Sujets)
Enfant d'âge préscolaire , Humains , Mâle , Encéphalomyélite aigüe disséminée/induit chimiquement , Sous-type H1N1 du virus de la grippe A/immunologie , Vaccins antigrippaux/effets indésirables , Noyaux du thalamus , Encéphalomyélite aigüe disséminée/anatomopathologie , Grippe humaine/prévention et contrôle , Imagerie par résonance magnétique , Noyaux du thalamus/anatomopathologieRésumé
The limbic structures play an important role in the control of the neuroendocrine and sympathical adrenal function in basal and stress conditions. This work was undertaken to evaluate plasma ACTH, adrenocortical activity, cardiac adrenoceptors density and affnity response to variable chronic stress (VCS) in anterodorsal thalamic nuclei (ADTN) lesioned rats. Thirty days after lesion, shamlesioned stressed animals increased plasma ACTH and corticosterone as compared to sham-lesioned unstressed animals (p<0.05); lesioned rats increased ACTH levels after VCS (p<0.05) as compared unstressed-lesioned rats. Whereas in sham-lesion plasma corticosterone (C) increased after stress. in lesioned animals (C) remained unchanged as compared to unstressed-lesioned animals. In the stressed groups, adrenal C contents were below those found in unstressed rats. Beta-receptors affinity, in all the experimental groups, was similar, but VCS sham-lesioned animals underwent a significant increase in cardiac D-adrenergic receptors density when compared with basal and lesioned groups (P<0.001). Our findings would demonstrate that the increment in cardiac Beta adrenoceptors density appears as a consequence of the increase in ACTH, plasma corticosterone and sympathetic response provoked by stress situations. ADTN lesion attenuated this hipophisoadrenal system response to chronic stress as well as the above mentioned cardiac beta adrenoceptors density increment.
Sujets)
Animaux , Femelle , Rats , Hormone corticotrope/sang , Corticostérone/sang , Ventricules cardiaques/anatomopathologie , Axe hypophyso-surrénalien/anatomopathologie , Récepteurs bêta-adrénergiques/physiologie , Stress physiologique/physiopathologie , Noyaux du thalamus/anatomopathologie , Hormone corticotrope/métabolisme , Analyse de variance , Maladie chronique , Corticostérone/métabolisme , Modèles animaux de maladie humaine , Ventricules cardiaques/anatomopathologie , Rat Wistar , Récepteurs bêta-adrénergiques/métabolisme , Noyaux du thalamus/anatomopathologieRésumé
Basados en datos anatómicos y clínicos creemos que el dolor talámico es producido por una lesión selectiva del núcleo ventrocaudal parvocelular (Vcpc) del tálamo. Por el contrario, la recuperación funcional de éste núcleo así como de las fibras A-delta y A-beta a nivel del núcleo ventral posterior (VP), puede aliviar o curar este tipo de dolor central.