RESUMO
BACKGROUND: Early appearance of serotonin in the fetal brain and its effects on brain morphogenesis support its neurotrophic role. OBJECTIVE: To determine the presence of serotonergic cells and the expression of tryptophan-5-hydroxylase (TPH), 5-hydroxytryptamine (5-HT), serotonin transporter (SERT), 5-HT1A receptor and Pet-1 during the development of the cerebral cortex, both in situ and in tissue cultures. MATERIAL AND METHODS: A descriptive, observational study was carried out in pregnant Wistar rats. The presence of the plug was regarded as the beginning of gestation. On days 13, 16 and 17, cesarean sections were performed to obtain the fetuses, and the brains were then immediately dissected to identify the presence of serotonergic cells, TPH, 5-HT, SERT, 5-HT1A and Pet-1 in tissue cultures and in situ by immunostaining detected on a confocal microscope. RESULTS: Serotonergic cells and terminals were observed in the midbrain on day 17 of gestation, and in neopallium cocultures on days 13 and 16. TPH, 5-HT, SERT and Pet-1 immunopositive cells were also observed in the neopallium on day 12 of culture. CONCLUSIONS: The presence of serotonergic cells and other elements of the serotonergic system in the early cerebral cortex was confirmed, which may be transient and participate in cortical maturation processes during brain development.
ANTECEDENTES: La aparición temprana de serotonina en el cerebro fetal y sus efectos en la morfogénesis cerebral apoyan su papel neurotrófico. OBJETIVO: Determinar la presencia de células serotoninérgicas y la expresión de triptófano-5-hidroxilasa (TPH), 5-hidroxitriptamina (5-HT), transportador de serotonina (SERT), receptor 5-HT1A y Pet-1 durante el desarrollo de la corteza cerebral, tanto in situ como en cultivo de tejidos. MATERIAL Y MÉTODOS: Se realizó estudio observacional descriptivo en ratas Wistar preñadas. La presencia del tapón se consideró el inicio de la gestación; en los días 13, 16 y 17 se practicaron cesáreas para obtener los fetos e inmediatamente se disecaron los cerebros para identificar células serotoninérgicas, TPH, 5-HT, SERT, 5-HT1A y Pet-1 en cultivo de tejido e in situ mediante inmunomarcaje detectado en un microscopio confocal. RESULTADOS: Células y terminales serotoninérgicas fueron observadas en el mesencéfalo el día 17 de gestación y en cocultivos de neopalio los días 13 y 16. También se observaron células inmunopositivas a TPH, 5-HT, SERT y Pet-1 en el neopalio en el día 12 del cultivo. CONCLUSIONES: Se confirmó la presencia de células serotoninérgicas y otros elementos del sistema serotoninérgico en la corteza cerebral temprana, la cual puede ser transitoria y participar en los procesos de maduración cortical durante el desarrollo cerebral.
Assuntos
Neurônios , Serotonina , Animais , Feminino , Gravidez , Ratos , Córtex Cerebral/metabolismo , Feto/metabolismo , Neurônios/metabolismo , Ratos Wistar , Serotonina/metabolismo , Serotonina/farmacologia , Triptofano Hidroxilase/metabolismo , Triptofano Hidroxilase/farmacologia , Modelos AnimaisRESUMO
Resumen Antecedentes: La aparición temprana de serotonina en el cerebro fetal y sus efectos en la morfogénesis cerebral apoyan su papel neurotrófico. Objetivo: Determinar la presencia de células serotoninérgicas y la expresión de triptófano-5-hidroxilasa (TPH), 5-hidroxitriptamina (5-HT), transportador de serotonina (SERT), receptor 5-HT1A y Pet-1 durante el desarrollo de la corteza cerebral, tanto in situ como en cultivo de tejidos. Material y métodos: Se realizó estudio observacional descriptivo en ratas Wistar preñadas. La presencia del tapón se consideró el inicio de la gestación; en los días 13, 16 y 17 se practicaron cesáreas para obtener los fetos e inmediatamente se disecaron los cerebros para identificar células serotoninérgicas, TPH, 5-HT, SERT, 5-HT1A y Pet-1 en cultivo de tejido e in situ mediante inmunomarcaje detectado en un microscopio confocal. Resultados: Células y terminales serotoninérgicas fueron observadas en el mesencéfalo el día 17 de gestación y en cocultivos de neopalio los días 13 y 16. También se observaron células inmunopositivas a TPH, 5-HT, SERT y Pet-1 en el neopalio en el día 12 del cultivo. Conclusiones: Se confirmó la presencia de células serotoninérgicas y otros elementos del sistema serotoninérgico en la corteza cerebral temprana, la cual puede ser transitoria y participar en los procesos de maduración cortical durante el desarrollo cerebral.
