Increased expression of gamma-aminobutyric acid transporter-1 in the forebrain of infant rats with corticotropin-releasing hormone-induced seizures but not in those with hyperthermia-induced seizures.

High affinity, gamma-aminobutyric acid (GABA) plasma membrane transporters (GATs) influence the availability of GABA, the main inhibitory neurotransmitter in the brain. Recent studies suggest a crucial role for GATs in maintaining levels of synaptic GABA in normal as well as abnormal (i.e., epileptic) adult brain. However, the role of GATs during development and specifically changes in their expression in response to developmental seizures are unknown. The present study examined GAT-1-immunolabeling in infant rats with two types of developmental seizures, one induced by corticotropin-releasing hormone (CRH) lasting about 2 h and the other by hyperthermia (a model of febrile seizures) lasting only 20 min. The number of GAT-1-immunoreactive (ir) neurons was increased in several forebrain regions 24 h after induction of seizures by CRH as compared to the control group. Increased numbers of detectable GAT-1-ir cell bodies were found in the hippocampal formation including the dentate gyrus and CA1, and in the neocortex, piriform cortex and amygdala. In contrast, hyperthermia-induced seizures did not cause significant changes in the number of detectable GAT-1-ir somata. The increase in GAT-1-ir somata in the CRH model and not in the hyperthermia model may reflect the difference in the duration of seizures. The brain regions where this increase occurs correlate with the occurrence of argyrophyllic neurons in the CRH model

Alzheimer\u27s Disease: From Animal Models to the Human Syndrome

Some animal models, genetically modified (such as murine) and sporadic (as others species), enable the study of the origin of specific lesions observed in human neurodegenerative diseases. In particular, Alzheimer\u27s disease (AD) models have been designed to test the hypothesis that certain lesions are associated with functional and morphological changes beginning with memory loss and impairment in activities of daily life. This review compares and evaluates the phenotypes of different AD animal models, on the basis of the specific objectives of each study, with the purpose of encompassing their contributions to the comprehension of the AD signs and symptoms in humans. All these models contribute to the comprehension of the human AD mechanisms regarding the heterogeneity of AD phenotypes: the overlap between AD and age‐related changes, the variability of AD onset (early or late), the probable reactiveness of amyloid‐β and tau proteins, the scarcity of senile plaques and/or neurofibrillary tangles in some AD cases, the spatial correlation of the pathology and cerebral blood vessels, and the immunological responses (microglial aging) and synaptopathy. Altogether, these considerations may contribute to find therapies to treat and prevent this disease

Selective Estrogen Receptor Modulators Regulate Dendritic Spine Plasticity in the Hippocampus of Male Rats

Some selective estrogen receptor modulators, such as raloxifene and tamoxifen, are neuroprotective and reduce brain inflammation in several experimental models of neurodegeneration. In addition, raloxifene and tamoxifen counteract cognitive deficits caused by gonadal hormone deprivation in male rats. In this study, we have explored whether raloxifene and tamoxifen may regulate the number and geometry of dendritic spines in CA1 pyramidal neurons of the rat hippocampus. Young adult male rats were injected with raloxifene (1 mg/kg), tamoxifen (1 mg/kg), or vehicle and killed 24 h after the injection. Animals treated with raloxifene or tamoxifen showed an increased numerical density of dendritic spines in CA1 pyramidal neurons compared to animals treated with vehicle. Raloxifene and tamoxifen had also specific effects in the morphology of spines. These findings suggest that raloxifene and tamoxifen may influence the processing of information by hippocampal pyramidal neurons by affecting the number and shape of dendritic spines

