Expresión y distribución de las Tioredoxinas durante asfixia perinatal. Su rol en la regulación del equilibrio redox / EXPRESSION AND DISTRIBUTION OF THIOREDOXINS IN PERINATAL ASPHYXIA

This article deals with the expression and distribution of Thioredoxins during perinatal asphyxia, and its roll in the regulation of the redox system. Disorders in the gaseous interchange through the placenta and the fetal lungs, can lead to what is known as the perinatal asphyxia (PA). The PA can involve all the organ systems, but has more severe effects on the Central Nervous System (CNS), producing damage as much as in the short term as in the long term. The disturbance recognized as oxidative stress, is considered as a disorder in the normal process of redox regulation. Thioredoxins are a group of proteins involucrated in the regulation of the cellular redox state. The aim of this report was to analyze the changes of the expression of Thioredoxins at a long term sustained on the hypothesis that the disorder at a short term induced by the perinatal asphyxia leds to substantial changes in a large term in the CNS.

Are astrocytes executive cells within the central nervous system? / ¿Son los astrocitos células ejecutivas dentro del Sistema Nervioso Central?

ABSTRACT Experimental evidence suggests that astrocytes play a crucial role in the physiology of the central nervous system (CNS) by modulating synaptic activity and plasticity. Based on what is currently known we postulate that astrocytes are fundamental, along with neurons, for the information processing that takes place within the CNS. On the other hand, experimental findings and human observations signal that some of the primary degenerative diseases of the CNS, like frontotemporal dementia, Parkinson’s disease, Alzheimer’s dementia, Huntington’s dementia, primary cerebellar ataxias and amyotrophic lateral sclerosis, all of which affect the human species exclusively, may be due to astroglial dysfunction. This hypothesis is supported by observations that demonstrated that the killing of neurons by non-neural cells plays a major role in the pathogenesis of those diseases, at both their onset and their progression. Furthermore, recent findings suggest that astrocytes might be involved in the pathogenesis of some psychiatric disorders as well.

RESUMEN Evidencias experimentales sugieren que los astrocitos desempeñan un rol crucial en la fisiología del sistema nervioso central (SNC) modulando la actividad y plasticidad sináptica. En base a lo actualmente conocido creemos que los astrocitos participan, en pie de igualdad con las neuronas, en los procesos de información del SNC. Además, observaciones experimentales y humanas encontraron que algunas de las enfermedades degenerativas primarias del SNC: la demencia fronto-temporal; las enfermedades de Parkinson, de Alzheimer, y de Huntington, las ataxias cerebelosas primarias y la esclerosis lateral amiotrófica, que afectan solo a los humanos, pueden deberse a astroglíopatía. Esta hipótesis se sustenta en hallazgos que demostraron que la muerte neuronal que en ellas ocurre es debida al compromiso de células no-neuronales que juegan rol principal en su iniciación y desarrollo. Más aún, observaciones recientes señalan que los astrocitos podrían estar implicados en la patogenia de algunas enfermedades psiquiátricas.

Striatal cytomegalic neurons containing nitric oxide are associated with experimental perinatal asphyxia: implication of cold treatment

Neuropathological mechanisms triggered by excitatory aminoacids are Known to involve nitric oxide (NO). Neurons containing NO are histochemically reactive to nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d), which labels NO synthase in CNS, Sprague-Dawley male rats subjected to perinatal asphyxia (PA) at 37 degreese Celsius, and PA plus 15 degreese Celsius hypothermia were evaluted when 6 months old by NADPH-d histochemical reaction. Computarized image analysis was used for quantification of stained sections. NADPH-d neurons in striatum from subsevere and severe PA showed a significant increment in soma size and dendritic process length versus control and hypothermic treated rats. Post-ischemic damage reurons are therefore involved in NO changes induced by PA that may be prevented by hypothermia treatment.