Abstract Background: Early appearance of serotonin in the fetal brain and its effects on brain morphogenesis support its neurotrophic role. Objective: To determine the presence of serotonergic cells and the expression of tryptophan-5-hydroxylase (TPH), 5-hydroxytryptamine (5-HT), serotonin transporter (SERT), 5-HT1A receptor and Pet-1 during the development of the cerebral cortex, both in situ and in tissue cultures. Material and methods: A descriptive, observational study was carried out in pregnant Wistar rats. The presence of the plug was regarded as the beginning of gestation. On days 13, 16 and 17, cesarean sections were performed to obtain the fetuses, and the brains were then immediately dissected to identify the presence of serotonergic cells, TPH, 5-HT, SERT, 5-HT1A and Pet-1 in tissue cultures and in situ by immunostaining detected on a confocal microscope. Results: Serotonergic cells and terminals were observed in the midbrain on day 17 of gestation, and in neopallium cocultures on days 13 and 16. TPH, 5-HT, SERT and Pet-1 immunopositive cells were also observed in the neopallium on day 12 of culture. Conclusions: The presence of serotonergic cells and other elements of the serotonergic system in the early cerebral cortex was confirmed, which may be transient and participate in cortical maturation processes during brain development.
RESUMO
INTRODUCTION: Diabetes mellitus (DM) inhibits brain serotonin biosynthesis through changes in tryptophan-5-hydroxylase (TPH) activity and expression. OBJECTIVES: To determine whether DM-induced changes in brain TPH1 or TPH2 expression and in the number of serotonergic neurons return to normal in diabetic rats treated with insulin. METHODS: Rats with streptozotocin-induced diabetes were divided in two groups: one treated with insulin and the other without treatment. On day 14, brain stems were obtained in order to quantify L-tryptophan and 5-hydroxytryptamine levels, as well as to determine TPH activity. The expression of TPH1 and TPH2 by West-ern blot, and the number of serotonergic neurons by immunohistochemistry. RESULTS: In diabetic rats, a decrease in the levels of L-tryptophan, 5-hydroxytryptamine, and TPH activity was confirmed, as well as lower TPH1 and TPH2 expression and lower numbers of serotonergic neurons. When diabetic rats were treated with insulin, L-tryptophan returned to normal, but not 5-hy-droxytryptamine, TPH expression, or the number of serotonergic neurons. CONCLUSIONS: DM chronically inhibits the synthesis of brain 5-hydroxytryptamine through changes in TPH1 and TPH2 expression and a decrease in the number of serotonergic neurons, which persist despite insulin treatment.
INTRODUCCIÓN: La diabetes mellitus (DM) inhibe la biosíntesis de serotonina cerebral mediante cambios en la actividad y expresión de la triptófano-5-hidroxilasa (TPH). OBJETIVOS: Determinar si los cambios en la expresión de TPH1 o TPH2 cerebral y en el número de neuronas serotoninérgicas causados por la DM retornan a la normalidad en las ratas con diabetes tratadas con insulina. MÉTODOS: Ratas con diabetes inducida con estreptozotocina se dividieron en dos grupos: uno tratado con insulina y otro sin tratamiento. En el día 14, se obtuvieron tallos cerebrales para cuantificar niveles de L-triptófano, 5-hidroxitriptamina y la actividad de la TPH. La expresión de TPH1 y TPH2 fue mediante Western blot y el número de neuronas serotoninérgicas por inmunohistoquímica. RESULTADOS: En las ratas con diabetes se confirmó disminución de los niveles de L-triptófano, 5-hidroxitriptamina y la actividad de la TPH, así como una menor expresión de TPH1 y 2 y un menor número de neuronas serotoninérgicas. Cuando las ratas diabéticas fueron tratadas con insulina, el L-triptófano regreso a la normalidad, no así la 5-hidroxitriptamina, la expresión de TPH y el número de neuronas serotoninérgicas. CONCLUSIONES: La DM inhibe crónicamente la síntesis de 5-hidroxitriptamina cerebral mediante modificaciones en la expresión de TPH1 y TPH2 y disminución de las neuronas serotoninérgicas, que persisten a pesar del tratamiento con insulina.
Assuntos
Diabetes Mellitus Experimental , Serotonina , Animais , Ratos , Serotonina/metabolismo , Triptofano/metabolismo , Núcleos da Rafe/metabolismo , Neurônios Serotoninérgicos/metabolismo , Estreptozocina/metabolismo , Diabetes Mellitus Experimental/tratamento farmacológico , Diabetes Mellitus Experimental/metabolismo , Triptofano Hidroxilase/metabolismo , Encéfalo/metabolismo , Insulina/metabolismoRESUMO
Resumen Introducción: La diabetes mellitus (DM) inhibe la biosíntesis de serotonina cerebral mediante cambios en la actividad y expresión de triptófano-5-hidroxilasa (TPH). Objetivos: Determinar si los cambios en la expresión de TPH1 y TPH2 cerebral y en el número de neuronas serotoninérgicas causados por la DM retornan a la normalidad en ratas con diabetes tratadas con insulina. Métodos: Ratas con diabetes inducida con estreptozotocina se dividieron en dos grupos uno tratado con insulina y otro sin tratamiento. En el día 14, se obtuvieron tallos cerebrales para cuantificar niveles de L-triptófano, 5-hidroxitriptamina y la actividad de la TPH. La expresión de TPH1 y TPH2 fue mediante Western blot y el número de neuronas serotoninérgicas por inmunohistoquímica. Resultados: En las ratas con diabetes se confirmó disminución de los niveles de L-triptófano, 5-hidroxitriptamina y la actividad de la TPH, así como menor expresión de TPH1 y TPH2 y menor número de neuronas serotoninérgicas. Cuando las ratas diabéticas fueron tratadas con insulina, el L-triptófano regresó a la normalidad, no así la 5-hidroxitriptamina, la expresión de TPH ni el número de neuronas serotoninérgicas. Conclusiones: La DM inhibe crónicamente la síntesis de 5-hidroxitriptamina cerebral mediante modificaciones en la expresión de TPH1 y TPH2 y disminución de las neuronas serotoninérgicas, que persisten a pesar del tratamiento con insulina.
