Excessive consumption of salt contributes to hypertension, which is the main risk factor for strokes, heart and kidney disease. Therefore it characterizes neuronal pathways that can control salt consumption is important to develop a new approach to reduce salt consumption. Here, we identify neurons in the Central Amygdala (CEA) mouse, nucleus paragraph lateral (LPBN), the core of the solitary channel (INTS) intermediary (INTS), and NTS Caudal (CNTS) which is activated and displays fos immunoreactivity in mice that have consumed salt to restore Salt debt, relative to full salt and thinning salt control.
Immunohistochemical studies The double label revealed that salt recovery rats had significantly activated neuron neuron density in CEA and INTS, while statistically significant changes in LPBN and CNT were not observed. Furthermore, in the CEA, the recovery of salt debt provides a significant increase in the density of active Caletretin neurons, while there are no changes relative to the control group in the density of active neurons expressed by C protein delta (PKC-Δ). Taken together, this study highlights the importance of opioid systems in CEA and INT in the neuron process associated with salt restoration, and can help develop pharmacological strategies and others to reduce salt consumption.
Analysis of cheap running styles for fenotyping behavior of the mouse model of neuromuscular diseases.
Animal support measurement is a general behavior tool used to describe phenotypes of certain diseases, injuries, or drug models. The method of analyzing the running style at a low cost exhibited here is the size of a simple but effective running style abnormality in Murine models. The footprints are analyzed by painting mouse feet with paint that cannot be washed without toxic and allow the subject to run through the tunnel on a piece of paper. Tunnel testing design utilizes natural mouse behavior and their affinity for small dark places.
The step length, step width, and the spread of each mouse is easily measured using a ruler and pencil. This is an established and reliable method, and produces several analogous metrics with digital systems. This approach is sensitive enough to detect changes in the first step in the phenotype presentation, and because of its non-invasive approach, this allows for group testing throughout the span of life or phenotypic presentation.
Standard Imaging Pipes for Fenotypical Mouse Laterality Defects and related heart malformations, on various scales and several stages.
Laterality defects are a disorder of developments produced from deviant left / right patterns. In the most severe case, such as in heterotaxy, they are associated with the Heart Complex Malformation. Progress in understanding the underlying physiopatological mechanism has been hampered by a lack of standard and complete procedures in mouse models for the phenotype / right asymmetry of all visceral organs. Here, we have developed a multimodality imaging pipe, which combines non-invasive micro-ultrasound imaging, micro-computing tomography (micro-CT) and high resolution episcopic microscope (HREM) to obtain 3D images at various stages of development and on multiple scales.
On the basis of the position in the uterine horn, we track in one individual, the development of organ asymmetry, the situation of all visceral organs in the thoracic or stomach environment, and the left / right acymetry is smooth anatomy. We provide anatomical image references and organ reconstruction in the mouse, and discuss differences with humans. This standard pipe, which we validated in a heterotaxy mouse model, offers a fast and easy to apply work framework. The extensive 3D phenotyping of organ asymmetry in the mouse uses clinical nomenclature for direct comparisons with patient phenotypes. It is compatible with automatic and quantitative image analysis, which is important to compare mutant phenotypes with incomplete penetration and to gain mechanistic insight into laterality defects.
Cognitive phenotyping assessment in congenital mice, which is genetically modified, and transgenic mouse models of Alzheimer’s disease.
Generally modified mouse models are used primarily to understand brain function and disease. The analysis of well-designed and controlled behavior from genetic modified mice has successfully led to identifying genes, understanding brain disease, and maintenance development. Recently, complex and higher cognitive functions have been checked in mice with genetic mutations.
Therefore, the research strategy for cognitive phenotypes must be sophisticated and evolved to convey the right meaning of findings and provide a strong translation tool to test the hypothesis and maintenance of development. This review discusses experimental design issues and discusses studies that have examined cognitive function using differences in mouse strains, genetically modified mice and transgenic mice for Alzheimer’s disease.