SUMMARY:The microtubule-associated protein MAP-2 is an integral part of the cytoskeleton and plays an important role in neural morphogenesis. This protein is an essential component of the dendritic cytoskeleton, especially in the adult brain, and its expression can be altered under experimental or pathological conditions. The purpose of this study was to evaluate the effect of infection with the rabies virus on MAP-2 immunoreactivity in the cerebral cortex of mice. The mice were inoculated with the rabies virus and the animals were sacrificed when the disease reached its advanced stage, together with uninfected animals of the same age. The brains were extracted after being previously perfusion-fixed with paraformaldehyde; coronal sections were obtained with a vibratome. The coronal sections were processed by immunohistochemistry to reveal the presence of the MAP-2 protein in neurons of the motor area of the cerebral cortex. Rabies-infected mice showed an increase in the immunoreactivity of the somata and apical dendrites in pyramidal neurons of the motor cortex. This is an unexpected result, as dendritic pathology has been previously demonstrated in rabies, and some studies on neurological disorders associate dendritic alterations with loss of expression of the MAP-2 protein. Therefore, whatever the alteration in the expression of this protein, decrease or increase, it could be causing a biochemical imbalance in the integrity and stability of the neuronal cytoskeleton.

A Zika virus (ZIKV) strain was isolated from an acute febrile patient during the Zika epidemics in Colombia. The strain was intraperitoneally inoculated into BALB/c mice, and 7 days postinoculation, neurological manifestations and ZIKV infection in the brain were demonstrated. The reported genome sequence is highly related to strains circulating in the Americas.

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Introducción. Algunos signos clínicos de la rabia y estudios experimentales previos sugieren que esta infección viral podría afectar al sistema GABAérgico. Objetivo. Evaluar el efecto de la infección con el virus de la rabia sobre la expresión de GABA en neuronas de la corteza cerebral de ratón. Materiales y métodos. Se inocularon ratones adultos con virus CVS de la rabia por vía intramuscular. Los animales se sacrificaron en la etapa terminal de la enfermedad y se fijaron por perfusión con paraformaldehído al 4% y glutaraldehído al 1%. Se procesaron cortes coronales de cerebro obtenidos en un Vibratome®, mediante inmunohistoquímica para identificar neuronas GABAérgicas en la corteza cerebral. Se realizaron conteos y análisis cuantitativo de las neuronas positivas para GABA en muestras de ratones normales e infectados. Resultados. En los animales infectados con rabia no se alteró el patrón de distribución de las neuronas GABAérgicas corticales pero su número disminuyó significativamente. El promedio de células positivas para GABA en 1 mm 2 de corteza fue de 293±32 en los controles y de 209±13 en los infectados. Por otra parte, el valor promedio del área de los perfiles neuronales positivos para GABA aumentó significativamente de 104±8 µm 2 en los controles a 122±10 µm 2 en las muestras infectadas, debido a que la pérdida de células positivas para GABA fue más evidente en las neuronas de menor tamaño. No obstante, el rango de tamaños de las células inmunopositivas para GABA fue similar en muestras de animales normales e infectados. Conclusiones. Este trabajo aporta nueva evidencia en favor de la hipótesis que propone la participación del GABA en la fisiopatología de la rabia.Palabras clave: ácido gamma-aminobutírico, agentes neurotransmisores, corteza cerebral, inmunohistoquímica, interneuronas, rabia.Decreased number neurons expressing GABA in the cerebral cortex of rabies-infected mice Introduction. GABAergic neurons synthesize and release gamma-aminobutyric acid, the predominant inhibitory neurotransmitter in the brain. Certain clinical signs of rabies and previous experimental studies have suggested that rabies viral infections affect the host GABAergic system. Objective. The effect of rabies virus infection on the expression of GABA was evaluated in neurons of the mouse cerebral cortex. Materials and methods. Adult mice were inoculated by intramuscular injection with the standard strain of rabies (CVS virus). The animals were sacrificed in the terminal stage of the illness and perfused with 4% paraformaldehyde and 1% glutaraldehyde. Frontal sections were obtained in a Vibratome® and treated with appropriate immunohistochemical reactions for identifying the GABAergic neurons in the cerebral cortex. Counts and comparative quantitative analysis of the GABA+ neurons were compared in samples of infected and normal mice. Results. In the animals infected with rabies virus, the distribution pattern of cortical GABAergic neurons was not changed, but their number diminished significantly. The mean value of GABA+ cells...

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