Abstract Introduction: Diabetes mellitus (DM) inhibits brain serotonin biosynthesis through changes in tryptophan-5-hydroxylase (TPH) activity and expression. Objectives: To determine whether DM-induced changes in brain TPH1 and TPH2 expression and in the number of serotonergic neurons return to normal in diabetic rats treated with insulin. Methods: Rats with streptozotocin-induced diabetes were divided in two groups: one treated with insulin and the other without treatment. On day 14, brain stems were obtained in order to quantify L-tryptophan and 5-hydroxytryptamine levels, as well as to determine TPH activity. The expressión of TPH1 and THP2 by Western blot, and the number of serotonergic neurons by immunohistochemistry. Results: In diabetic rats, a decrease in the levels of L-tryptophan, 5-hydroxytryptamine and TPH activity was confirmed, as well as lower TPH1 and TPH2 expression and lower numbers of serotonergic neurons. When diabetic rats were treated with insulin, L-tryptophan returned to normal, but not 5-hydroxytryptamine, TPH expression, or the number of serotonergic neurons. Conclusions: DM chronically inhibits the synthesis of brain 5-hydroxytryptamine through changes in TPH1 and TPH2 expression and a decrease in the number of serotonergic neurons, which persist despite insulin treatment.
RESUMO
This review aimed to describe and comment on how experimental intrauterine nutritional stress in animals produced some changes in tryptophan-5-hydroxylases (TPH) 1 and 2 in the brain and other key proteins such as plasma albumin, and how the intrauterine nutritional stress could produce long-lasting alterations in serotonin function in the brain of human infants.
El objetivo de esta revisión es describir y comentar cómo el estrés nutricional intrauterino experimental en animales produjo algunos cambios en las triptófano-5-hidroxilasas 1 y 2 en el cerebro y en otras proteínas clave, como la albúmina plasmática, y de qué manera el estrés nutricional intrauterino podría producir alteraciones duraderas en la función de la serotonina en el cerebro de lactantes.
Assuntos
Retardo do Crescimento Fetal , Serotonina , Animais , Encéfalo , HumanosRESUMO
This report describes the presence of Aedes albopictus Skuse (Diptera: Culicidae) in Yucatan Peninsula and represents the first record of the Asian tiger invasive mosquito in Campeche State, southeastern Mexico. We collected specimens using 11,326 ovitraps put into houses of urban and rural areas, as part of the entomological surveillance by the local Ministry of Health from January 2019 to February 2020. We found Ae. albopictus in five of the 12 municipalities of Campeche (San Francisco de Campeche, Tenabo, Hecelchakán, Calkíni and Escárcega). We record 68 positive ovitraps and 226 Ae. albopictus larvae. This finding increases the number of mosquito species recorded in Campeche, Mexico, and possibly the potential for 22 arbovirus transmission.
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Aedes/fisiologia , Distribuição Animal , Mosquitos Vetores/fisiologia , Aedes/crescimento & desenvolvimento , Animais , Larva/crescimento & desenvolvimento , Larva/fisiologia , México , Mosquitos Vetores/crescimento & desenvolvimentoRESUMO
BACKGROUND: The diabetic cardiomyopathy occurs in both type 1 and type 2 diabetes mellitus. Hyperglycemia and associated metabolic changes participate in the pathogenesis of this disease. OBJECTIVE: To characterizes various pathological changes occurring during the development of diabetic cardiomyopathy in rats. METHODS: Diabetic rats were used for streptozotocin administration. At 7, 14, 21 and 30 days after toxic administration, the heart was obtained and placed in a Hartman solution and 4% p-formaldehyde. Five-micrometer thick sections were stained with hematoxylin-eosin, Masson trichrome and immunocytochemistry using anti-ß-tubulin antibody. RESULTS: At 14 days after application of streptozotocin, dilated sinusoids with endothelial lining in the myocardium and collagen deposits in the cardiac interstitium and between the Purkinje fibers were observed. At 21 days there was a slight decrease of the arteriolar lumen due to hyperplasia of the medial layer. It is important to note that cardiac sinusoids as well as collagen deposits became more evident at 30 day of the study, as well as a major derangement of the microtubular system of the cardiomyocytes. CONCLUSIONS: Cardiac sinusoids representing fetal vascular pattern and interstitial fibrosis in the myocardium and the microtubular derangement of cardiomyocytes support the fact that the pathophysiological mechanism of diabetic cardiomyopathy begins in the coronary microcirculation due to changes in cardiac metabolism, contributing to the development of myocardial dysfunction in diabetes.
