Nutrients
February 2024
The use of aspartame (ASP) and potassium acesulfame (ACK) to reduce weight gain is growing; however, contradictory effects in body mass index control and neurobiological alterations resulting from artificial sweeteners consumption have been reported. This study aimed to evaluate the impact of the chronic consumption of ASP and ACK on mood-related behavior and the brain expression of serotonin genes in male Wistar rats. Mood-related behaviors were evaluated using the swim-forced test and defensive burying at two time points: 45 days (juvenile) and 95 days (adult) postweaning.
View Article and Find Full Text PDFArtificial sweeteners are mainly used as substitutes for sucrose derivates. In this study, we analyzed if the chronic consumption of aspartame or acesulfame potassium at an early age, produces histological alterations, astrogliosis and decreased neuronal viability, in hippocampus, prefrontal cortex, amygdala and hypothalamus of male Wistar rats. A histological analysis was performed on male Wistar rats that consumed aspartame or acesulfame potassium during 90 days, initiating the consumption of sweeteners immediately after weaning.
View Article and Find Full Text PDFIn this study, we evaluated the expression profile changes of genes that intervene in the calcium signaling pathway, in young and adult Wistar rats, using the animal model of neonatal lesion in ventral hippocampus (NLVH) (a recognized animal model for schizophrenia) and compared to the group of control animals (Sham). Through microarray technology, gene expression profiles were obtained from the three brain areas (nucleus accumbens, prefrontal cortex, and hippocampus) of young male Wistar rats (45 days) and adults (90 days) whether or not subjected to NLVH. The calcium signaling pathway reported a greater number of differentially expressed genes with z-score two values, > 2 (over-expression) and < - 2 (under-expression), in the three evaluated areas.
View Article and Find Full Text PDFIntroduction: It has been suggested that schizophrenia may be induced by “accidents” or injuries that occur during early brain development and result in a reduction of the neural connections in different regions. In this study, we evaluated differences in the expression of brain genes using a recognized experimental prototype of schizophrenia: the animal model of ventral hippocampal lesion in neonate rats (VHLN) compared to control animals.
Methods: Using microarray technology, we obtained gene expression profiles of three brain areas (nucleus accumbens, prefrontal cortex and hippocampus) of juvenile (45 days) and adult (90 days) Wistar male rats that underwent either VHLN or sham VHLN.