Metadata
Author: scielo-abstract
Data
English[en]
Several lines of evidence based on experimental models of focal cerebral ischemia have demonstra ted exofocal changes in differentneuronal markers such us benzodiazepine receptors, glial fibrillary acidic protein and microtubule-associated -protein 2, that may contribute to the expression of these affective symptoms. In our study we observed that these changes involved sustantia nigra, periaqueductal gray matter and raphe nuclei, áreas connected with the infarcted área. A physiopathological hypothesis is formulated considering the relationship between corticostriato- thalamic circuits and their main system of regulation i.e. dopamine, serotonin, norepinephrine and acetilcholine.
Spanish[es]
Datos de modelos de isquemia experimental focal, en las que se establecen cambios en los receptores de benzodiacepinas, en proteínas asociadas a los microtúbulos (MAP2) y en la proteína acídica fibrilar glial (GFAP) en sectores alejados del foco isquémico y relacionados con las estructuras límbicas, sustancia negra o sustancia gris periacueductal, permiten formular una hipótesis fisiopatológica que implica los circuitos cortícoestriato-tálamo-corticales y los diferentes sistemas de modulación provenientes del tallo cerebral como: serotonina, norepinefrina, dopamina y acetilcolina.