Antecedentes: la miocardiopatía diabética ocurre en ambos tipos de diabetes mellitus y en su patogenia intervienen la hiperglucemia y los cambios metabólicos asociados. Objetivo: caracterizar los diferentes cambios patológicos que aparecen durante la evolución de la miocardiopatía diabética en la rata. Material y métodos: estudio transversal comparativo en dos grupos de ratas diabéticas por la administración de estreptozotocina. A los 14, 21 y 30 días de la administración del tóxico se obtuvieron los corazones, que se colocaron en p-formaldehído al 4%. Se efectuaron cortes de 5 µm y se tiñeron con hematoxilina-eosina, tricrómica de Masson e inmunocitoquímica con anticuerpos anti ß-tubulina. Resultados: a los 14 días de la aplicación de la estreptozotocina se observaron en el miocardio sinusoides dilatadas y depósito de colágena entre las fibras de Purkinje e intersticio cardiaco. A los 21 días disminuyó la luz arteriolar por hiperplasia de la capa media. A los 30 días del estudio se hicieron más evidentes los sinusoides cardiacos y los depósitos de colágena y un importante desarreglo del sistema microtubular de los cardiomiocitos. Conclusiones: los sinusoides cardiacos, que representan un patrón vascular fetal y la fibrosis intersticial en el miocardio y el desarreglo microtubular de los cardiomiocitos, apoyan el hecho de que el mecanismo fisiopatológico de la miocardiopatía diabética se inicia en la microcirculación coronaria debido a cambios en el metabolismo cardiaco que contribuyen a la disfunción miocárdica durante el estado diabético.
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Cardiomiopatias/patologia , Complicações do Diabetes/patologia , Diabetes Mellitus Experimental/patologia , Animais , Glicemia/análise , Peso Corporal , Capilares/patologia , Cardiomiopatias/etiologia , Colágeno/análise , Circulação Coronária , Citoesqueleto/ultraestrutura , Angiopatias Diabéticas/patologia , Ingestão de Alimentos , Fibrose , Masculino , Microcirculação , Microtúbulos/ultraestrutura , Miócitos Cardíacos/patologia , Ratos , Ratos Wistar , Estreptozocina , Tubulina (Proteína)/análiseRESUMO
Introducción: El objetivo de este trabajo fue determinar la prevalencia de disfunción diastólica subclínica del ventrículo izquierdo (DDVI) y su asociación con el descontrol metabólico en adolescentes con diabetes tipo 1. Métodos: Se trató de un estudio en 53 adolescentes con diabetes tipo 1 en dos fases: primero, un estudio transversal descriptivo y, después de realizar un ecocardiograma, un transversal comparativo. Se consideró DDVI cuando tuvieron tres o más datos ecocardiográficos alterados: velocidad de contracción auricular (relación E/A), tiempo de desaceleración (TD), tiempo de relajación volumétrico (TRIVI) y función sistólica mayor de 50%. Además, se les determinaron los niveles de glucosa, de hemoglobina glucosilada y microalbuminuria. Resultados: El 16.98% de los adolescentes diabéticos mostraron datos ecocardiográficos de DDVI, y el 15.10% correspondió al sexo masculino. El patrón pseudonormalizado se observó en 7.54%, en relación con el 5.66% del patrón de alteración de la relajación y del 3.77% del restrictivo. Estos pacientes, además, mostraron mayor tiempo de la enfermedad, obesidad y un aumento en la glucemia, en la hemoglobina glucosilada y de la microalbuminuria. Conclusiones: La DDVI es una complicación frecuente en los adolescentes con diabetes tipo 1. Aquellos con DDVI presentaron con mayor frecuencia obesidad, mayor tiempo de evolución de la enfermedad y un peor control metabólico. Se propone que en estos pacientes se realice un diagnóstico oportuno y sistemático a través de un ecocardiograma.
Background: To determine the prevalence of subclinical left ventricular diastolic dysfunction (LVDD) and its association with metabolic control in adolescents with type 1diabetes. Methods: We carried out a study in 53 adolescents with type 1 diabetes in two phases: cross-sectional and after performing two-dimensional M-mode echocardiogram and color Doppler, a cross-sectional comparison. Subjects were divided into two groups: the first without LVDD and the second with LVDD. LVDD was considered when there were three or more alterations according to echocardiographic data (rate of atrial contraction, time of deceleration, time of volumetric relaxation) accompanied by systolic function >50%. We also determined glucose, hemoglobin, glycosylate, and microalbuminuria. Results: Of the adolescents with diabetes, 16.98% showed echocardiographic data of LVDD; 15.10% were male. Pseudonormalized pattern was observed in 7.54% compared to 5.66% with impaired relaxation pattern and 3.77% with restrictive pattern. Furthermore, there was a longer time of disease evolution, obesity and a significant increase of glycemia, glycosylated hemoglobin and microalbuminuria. Conclusions: LVDD is a frequent complication in adolescents with type 1 diabetes. Those with LVDD had a higher prevalence of obesity, longer time of disease, and poorer metabolic control. Therefore, we propose that a timely and systematic search with echocardiogram is important in patients with type 1 diabetes.
