Distribución de calbindina y parvoalbúmina y efecto del virus de la rabia sobre su expresión en la médula espinal de ratones / Calbindin and parvalbumin distribution in spinal cord of normal and rabies-infected mice

Introducción. Aunque se trata de una enfermedad infecciosa del sistema nervioso, poco se conoce sobre los mecanismos patogénicos de la infección con el virus de la rabia. En particular, son escasos los estudios sobre su histopatología en la médula espinal. Objetivo. Estudiar la distribución de las proteínas calbindina y parvoalbúmina, en la médula espinal de ratones y evaluar el efecto de la infección con el virus de la rabia sobre su expresión. Materiales y métodos. Se inocularon ratones con virus de la rabia, por vía intracerebral o intramuscular, y se extrajo la médula espinal para hacer cortes transversales, los cuales se sometieron a tratamiento inmunohistoquímico con anticuerpos monoclonales para revelar la presencia de las dos proteínas en ratones normales y en animales infectados. Se llevó a cabo el análisis cualitativo y cuantitativo de la inmunorreacción de las dos proteínas. Resultados. Las proteínas calbindina y parvoalbúmina se distribuyeron de manera diferencial en las láminas de Rexed. La infección con el virus de la rabia produjo una disminución en la expresión de calbindina. Por el contrario, la infección provocó un incremento en la expresión de parvoalbúmina. El efecto de la rabia sobre las dos proteínas fue similar al comparar las dos vías de inoculación. Conclusión. El efecto diferencial de la infección con el virus de la rabia sobre calbindina y parvoalbúmina en la médula espinal de ratones, es similar al reportado anteriormente para áreas encefálicas. Esto sugiere uniformidad en su respuesta a la infección en todo el sistema nervioso central y es un aporte importante para el conocimiento de la patogénesis de la rabia.

Introduction: Rabies is a fatal infectious disease of the nervous system; however, the knowledge about the pathogenic neural mechanisms in rabies is scarce. In addition, there are few studies of rabies pathology of the spinal cord. Objective: To study the distribution of calcium binding proteins calbindin and parvalbumin and assessing the effect of rabies virus infection on their expression in the spinal cord of mice. Materiales y methods: Mice were inoculated with rabies virus, by intracerebral or intramuscular route. The spinal cord was extracted to perform some crosscuts which were treated by immunohistochemistry with monoclonal antibodies to reveal the presence of the two proteins in normal and rabies infected mice. We did qualitative and quantitative analyses of the immunoreactivity of the two proteins. Results: Calbindin and parvalbumin showed differential distribution in Rexed laminae. Rabies infection produced a decrease in the expression of calbindin. On the contrary, the infection caused an increased expression of parvalbumin. The effect of rabies infection on the two proteins expression was similar when comparing both routes of inoculation. Conclusion: The differential effect of rabies virus infection on the expression of calbindin and parvalbumin in the spinal cord of mice was similar to that previously reported for brain areas. This result suggests uniformity in the response to rabies infection throughout the central nervous system. This is an important contribution to the understanding of the pathogenesis of rabies.

Environmental enrichment during early postnatal development decreases parvalbumin expression in the rat somatosensory cortex

In the rat brain, parvalbumin (PV) expression starts on postnatal day 8 and comprises a heterogeneous population of nonpyramidal GABAergic neurons. In the present work, an immunohistochemical study was done on control and experimental rats submitted to enriched environmental conditions between postnatal days 3 to 18 or 3 to 24. Counts of PV+ neurons were made in the dorsomedial and in the ventrolateral regions of the somatosensory cortex. In control animals, PV+ neurons reached a peak on day 24 declining towards day 120. In these rats a peculiar distribution pattern was detected in which immunoreactive neurons are more numerous in the dorsomedial than ventrolateral regions as well in infragranular than supragranular layers and in posterior regions than anterior ones. Differences observed in these three dimensions were well established on day 24. Rats exposed to the enriched environment from day 3 to day 24 show a reduction (26 por ciento) in the number of PV+ neurons. The effects of the enrichment persisted for at least 12 days since animals submitted to the enriched condition from day 3 to day 18 and sacrificed on day 30 present a similar reduction (29 por ciento) in the number of PV immunoreactive neurons. Environmental enrichment induces a significant reduction of PV+ neurons but the overall distribution is retained. This finding suggests some degree of stability in the expression of PV in the rat somatosensory cortex.