Transmissão Sináptica/efeitos dos fármacos
Ácido gama-Aminobutírico/metabolismo
-Região CA1 Hipocampal/metabolismo
Inibição Neural/efeitos dos fármacos
Inibição Neural/fisiologia
Ratos Wistar
Sinapses/efeitos dos fármacos
Sinapses/fisiologia
Limites: Animais
Masculino
Ratos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


  3 / 13 LILACS  
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Texto completo
Id: lil-505427
Autor: Margatho, L. O; Elias, L. L. K; Antunes-Rodrigues, J.
Título: GABA in the central amygdaloid nucleus modulates the electrolyte excretion and hormonal responses to blood volume expansion in rats
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;42(1):114-121, Jan. 2009. ilus.
Idioma: en.
Conferência: Apresentado em: Miguel R. Covian Symposium, 4, Ribeirão Preto, May 23-25, 2008.
Projeto: FAPESP; . CNPq.
Resumo: We investigated the involvement of GABAergic mechanisms of the central amygdaloid nucleus (CeA) in unanesthetized rats subjected to acute isotonic or hypertonic blood volume expansion (BVE). Male Wistar rats bearing cannulas unilaterally implanted in the CeA were treated with vehicle, muscimol (0.2 nmol/0.2 µL) or bicuculline (1.6 nmol/0.2 µL) in the CeA, followed by isotonic or hypertonic BVE (0.15 or 0.3 M NaCl, 2 mL/100 g body weight over 1 min). The vehicle-treated group showed an increase in sodium excretion, urinary volume, plasma oxytocin (OT), and atrial natriuretic peptide (ANP) levels compared to control rats. Muscimol reduced the effects of BVE on sodium excretion (isotonic: 2.4 ± 0.3 vs vehicle: 4.8 ± 0.2 and hypertonic: 4.0 ± 0.7 vs vehicle: 8.7 ± 0.6 µEq·100 g-1·40 min-1); urinary volume after hypertonic BVE (83.8 ± 10 vs vehicle: 255.6 ± 16.5 µL·100 g-1·40 min-1); plasma OT levels (isotonic: 15.3 ± 0.6 vs vehicle: 19.3 ± 1 and hypertonic: 26.5 ± 2.6 vs vehicle: 48 ± 3 pg/mL), and ANP levels (isotonic: 97 ± 12.8 vs vehicle: 258.3 ± 28.1 and hypertonic: 160 ± 14.6 vs vehicle: 318 ± 16.3 pg/mL). Bicuculline reduced the effects of isotonic or hypertonic BVE on urinary volume and ANP levels compared to vehicle-treated rats. However, bicuculline enhanced the effects of hypertonic BVE on plasma OT levels. These data suggest that CeA GABAergic mechanisms are involved in the control of ANP and OT secretion, as well as in sodium and water excretion in response to isotonic or hypertonic blood volume expansion.
Descritores: Tonsila do Cerebelo/efeitos dos fármacos
Bicuculina/farmacologia
Volume Sanguíneo/efeitos dos fármacos
Agonistas GABAérgicos/farmacologia
Antagonistas GABAérgicos/farmacologia
Muscimol/farmacologia
-Tonsila do Cerebelo/fisiologia
Fator Natriurético Atrial/sangue
Bicuculina/administração & dosagem
Volume Sanguíneo/fisiologia
Diurese/efeitos dos fármacos
Diurese/fisiologia
Agonistas GABAérgicos/administração & dosagem
Antagonistas GABAérgicos/administração & dosagem
Muscimol/administração & dosagem
Ocitocina/sangue
Ratos Wistar
Sódio/urina
Limites: Animais
Masculino
Ratos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