RESUMO
The aim of this study was to determine whether intrauterine malnutrition (IUM) produces a change in the expression of tryptophan-5-hydroxylase (TPH) 1 and/or 2 as the primary mechanism to explain the observed chronic cerebral acceleration of the synthesis of 5-hydroxytryptamine (5-HT). We used an IUM model and controls with ages of 1, 15 and 21 days. The brainstem was obtained to determine L-tryptophan, 5-HT and TPH activity. Expression of TPH1 and TPH2 via specific antibodies for each was also evaluated by immunocytochemistry and Western blot. Malnourished offspring had a significant elevation of L-Trp, TPH activity and 5-HT in the brainstem. Both isoforms (1 and 2) of TPH were expressed from birth in both groups; however, TPH1 expression was significantly higher in offspring with IUM in relation to the controls. Importantly, these malnourished offspring showed reduced expression of TPH2 compared to controls. It was confirmed that IUM produces an increase in 5-HT in the brainstem and also showed increased expression of TPH1 at birth, with decreased expression of TPH2. These findings together allow us to propose that chronic elevation of synthesis of 5-HT observed in the brain of the offspring with IUM is probably due to a change in the expression and activity of TPH1 induced from fetal life.
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Tronco Encefálico/metabolismo , Transtornos da Nutrição Fetal/patologia , Regulação da Expressão Gênica no Desenvolvimento/fisiologia , Triptofano Hidroxilase/metabolismo , Fatores Etários , Animais , Animais Recém-Nascidos , Peso Corporal/fisiologia , Tronco Encefálico/crescimento & desenvolvimento , Modelos Animais de Doenças , Feminino , Masculino , Gravidez , Ratos , Ratos Wistar , Serotonina/metabolismoRESUMO
The aim of this study was to determine the differences between two groups of adolescents with metabolic syndrome (MetS) and normal controls in relation to brain serotonergic activity through intensity-dependent auditory-evoked potentials (IDAEPs) and plasma free fraction of L-tryptophan. Eighteen adolescents with MetS and thirteen controls were studied. Free fraction, bound and total plasma L-tryptophan, glucose, cholesterol, triglycerides, HDL-cholesterol, albumin and IDAEPs were determined. Glycemia, triglycerides were significantly elevated, and HDL-cholesterol in plasma was significantly reduced. Free fraction and free fraction/total L-tryptophan ratio were decreased. The slope of the amplitude/stimulus intensity function of the N1/P2 component significantly increased in adolescents with MetS. Decrease of free fraction of L-tryptophan in plasma and increase of the slope of the N1/P2 component suggest a low brain serotonin tone. Cortex responses are regulated by serotonergic innervations and may show a different behavior in young patients with MetS. Therefore, the slope of the N1/P2 component along with the free fraction of L-tryptophan in plasma, indicate that in adolescents with MetS the state of serotonergic brain activity is depressed and possibly related to psychiatric disorders.
Assuntos
Potenciais Evocados Auditivos/fisiologia , Síndrome Metabólica , Serotonina/metabolismo , Triptofano/metabolismo , Adolescente , Córtex Auditivo/metabolismo , Córtex Auditivo/fisiologia , Glicemia/metabolismo , Química Encefálica , Criança , HDL-Colesterol/sangue , HDL-Colesterol/metabolismo , Estudos Transversais , Feminino , Humanos , Masculino , Síndrome Metabólica/metabolismo , Síndrome Metabólica/fisiopatologia , Triglicerídeos/sangue , Triglicerídeos/metabolismo , Triptofano/sangueRESUMO
The aim of this study was to determine whether intrauterine growth restriction produces an increase of dihydropteridine reductase activity as a compensatory mechanism that maintains the necessary concentration of cofactor, tetrahydrobiopterin, during accelerated brain serotonin biosynthesis. Intrauterine growth-restricted offspring and controls were used. On days 1, 10, 15 and 21 of life, the brainstem was dissected and l-tryptophan, serotonin, tryptophan-5-hydroxylase and dihydropteridine reductase activities were determined. Intrauterine growth-restricted pups showed a significant increase of l-tryptophan, 5-hydroxytryptamine, tryptophan-5-hydroxylase and also dihydropteridine activity in the brainstem in comparison to normal pups. These results confirm that intrauterine growth restriction produces an increase of serotonin biosynthesis in the brainstem. This is accompanied by an increase in dihydropteridine activity that appears to be a compensatory mechanism to maintain sufficient tetrahydrobiopterin for the donation of electrons during the accelerated synthesis of brain serotonin in intrauterine growth-restricted rats.
