Norepinephrine plays an important role in modulating memory through its beta-adrenergic receptors (Adrβ: β, β and β). Here, we hypothesized that multisensory stimulation would reverse memory impairment caused by the inactivation of Adrβ (AdrβKO) with consequent inhibition of sustained glial-mediated inflammation. To test this, 21- and 86-day-old AdrβKO mice were exposed to an 8-week multisensory stimulation (MS) protocol that comprised gustatory and olfactory stimuli of positive and negative valence; intellectual challenges to reach food; the use of hidden objects; and the presentation of food in ways that prompted foraging, which was followed by analysis of GFAP, Iba-1 and EAAT2 protein expression in the hippocampus (HC) and amygdala (AMY).
View Article and Find Full Text PDFIntroduction: A polymorphism in the type 2 deiodinase (Thr92Ala-DIO2) gene has been associated with behavioral and cognitive dysfunction as well as neurodegeneration and oxidative stress in the central nervous system.
Objective: To test whether the minor allele (Ala92) frequency (MAF) is increased in children in the autism spectrum disorder (ASD), and whether carriers of the minor allele exhibit more severe symptoms and/or worse adaptive behavior.
Study Design: ASD children were evaluated at baseline and yearly throughout the study by psychologists using the following tools: autism behavior checklist, Vineland Adaptative Behaviour Scales II, non-verbal intelligence test SON-R 2-7, SON-R 6-40, Weschler scale for intelligence, and autism treatment evaluation checklist.
Braz J Med Biol Res
August 2018
Attention and emotion have a positive impact on memory formation, which is related to the activation of the noradrenergic system in the brain. The hippocampus and amygdala are fundamental structures in memory acquisition, which is modulated by noradrenaline through the noradrenergic receptors. Pharmacological studies suggest that memory acquisition depends on the action of both the β3 (β3-AR) and β2 (β2-AR) receptor subtypes.
View Article and Find Full Text PDFC57Bl/6J mice are the gold standard animal model of diet-induced obesity. These animals become obese with higher adiposity, blood fasting glucose, triglycerides, and total cholesterol when fed a high-fat diet (HFD). Conversely, the FVB/N mouse line is thought to be resistant to diet-induced obesity, with low or no weight gain and adiposity in response to a HFD In this study, we investigated whether FVB/N mice are resistant or susceptible to metabolic disorder that is promoted by a HFD Biometric parameters and blood chemistry were analyzed in C57Bl/6J and FVB/N mice that were fed a chow diet or HFD Glucose and insulin sensitivity were assessed by performing the glucose tolerance test and measuring serum insulin/glucose and homeostasis model assessment-insulin resistance.
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