  4 / 13 LILACS  
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Texto completo
Id: lil-431562
Autor: Duarte, T. T; Corrêa, S. A. L; Santana, U. J; Pereira, A. S. F; Hoffmann, A.
Título: Agonistic-like responses from the torus semicircularis dorsalis elicited by GABA A blockade in the weakly electric fish Gymnotus carapo
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;39(7):945-955, July 2006. ilus.
Idioma: en.
Projeto: Fundação de Amparo à Pesquisa do Estado de São Paulo.
Resumo: Findings by our group have shown that the dorsolateral telencephalon of Gymnotus carapo sends efferents to the mesencephalic torus semicircularis dorsalis (TSd) and that presumably this connection is involved in the changes in electric organ discharge (EOD) and in skeletomotor responses observed following microinjections of GABA A antagonist bicuculline into this telencephalic region. Other studies have implicated the TSd or its mammalian homologue, the inferior colliculus, in defensive responses. In the present study, we explore the possible involvement of the TSd and of the GABA-ergic system in the modulation of the electric and skeletomotor displays. For this purpose, different doses of bicuculline (0.98, 0.49, 0.245, and 0.015 mM) and muscimol (15.35 mM) were microinjected (0.1 æL) in the TSd of the awake G. carapo. Microinjection of bicuculline induced dose-dependent interruptions of EOD and increased skeletomotor activity resembling defense displays. The effects of the two highest doses showed maximum values at 5 min (4.3 ± 2.7 and 3.8 ± 2.0 Hz, P < 0.05) and persisted until 10 min (11 ± 5.7 and 8.7 ± 5.2 Hz, P < 0.05). Microinjections of muscimol were ineffective. During the interruptions of EOD, the novelty response (increased frequency in response to sensory novelties) induced by an electric stimulus delivered by a pair of electrodes placed in the water of the experimental cuvette was reduced or abolished. These data suggest that the GABA-ergic mechanisms of the TSd inhibit the neural substrate of the defense reaction at this midbrain level.
Descritores: Comportamento Animal/fisiologia
Bicuculina/farmacologia
Gimnotiformes/fisiologia
Mesencéfalo/fisiologia
Muscimol/farmacologia
-Comportamento Animal/efeitos dos fármacos
Bicuculina/administração & dosagem
Mecanismos de Defesa
Interações Medicamentosas/fisiologia
Estimulação Elétrica
Órgão Elétrico/efeitos dos fármacos
Órgão Elétrico/fisiologia
Agonistas GABAérgicos/farmacologia
Antagonistas GABAérgicos/farmacologia
Microinjeções
Mesencéfalo/efeitos dos fármacos
Movimento/efeitos dos fármacos
Movimento/fisiologia
Muscimol/administração & dosagem
Vias Neurais/efeitos dos fármacos
Vias Neurais/fisiologia
Limites: Animais
Responsável: BR1.1 - BIREME


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Id: lil-319818
Autor: Donoso, A. O; Seltzer, A. M; Navarro, C. E; Cabrera, R. J; López, F. J; Negro-Vilar, A.
Título: Regulation of luteinizing hormone-releasing hormone and luteinizing hormone secretion by hypothalamic amino acids
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;27(4):921-932, Apr. 1994.
Idioma: en.
Resumo: 1. The present review discusses the proposed roles of the amino acids glutamate and GABA in the central regulation of luteinizing hormone-releasing hormone (LHRH) and in luteinizing hormone (LH) secretion. 2. Descriptions of the mechanisms of action of these neurotransmitters have focused on two diencephalic areas, namely, the preoptic-anterior hypothalamic area where the cell bodies of LHRH neurons are located, and the medial basal hypothalamus which contains the nerve endings of the LHRH system. Increasing endogenous GABA concentration by drugs, GABA agonists, or blockade of glutamatergic neurotransmission by selective antagonists in rats and non-human primates prevents ovulation and pulsatile LH release, and blunts the LH surges induced by estrogen or an estrogen-progesterone combination. In contrast, glutamate and different glutamate agonists such as NMDA, AMPA and kainate, can increase LHRH/LH secretion. 3. The simultaneous enhancement of glutamatergic activity and a decrease of GABAergic tone may positively influence the maturation of the pituitary-gonadal system in rats and non-human primates. Administration of glutamate receptor agonists has been shown to significantly advance the onset of puberty. Conversely, glutamate antagonists or increased endogenous GABA levels may delay the onset of puberty. The physiological regulation of LHRH/LH secretion may thus involve a GABA-glutamate interaction and a cooperative action of the various types of ionotropic glutamate receptors. 4. The inhibitory actions of GABA on LH release and ovulation may be exerted at the level of afferent nerve terminals that regulate LHRH secretion. A likely candidate is noradrenaline, as suggested by the synaptic connections between noradrenergic nerve terminals and GABAergic interneurons in the preoptic area. Recent experiments have provided complementary evidence for the physiological balance between inhibitory and excitatory transmission resulting in modulation of the action of noradrenaline to evoke LHRH release.
Descritores: Ácido gama-Aminobutírico/fisiologia
Glutamatos
Hormônio Liberador de Gonadotropina
Hipotálamo
Hormônio Luteinizante
-Ácido gama-Aminobutírico/farmacologia
Antagonistas de Aminoácidos Excitatórios
Antagonistas GABAérgicos
Glutamatos
Hormônio Liberador de Gonadotropina
Hipotálamo/efeitos dos fármacos
Hormônio Luteinizante
Norepinefrina
Receptores de GABA
Receptores de Glutamato
Maturidade Sexual
Limites: Animais
Masculino
Feminino
Ratos
Responsável: BR1.1 - BIREME