Assuntos
Tronco Encefálico/enzimologia , Di-Hidropteridina Redutase/metabolismo , Retardo do Crescimento Fetal , Animais , Biopterinas/análogos & derivados , Biopterinas/metabolismo , Restrição Calórica , Feminino , Masculino , Estado Nutricional , Gravidez , Ratos , Ratos Wistar , Serotonina/biossíntese , Triptofano Hidroxilase/metabolismoRESUMO
Objetivo: Caracterizar morfológica y bioquímicamente células productoras de serotonina durante el desarrollo del tejido cardiaco. Material y métodos: Se utilizaron ratas gestantes de la cepa Wistar. A los días 10, 12, 16 y 20 de gestación se obtuvieron los fetos por cesárea, a los cuales se les disecaron los corazones, que se fijaron para los ensayos de inmunohistoquímica para triptófano- 5-hidroxilasa (Tph), además se efectuó Western Blot para la enzima; se determinó la concentración de serotonina y la actividad de Tph por cromatografía de líquidos de alta resolución. Los resultados fueron analizados mediante U de Mann-Whitney, aceptando un nivel de significación de p < 0.05. Resultados: En los cortes de corazón fetal, desde el día 10 de gestación se observaron células inmunorreactivas para Tph, con metacromasia en su interior. Fibras nerviosas inmunorreactivas para la misma enzima que hacen contacto probablemente con las células serotoninérgicas. La actividad enzimática y la concentración de la serotonina aumentaron con la edad gestacional, además, se encontró la proteína enzimática por Western- Blot en el corazón fetal de 16 días de gestación. Conclusiones: Se demostró la presencia de células productoras de serotonina en el miocardio fetal, cuyo fenotipo corresponde a mastocitos cardiacos, lo cual sugiere que la serotonina puede ser importante en el desarrollo del tejido cardiaco y que también participa en los mecanismos fisiopatológicos de los defectos cardiacos estructurales o en la predisposición a enfermedades cardiovasculares en el adulto.
BACKGROUND: We undertook this study to present biochemical and morphological characterization of serotonergic cells during fetal heart development. METHODS: Wistar rats (10, 12, 16 and 20 days of gestation) were used. After obtaining the fetuses by Cesarean section, the hearts were removed and fixed for immunohistochemical assay of tryptophan-5-hydroxylase (Tph), in addition to Western blot for enzyme. Serotonin concentration and Tph were also evaluated with high-performance liquid chromatography. Results were analyzed using Mann-Whitney U test with a significance level of p <0.05. RESULTS: Metachromatic cells immunoreactive for Tph were observed from day 10 of gestation. Nerve fibers were also labeled, apparently making contact with serotonergic cells. Tph activity was measurable and serotonin levels increased with gestational age. The presence of Tph protein was confirmed by Western blot on day 16. CONCLUSIONS: The present results support the existence of cells located in the fetal myocardium, capable of producing serotonin whose phenotype belongs to cardiac mast cells. Their presence in this tissue strongly suggests that serotonin may play a key role in normal and abnormal development of cardiac tissue.
Assuntos
Animais , Masculino , Feminino , Ratos , Coração/embriologia , Miocárdio/citologia , Miocárdio/metabolismo , Serotonina/biossíntese , Ratos WistarRESUMO
BACKGROUND: We undertook this study to present biochemical and morphological characterization of serotonergic cells during fetal heart development. METHODS: Wistar rats (10, 12, 16 and 20 days of gestation) were used. After obtaining the fetuses by Cesarean section, the hearts were removed and fixed for immunohistochemical assay of tryptophan-5-hydroxylase (Tph), in addition to Western blot for enzyme. Serotonin concentration and Tph were also evaluated with high-performance liquid chromatography. Results were analyzed using Mann-Whitney U test with a significance level of p <0.05. RESULTS: Metachromatic cells immunoreactive for Tph were observed from day 10 of gestation. Nerve fibers were also labeled, apparently making contact with serotonergic cells. Tph activity was measurable and serotonin levels increased with gestational age. The presence of Tph protein was confirmed by Western blot on day 16. CONCLUSIONS: The present results support the existence of cells located in the fetal myocardium, capable of producing serotonin whose phenotype belongs to cardiac mast cells. Their presence in this tissue strongly suggests that serotonin may play a key role in normal and abnormal development of cardiac tissue.
Assuntos
Coração/embriologia , Miocárdio/citologia , Miocárdio/metabolismo , Serotonina/biossíntese , Animais , Feminino , Masculino , Ratos , Ratos WistarRESUMO
BACKGROUND: The present study was aimed to obtain information on the interaction kinetics of L-tryptophan (L-Trp) with plasma albumin from normal, intrauterine growth-restricted (IUGR) and nutritionally recovered (NR) newborn infants. METHODS: A case study cohort was planned in 37 newborns during the first 3 months of life. At birth two groups were formed. The first group included 20 newborns with IUGR. The control group (C) included 17 appropriate for gestational age newborns. At 30 days of age, 9 infants of the IUGR group showed a return to normal of the anthropometric parameters, these infants formed the NR group. Free, bound and total L-Trp were measured. To assess binding kinetics albumin was freed of fatty acids and tested in mole to mole samples from IUGR, NR and control babies. RESULTS: Plasma free L-Trp was increased, K(d) (dissociation constant) elevated and B(max )(maximal binding)decreased in IUGR patients up to postnatal day 90. These changes remained even after nutritional recovery. CONCLUSIONS: Abnormal kinetics of L-Trp binding to albumin explains the increased availability of this precursor amino acid in the plasma of IUGR infants. This finding corroborates previous results in IUGR rats and newborn babies, indicating enhanced potential for brain serotonergic synthesis.
