Urea metabolism in the digestive tract of the pig ; preliminary quantitative and qualitative data

La méthode directe d’étude des échanges de nutriments entre le sang et les contenus digestifs, déjà exposée ici (Rerat, 1977) a été appliquée à l'étude du passage de l’urée sanguine vers la lumière intestinale et de sa métabolisation en ammoniac chez le porc au cours de cinq répétitions à niveaux alimentaires différents permettant de comparer chez un même animal des régimes à 12 p. 100 de protéines contenant ou non de l’urée (3 p. 100). Il se produit une sécrétion brute permanente d urée en provenance du sang vers le tube digestif qui s’élève à près d’un gramme par heure au cours de la digestion de repas équilibrés chez des sujets en bonne santé. L’urée sécrétée n’est que partiellement dégradée (moins de 50 p. 100) en ammoniac. L’urée fournie par voie alimentaire est rapi dement absorbée (en cinq heures environ), et son addition au régime ne se traduit pas par une élévation significative des quantités d’ammoniac produites au cours de la période d’étude postprandiale (8 h) chez des animaux non adaptés à cette addition d urée.The previously reported direct method of determination of the exchanges of nutriments between blood and digestive contents (Rerat, 1977) was applied to the study of the passage of blood urea towards the intestinal lumen and its meta- bolization into ammonia in the pig. Using five replications at different feeding levels it was possible to compare in one and the same animal diets containing 12 p. 100 protein and either no urea or 3 p. 100. The amount of blood urea permanently secreted in the gut during digestion of a balanced meal in healthy animals ranged around 1 gramme per hour. The urea secreted was only partially degraded ( less than 50 p. 100) into ammonia. Dietary urea was rapidly absorbed (within about 5 hours) and its addition to the diet did not lead to a significant elevation in the amounts of ammonia produced during the postprandial period (8 h) in animals non adapted to this addition of urea

Neurodevelopmental Disruption of Cortico-Striatal Function Caused by Degeneration of Habenula Neurons

The habenula plays an important role on cognitive and affective functions by regulating monoamines transmission such as the dopamine and serotonin, such that its dysfunction is thought to underlie a number of psychiatric conditions. Given that the monoamine systems are highly vulnerable to neurodevelopmental insults, damages in the habenula during early neurodevelopment may cause devastating effects on the wide-spread brain areas targeted by monoamine innervations.Using a battery of behavioral, anatomical, and biochemical assays, we examined the impacts of neonatal damage in the habenula on neurodevelopmental sequelae of the prefrontal cortex (PFC) and nucleus accumbens (NAcc) and associated behavioral deficits in rodents. Neonatal lesion of the medial and lateral habenula by ibotenic acid produced an assortment of behavioral manifestations consisting of hyper-locomotion, impulsivity, and attention deficit, with hyper-locomotion and impulsivity being observed only in the juvenile period, whereas attention deficit was sustained up until adulthood. Moreover, these behavioral alterations were also improved by amphetamine. Our study further revealed that impulsivity and attention deficit were associated with disruption of PFC volume and dopamine (DA) receptor expression, respectively. In contrast, hyper-locomotion was associated with decreased DA transporter expression in the NAcc. We also found that neonatal administration of nicotine into the habenula of neonatal brains produced selective lesion of the medial habenula. Behavioral deficits with neonatal nicotine administration were similar to those caused by ibotenic acid lesion of both medial and lateral habenula during the juvenile period, whereas they were different in adulthood.Because of similarity between behavioral and brain alterations caused by neonatal insults in the habenula and the symptoms and suggested neuropathology in attention deficit/hyperactivity disorder (ADHD), these results suggest that neurodevelopmental deficits in the habenula and the consequent cortico-striatal dysfunctions may be involved in the pathogenesis and pathophysiology of ADHD