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Id: lil-312325
Autor: Abud Mendoza, Carlos; Moreno Valdés, R; Wade, C; Cuevas Orta, E.
Título: GAbapentina (Gp): una herramienta útil en el tratamiento del dolor en pacientes con fibromialgia (FM): informe preliminar / Gabapentine as a tool for treating pain in fybromialgia patients
Fonte: Rev. mex. reumatol;16(6):367-371, nov.-dic. 2001. tab, graf.
Idioma: es.
Resumo: Introducción: La fibromialgia (FM) tiene una prevalencia del 2 por ciento en la población general, y es una de las causas principales de dolor musculoesquelético crónico. La gabapentina (Gp) es un fármaco de utilidad para el dolor neuropático. Recientemente se han implicado algunas alteraciones del sistema nervioso autónomo en la fisiopatología de la FM. La Gp pudiera ser útil en el control del dolor en esta enfermedad. Objetivo: Evaluar la eficacia de Gp en pacientes con FM. Pacientes y métodos: Estudio piloto, prospectivo, en pacientes con FM de acuerdo con los criterios establecidos por el Colegio Americano de Reumatología (CAR). Todos los pacientes se evaluaron clínicamente; se registraron al inicio y a las 6 semanas de tratamiento: 1) Escala visual análoga del dolor (EVA); 2) Inventario de Beck para la depresión y 3) Número de puntos dolorosos (IPD) de 0 a 18. Se administró Gp de 900 a 1200 mg/d al tratamiento previo de cada paciente. El análisis estadístico fue mediante prueba de Wilcoxon. Resultados: Incluimos a 16 mujeres de 15 a 78 años de edad (promedio 44). Dos pacientes se excluyeron por no adhesión al tratamiento; 7/14 restantes (50 por ciento) tuvieron FM asociada a otra enfermedad reumática. La respuesta fue significativamente mejor en el grupo Gp (p<0.05). El tratamiento previo consistió en fluoxetina (4 pacientes), amitriptilina (2), analgésico (1), AINE (10), prednisona (3), metotrexato (4) y 3 no recibían tratamiento previo. Cinco pacientes tuvieron eventos adversos que no ameritaron la suspensión del tratamiento. Conclusión: La Gp ya sea como monoterapia o como terapia concomitante, es de utilidad en el tratamiento a corto plazo en pacientes con FM. Requerimos de estudios controlados, doble ciego y a largo plazo, para definir el papel de la Gp en la FM, así como dosis y duración del tratamiento.
Descritores: Fibromialgia
Antagonistas GABAérgicos
Dor
-Doenças Reumáticas/tratamento farmacológico
Limites: Humanos
Feminino
Adolescente
Adulto
Pessoa de Meia-Idade
Responsável: MX1.1 - CENIDSP - Centro de Información para Decisiones en Salud Pública


  7 / 13 LILACS  
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Id: lil-307313
Autor: Martinez-Villa, Eduardo; Irimia-Sierra, P; Gallego-Culleré, J.
Título: Situación actual de la neuroprotección en el ictus / Current situation of neuroprotection in stroke
Fonte: Acta neurol. colomb;16(1):52-65, jan. 2000.
Idioma: es.
Resumo: La isquemia cerebral focal o global representa en los países desarrollados una de las causas más importantes de muerte y deterioro neurológico. Las dos orientaciones terapéuticas más importantes en el paciente con isquemia cerebral aguda consisten en mejorar el flujo sanguíneo cerebral y reducir o bloquear las consecuencias metabólicas a nivel subcelular y celular. Los importantes avances producidos en la última década en el conocimiento de los mecanismos fisiopatológicos de la isquemia cerebral y en el desarrollo de nuevos fármacos ha planteado expectativas reales de tratamiento y el rechazo de actitudes nihilistas. Se revisan las nuevas tendencias en neuroprotección en isquemia cerebral focal y los resultados de los ensayos clínicos publicados
Descritores: Isquemia Encefálica
Bloqueadores dos Canais de Cálcio
Canais de Cálcio
Antagonistas GABAérgicos
Gangliosídeos
Canais Iônicos
Responsável: CO5.1 - Centro de Información y Conocimiento


