van den Brandt, J. | Search bioRxiv

bioRxiv2019

Obesity alters mobility and adult neurogenesis, but not hippocampal dependent learning in ob/ob mice

AbstractsO_ST_ABSBackgroundC_ST_ABSObesity has become a severe problem among the worlds population with clearly increasing prevalence over the last decades. Because obesity is associated with several comorbidities (e.g. hypertension or cancer) it constitutes an increasing burden for the health care system. Correlations between obesity and cognition have been studied in humans with ambivalent results. Here, we studied the effects of obesity on hippocampus dependent learning and memory and cell morphology in a mouse model of obesity. MethodsThe body mass of male and female Lep+/+(wt) and Lepob/ob(ob/ob) animals with access to food and water ad libitum was measured between postnatal day 60-200 and animals with clear adiposity (4-6 months) were further analyzed. Adult hippocampal neurogenesis in the dentate gyrus was examined using phosphohistone H3 as a marker for proliferation, doublecortin as a marker for differentiation and caspase3 as a marker for apoptosis. Moreover, the density of dendritic spines on apical and basal dendrites of pyramidal neurons of the cornu ammonis 1 (CA1) were analyzed using Golgi impregnation. In addition, mice were subjected to the open field and Morris water maze test in order to analyze locomotor activity and spatial learning. ResultsThe body weight of ob/ob mice nearly doubled during the first 120 postnatal days. Adult hippocampal neurogenesis was reduced in ob/ob mice due to reduced cell proliferation. Dendritic spine densities in the hippocampal area CA1 were not altered in ob/ob mice. Four to six months old ob/ob mice showed reduced locomotor activity in the open field test but similar performance in the Morris water maze compared to control mice. ConclusionOur data show that alterations in adult neurogenesis in leptin-deficient mice are not associated with an impairment in spatial learning abilities. Moreover, ob/ob mice are inconspicuous in the Morris water maze and do not display altered spine densities in the hippocampus, suggesting that obesity does not have a severe impact upon hippocampal neuronal plasticity and spatial learning.

neuroscience↗

bioRxiv2017

Natural Colonization of Laboratory Mice with Staphylococcus aureus Primes a Systemic Immune Response

BackgroundWhether mice are an appropriate model for S. aureus infection and vaccination studies is a matter of debate, because they are not considered as natural hosts of S. aureus. Sparked by an outbreak of S. aureus infections in laboratory mice, we investigated whether laboratory mice are commonly colonized with S. aureus and whether this might impact on infection experiments.\n\nMethodsWe characterized 99 S. aureus isolates from laboratory mice (spa typing, virulence gene PCR), and quantified murine antibodies using FlexMap technology.\n\nResultsSpecific-pathogen-free mice from various vendors were frequently colonized with S. aureus (0-21%). S. aureus was readily transmitted from murine parents to offspring, which became persistently colonized. Most murine isolates belonged to the lineage CC88 (54%). Murine strains showed features of host adaptation, such as absence of hlb-converting phages and superantigen genes, as well as enhanced coagulation of murine plasma. Importantly, S. aureus colonization induced a systemic IgG response specific for numerous S. aureus proteins, including several vaccine candidates.\n\nConclusionLaboratory mice are natural hosts of S. aureus and, therefore, provide better infection models than previously assumed. Pre-exposure to S. aureus is a possible confounder in S. aureus infection and vaccination studies.

immunology↗