Assuntos
Retardo do Crescimento Fetal/sangue , Serotonina/sangue , Albumina Sérica/metabolismo , Triptofano/sangue , Estatura , Índice de Massa Corporal , Peso Corporal , Estudos de Coortes , Ácidos Graxos não Esterificados/sangue , Retardo do Crescimento Fetal/fisiopatologia , Humanos , Lactente , Recém-Nascido , Estado Nutricional , Ligação ProteicaRESUMO
INTRODUCTION: High birth and immigration rates in the US-Mexico border region have led to large population increases in recent decades. Two national, 10 state, and more than 100 local government entities deliver reproductive health services to the region's 14 million residents. Limited standardized information about health risks in this population hampers capacity to address local needs and assess effectiveness of public health programs. METHODS: We worked with binational partners to develop a system for reproductive health surveillance in the sister communities of Matamoros, Tamaulipas, Mexico, and Cameron County, Texas, as a model for a broader regional approach. We used a stratified, systematic cluster-sampling design to sample women giving birth in hospitals in each community during an 81-day period (August 21-November 9) in 2005. We conducted in-hospital computer-assisted personal interviews that addressed prenatal, behavioral, and lifestyle factors. We evaluated survey response rates, data quality, and other attributes of effective surveillance systems. We estimated population coverage using vital records data. RESULTS: Among the 999 women sampled, 947 (95%) completed interviews, and the item nonresponse rate was low. The study sample included 92.7% of live births in Matamoros and 98.3% in Cameron County. Differences between percentage distributions of birth certificate characteristics in the study and target populations did not exceed 2.0. Study population coverage among hospitals ranged from 92.9% to 100.0%, averaging 97.3% in Matamoros and 97.4% in Cameron County. CONCLUSION: Results indicate that hospital-based sampling and postpartum interviewing constitute an effective approach to reproductive health surveillance. Such a system can yield valuable information for public health programs serving the growing US-Mexico border population.
Assuntos
Cooperação Internacional , Serviços de Saúde Reprodutiva/organização & administração , Serviços de Saúde da Mulher/organização & administração , Coleta de Dados/economia , Feminino , Hispânico ou Latino , Administração Hospitalar , Humanos , México , Projetos Piloto , Vigilância da População , Serviços de Saúde Reprodutiva/economia , Texas , Serviços de Saúde da Mulher/economiaRESUMO
Barrel formation is delayed in nutritionally restricted rats. The underlying cause of such delay is yet unclear. Because barrels appear upon the arrival of somatosensory thalamo-cortical afferents and the reorientation of the dendritic arborizations of cortical spiny stellate neurons, it is likely that at least one of these processes is altered by nutritional restriction. Also, the serotoninergic afferent system has been implicated in regulating barrel segregation and growth during early postnatal life. We then evaluated the pattern of immunostaining of the serotonin transporter (SERT) and of the serotonin receptor 1B (5-HT(1B)), as well as the growth and arrival time of somatosensory thalamo-cortical afferents, to infer the contribution of these elements in the delayed formation of barrels observed in nutritionally restricted rats. It was found that the rates of development and the segregation of thalamo-cortical fibers were normal in nutritionally restricted rats. SERT, but not 5-HT(1B) immunoreactivity, was decreased in the primary somatosensory cortex during barrel specification. The availability of both proteins in nutritionally restricted rats was lower than that observed in their well fed counterparts at later developmental times. It is concluded that the delayed formation of barrels observed in nutritionally restricted rats is due to a retarded reorientation of dendritic arbors of cortical neurons. This might happen as a secondary effect of decreasing the availability of SERT and/or increasing the availability of 5-HT(1B) receptor early in postnatal life.