  8 / 13 LILACS  
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Id: lil-292195
Autor: Santiago Avila, Marco Aurelio; Garfías Arvizu, Alfonso; Cobos Zapiaín, Guillermo; Islas Marroquín, Jorge.
Título: Efecto de la aplicación de penicilina cristalina en el núcleo caudado en procesos de comportamiento condicionado en ratas / Results of crystalline penicillin application in nucleus caudatus in modification of conditioning behaviour in rats
Fonte: Rev. sanid. mil;54(5):240-3, sept.-oct. 2000. ilus, graf.
Idioma: es.
Resumo: Se estudió el papel que tiene el GABA presente en el núcleo caudado (NC), en la retención de una prueba de prevención pasiva, aplicando de manera bilateral una dosis de penicilina sódica cristalina (500 UI/µ). La aplicación se llevó a cabo dos minutos después de la fase de adquisición de una tarea de inhibición en una caja de dos compartimientos. Veinticuatro y 48 horas después, se midió la latencia de retención (LR). A las 24 horas, las LR fueron en promedio de 598 ñ 3.3 s para el control íntegro (CI) y para el control solución salina (CSS) fue de 505.4 ñ 119.5, mientras que para el grupo experimental (GE) fue de 319 ñ 125.6 s. A las 48 horas esta latencia fue de 600 s para el CI y el grupo CSS, mientras que para el GE fue de 25 ñ 5.64 s. El procesamiento estadístico demuestra que a las 24 horas, existe diferencia estadísticamente significativa (p < 0.05) entre el grupo CI y los grupos CSS y GE, este efecto es probablemente secundario al efecto mecánico por la aplicación de la solución salina. A las 48 horas, no hay diferencia significativa (p > 0.05) entre los grupos CI y CSS, pero entre éstos y el grupo GE es significativa (p < 0.05), lo que puede estar dado por el disturbio eléctrico producido por la penicilina y que implica que la actividad GABAérgica de alguna manera se encuentra involucrada en los procesos de aprendizaje y memoria a largo plazo.
Descritores: Antagonistas GABAérgicos
Aprendizagem/efeitos dos fármacos
Núcleo Caudado
Penicilinas/efeitos adversos
-Memória/efeitos dos fármacos
Limites: Animais
Ratos
Masculino
Responsável: MX1.1 - CENIDSP - Centro de Información para Decisiones en Salud Pública


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Texto completo SciELO Brasil
Texto completo
Id: lil-281622
Autor: Yokoro, C. M; Pesquero, S. M. S; Turchetti-Maia, R. M. M; Francischi, J. N; Tatsuo, M. A. K. F.
Título: Acute phenobarbital administration induces hyperalgesia: pharmacological evidence for the involvement of supraspinal GABA-A receptors
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;34(3):397-405, Mar. 2001. ilus.
Idioma: en.
Resumo: The aim of the present study was to determine if phenobarbital affects the nociception threshold. Systemic (1-20 mg/kg) phenobarbital administration dose dependently induced hyperalgesia in the tail-flick, hot-plate and formalin tests in rats and in the abdominal constriction test in mice. Formalin and abdominal constriction tests were the most sensitive procedures for the detection of hyperalgesia in response to phenobarbital compared with the tail-flick and hot-plate tests. The hyperalgesia induced by systemic phenobarbital was blocked by previous administration of 1 mg/kg ip picrotoxin or either 1-2 mg/kg sc or 10 ng icv bicuculline. Intracerebroventricular phenobarbital administration (5 æg) induced hyperalgesia in the tail-flick test. In contrast, intrathecal phenobarbital administration (5 æg) induced antinociception and blocked systemic-induced hyperalgesia in this test. We suggest that phenobarbital may mediate hyperalgesia through GABA-A receptors at supraspinal levels and antinociception through the same kind of receptors at spinal levels
Descritores: Hiperalgesia/fisiopatologia
Hipnóticos e Sedativos/administração & dosagem
Fenobarbital/administração & dosagem
Receptores de GABA-A/efeitos dos fármacos
Medula Espinal/efeitos dos fármacos
-Análise de Variância
Bicuculina/farmacologia
Relação Dose-Resposta a Droga
Antagonistas GABAérgicos/farmacologia
Hiperalgesia/induzido quimicamente
Atividade Motora/efeitos dos fármacos
Medição da Dor
Picrotoxina/farmacologia
Ratos Sprague-Dawley
Limites: Animais
Masculino
Ratos
Camundongos
Responsável: BR1.1 - BIREME


  10 / 13 LILACS  
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Fotocópia
Id: lil-269811
Autor: Velasco Venegas, Maritza.
Título: Neuropatía diabética / Diabetic neuropathy
Fonte: Dolor;5(23):10-3, dic. 1997. tab.
Idioma: es.
Descritores: Neuropatias Diabéticas/tratamento farmacológico
-Antagonistas GABAérgicos/uso terapêutico
Neuropatias Diabéticas/classificação
Estimulação Elétrica Nervosa Transcutânea
Limites: Humanos
Responsável: CL10.1 - Biblioteca Biomédica



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