Estudio teórico y experimental del sistema 9 Be + 51 V y sistemas similares

En este trabajo de tesis se presenta el estudio sistemático de los sistemas 7Li + 51V, 9Be + 51V y 8B + 58Ni. Para los sistemas ( 7Li, 9 Be) + 51V se midieron las secciones eficaces de fusión a energías cercanas a la barrera Coulombiana (EB,lab=11.75 y 16.16 MeV, respectivamente) empleando la técnica de rayos γ. El experimento para medir la fusión se llevó a cabo en el Laboratorio del Acelerador Tan- dem, del Instituto Nacional de Investigaciones Nucleares (ININ), siendo éstas las primeras mediciones realizadas para estos proyectiles a las energías consideradas. De forma simultánea, se hizo el análisis de los posibles núcleos residuales usando los códigos computacionales de fusión-evaporación PACE2, LILITA y CASCADE. Los resultados obtenidos fueron comparados con los datos experimentales me- didos. De forma preliminar, para el sistema 7Li + 51V, se hicieron cálculos usando la teoría de canales acoplados de reacción para estimar la contribución de la sección eficaz de transferencia de un protón a la producción del núcleo residual 52Cr. Para el sistema 8B + 58Ni, se hizo un análisis teórico de canales acoplados con el continuo discretizado y canales acoplados de reacción para estudiar los procesos de rompimiento y de transfe- rencia de un protón, 58Ni(8B,7Be)59Cu, a energías alrededor de la barrera Coulombiana (EB,lab=22.95 MeV). Para calcular las secciones eficaces correspondientes se usó un potencial de Modelo Óptico se- mimicroscópico, el cual combina un potencial real de doble convolución, un potencial de polarización y un potencial imaginario tipo Woods-Saxon. A partir de la comparación de nuestros cálculos con datos experimentales se determinaron los factores espectroscópicos Sexpt y astrofísicos S17(0) del protón en la interacción 8B → 7Be+p

Anti-tumour necrosis factor discontinuation in inflammatory bowel disease patients in remission: study protocol of a prospective, multicentre, randomized clinical trial

Background: Patients with inflammatory bowel disease who achieve remission with anti-tumour necrosis factor (anti-TNF) drugs may have treatment withdrawn due to safety concerns and cost considerations, but there is a lack of prospective, controlled data investigating this strategy. The primary study aim is to compare the rates of clinical remission at 1?year in patients who discontinue anti-TNF treatment versus those who continue treatment. Methods: This is an ongoing, prospective, double-blind, multicentre, randomized, placebo-controlled study in patients with Crohn?s disease or ulcerative colitis who have achieved clinical remission for ?6?months with an anti-TNF treatment and an immunosuppressant. Patients are being randomized 1:1 to discontinue anti-TNF therapy or continue therapy. Randomization stratifies patients by the type of inflammatory bowel disease and drug (infliximab versus adalimumab) at study inclusion. The primary endpoint of the study is sustained clinical remission at 1?year. Other endpoints include endoscopic and radiological activity, patient-reported outcomes (quality of life, work productivity), safety and predictive factors for relapse. The required sample size is 194 patients. In addition to the main analysis (discontinuation versus continuation), subanalyses will include stratification by type of inflammatory bowel disease, phenotype and previous treatment. Biological samples will be obtained to identify factors predictive of relapse after treatment withdrawal. Results: Enrolment began in 2016, and the study is expected to end in 2020. Conclusions: This study will contribute prospective, controlled data on outcomes and predictors of relapse in patients with inflammatory bowel disease after withdrawal of anti-TNF agents following achievement of clinical remission. Clinical trial reference number: EudraCT 2015-001410-1

Doctor José María Cantú Garza (1938-2007) [Doctor José María Cantú Garza (1938-2007)]

[No abstract available

Doctor José María Cantú Garza (1938-2007) [Doctor José María Cantú Garza (1938-2007)]

[No abstract available

Psychobiological studies showing the serotonin involvement in cognition-related behavioral performance

Serotonin most often acts as an inhibitory neurotransmitter which also modulates post-synaptic activity within other neurotransmitter systems. Serotonin is synthesized from the essential amino acid tryptophan in Raphe complex neurons which innervate extensive brain regions including the cerebral cortex, hippocampus, basal ganglia and cerebellum. Cognitive information is processed through synaptic connections with other regions of the brain, forming neural circuits as well as sub-serving systems that influence behavior. Previously investigations have concluded that serotonin has a modulatory role in neural systems, causing functional activity in the organization of various processes that relate to cognitive activity such as learning, memory, maintaining attention and behavioral switching. Serotonergic modulatory mechanisms include plastic changes at different biological organizational levels ranging from the molecular level, to adaptive behavior. Several psychopathological entities are associated with abnormal variations in brain serotonin levels. However, these involve other neurotransmitter systems such as dopamine, norepinephrine or acetylcholine. Therefore, an experimental study of the physiological interaction between serotonin and other neurotransmitter systems in normal and atypical cognitive abilities would be crucial for the improvement of therapeutic strategies applied to patients showing psychopathologies associated with dysfunctional serotonin neurotransmission. © 2013 by Nova Science Publishers, Inc. All rights reserved