Assuntos
Desnutrição/complicações , Receptor 5-HT1B de Serotonina/metabolismo , Proteínas da Membrana Plasmática de Transporte de Serotonina/metabolismo , Serotonina/metabolismo , Córtex Somatossensorial/crescimento & desenvolvimento , Tálamo/crescimento & desenvolvimento , Envelhecimento/fisiologia , Animais , Animais Recém-Nascidos , Restrição Calórica , Comunicação Celular/fisiologia , Diferenciação Celular/fisiologia , Transtornos da Nutrição Infantil/complicações , Pré-Escolar , Sinais (Psicologia) , Deficiências do Desenvolvimento/metabolismo , Deficiências do Desenvolvimento/patologia , Deficiências do Desenvolvimento/fisiopatologia , Privação de Alimentos/fisiologia , Cones de Crescimento/metabolismo , Cones de Crescimento/patologia , Humanos , Imuno-Histoquímica , Lactente , Desnutrição/fisiopatologia , Vias Neurais/crescimento & desenvolvimento , Vias Neurais/metabolismo , Vias Neurais/fisiopatologia , Ratos , Ratos Wistar , Córtex Somatossensorial/metabolismo , Córtex Somatossensorial/fisiopatologia , Tálamo/metabolismo , Tálamo/fisiopatologiaRESUMO
Introducción. Se ha demostrado que la desnutrición gestacional produce desde la etapa fetal una aceleración de la síntesis de 5-hidroxitriptamina cerebral (5-HT), secundaria a un aumento de la afinidad de la triptófano-5-hidroxilasa (T5-H) por el L-triptófano (L-Trp) y una mayor capacidad de fosforilación. Estos hallazgos han sugerido un cambio conformacional de la enzima durante el desarrollo cerebral como mecanismo principal que explique la aceleración de la síntesis de 5-HT. El objetivo de este trabajo fue evaluar los diferentes cambios que se producen en el cerebro de las ratas desnutridas durante la gestación y que al nacer son sometidas a un esquema de rehabilitación nutricia, con el propósito de obtener información que nos permita apoyar la hipótesis de que el mecanismo de activación de la síntesis de 5-HT cerebral es debida a un cambio estructural de la T5-H. Material y Métodos. Se seleccionaron ratas cepa Wistar, adaptadas a condiciones ambientales estándar. Al término de este período se formaron dos grupos: uno con desnutrición proteínico-calórico (D) y el otro control (C). Las hembras fueron pareadas con machos normales. Al nacimiento las crías de ambos grupos fueron mezcladas y redistribuidas al azar a madres del mimsmo grupo; ademas se realizó un entrecruzamiento de las crías de estos grupos para formar dos subgrupos; el desnutrido recuperado (DR) y el desnutrido en la lactancia (DL). A las edades de 1, 10, 15 y 21 días, se obtuvo el encéfalo para los ensayos bioquímicos. Además se realizaron curvas de peso corporal, cerebral y de la longitud céfalo-sacra. Resultados. Los grupos D y DL mostraron un retraso significativo del crecimiento corporal, cerebral y de la longitud céfalo desde el primer día hasta los 21 días de edad en comparación a los controles. El mismo patrón se observó en las proteínas tisulares. El grupo DR alcanzó una recuperación física a los 15 días de edad. La actividad de la enzima en los desnutridos mostró un aumento significativo en todas las edades estudiadas; la misma elevación significativa persistió en el grupo DR hasta los 21 días en comparación al grupo control y una elevación significativa en la concentración de 5-HT. Conclusiones: Los resultados confirman que la desnutrición gestacional y posnatal producen una deficiencia en la composición corporal, cerebral y una aceleración en la síntesis de 5-hidroxitriptamina. Además apoyan el hecho de que la rebilitación nutricional neonatal produce una recuperación en la composición corporal. Sin embargo los hallazgos de que el L-Trp cerebral se normalice en el animal rehabilitado, de que la actividad de la T5-H permanezca elevada y persista un aumento en la síntesis de neurotransmisor, 5-HT, apoya indirectamente la hipótesis de que el mecanismo de activación de esta importante vía biosintética cerebral, es posiblemente debiido a un cambio relacionado a la estructura de la triptófano-5-hidroxilasa inducido por la desnutrición ontogénica. Desnutrición gestacional; 5-hidroxitriptamina; cerebro; rehabilitación nutricional; triptófano-5-hidroxilasa
Assuntos
Ratos , Animais , Feminino , Cérebro/enzimologia , Cérebro/metabolismo , Desnutrição Proteico-Calórica/enzimologia , Desnutrição Proteico-Calórica/reabilitação , Serotonina/análise , Serotonina/síntese química , Ratos Wistar/metabolismoRESUMO
La desnutrición temprana induce cambios metabólicos específicos sobre el sistema serotoninergico cerebral, en animales de experimentación. La síntesis de serotonina cerebral se encuentra elevada, lo que depende del incremento de su precursor que es el triptófano plasmático libre; la relación del triptófano unido a albúmina con la fracción libre, determina la disponibilidad del precursor para su paso a través de la barrera hematoencefálica. En el presente estudio reportamos los resultados del metabolismo de la serotonina periférica, en dos grupos de recién nacidos humanos con desnutrición intrauterina y sus controles normales. La fracción libre del L-triptófano fue significativamente elevada, los aminoácidos neutros apresentaron modificaciones substanciales y la fracción unida a albúmina del triptófano y las proteínas del plasma fueron significativamente menores al compararse con los recién nacidos con peso adecuado para la edad gestacional. La elevación de la fracción libre del triptófano plasmático en recién nacidos con desnutrición temprana sugiere un incremento del transporte de esta aminoácido al cerebro con un aumento de la síntesis del neurotransmisor
Assuntos
Humanos , Masculino , Feminino , Aminoácidos/sangue , Doenças Placentárias/sangue , Recém-Nascido/sangue , Serotonina/sangue , Triptofano/sangue , Recém-Nascido PrematuroRESUMO
Se determinó la exposición a vibraciones generales en 12 puestos de trabajo de la industria, del transporte, la agricultura y la construcción, en las condiciones más comunes de trabajo. Estas se realizaron en el piso, en el caso de obreros que que laboraban de pie y en el asiento y espaldar cuando el trabajo se realizaba sentado. Se halló el valor eficaz (RMS) de la aceleración en el eje Z y en las bandas de 1/3 de octavas comprendidas entre 2 y 80 Hz. Se brindan los resultados de estas mediciones y su comparación con la norma cubana, lo que evidencia la importancia de este riesgo en dos actividades fundamentales de nuestra economía: maquinaria agrícola y transporte