The purpose of the Neuroanatomy and Neurophysiology core will be to provide expertise, technical assistance and centralized equipment and facilities for all neuroanatomical and sympathetic nerve recording aspects of the program project experiments. The facilities available will allow investigators to access equipment and materials necessary for preparation of the high quality microscopic material and state-of-the-art technique to study sympathetic nervous system activity, all essential for successful completion and interpretation of experiments performed on the brain. As a new addition, a subcontract of the core located at Weill Cornell Medical College will perform ER stress biomarker analysis. This will be achieved in a cost-effective manner by the centralization of facilities and expertise. Specifically, the core will provide: i) Expertise and instrumentation for gene transfer into the mouse brain nuclei in highly specific manner;ii) A full service for the preparation of morphological and immunocytochemical material for analysis with light and electron microscopy. This will include fixation, thin and ultrathin sectioning, and pre-embedding immunocytochemistry, etc. Expertise in the analysis and interpretation of this material will be provided;iii) Quantitative methods for determining cell numbers, etc., and planning, designing and implementing neuroanatomical experiments;iv) Expertise and instrumentation for sympathetic nerve recording, including data analysis and interpretation;v) Training in experimental neuroanatomy and neurophysiology for principal and co-investigators and associated postdoctoral and other students;vi) Measurements of ER stress biomarkers in brain micropunches harvested for Projects 2 and 3 by this Core B at Ul, and harvested at Cornell by Project 1. The core will perform experiments involving a) the precise targeting of brain regions with adenoviral vectors b) the identification of specific neuronal populations in complex brain regions through the use of antibodies and other markers;c) the use of electron microscopic methods to determine the presence of morphological changes associated with ER stress, the interactions of neural elements, and the subcellular localization of antigens not resolvable with light microscopy, d) nerve recordings from sympathetic and other afferent fibers innervating the kidney, muscle and adipose tissue, and e) measures of ER stress biomarkers.

Public Health Relevance

Core B mission is to facilitate research carried out by the entire PPG and to accelerate discovery by providing a seamless pipeline for the analysis of neuroanatomical features in mice, direct measurement of sympathetic nervous system activity subserving various beds, and measurements of endoplasmic reticulum stress.

National Institute of Health (NIH)
National Heart, Lung, and Blood Institute (NHLBI)
Research Program Projects (P01)
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Special Emphasis Panel (ZHL1-PPG-J (F1))
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University of Iowa
Iowa City
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Littlejohn, Nicole K; Keen, Henry L; Weidemann, Benjamin J et al. (2016) Suppression of Resting Metabolism by the Angiotensin AT2 Receptor. Cell Rep 16:1548-60
Mukohda, Masashi; Stump, Madeliene; Ketsawatsomkron, Pimonrat et al. (2016) Endothelial PPAR-γ provides vascular protection from IL-1β-induced oxidative stress. Am J Physiol Heart Circ Physiol 310:H39-48
von Holstein-Rathlou, Stephanie; BonDurant, Lucas D; Peltekian, Lila et al. (2016) FGF21 Mediates Endocrine Control of Simple Sugar Intake and Sweet Taste Preference by the Liver. Cell Metab 23:335-43
Lu, Ko-Ting; Keen, Henry L; Weatherford, Eric T et al. (2016) Estrogen Receptor α Is Required for Maintaining Baseline Renin Expression. Hypertension 67:992-9
Guo, Deng-Fu; Cui, Huxing; Zhang, Qihong et al. (2016) The BBSome Controls Energy Homeostasis by Mediating the Transport of the Leptin Receptor to the Plasma Membrane. PLoS Genet 12:e1005890
Shinohara, Keisuke; Liu, Xuebo; Morgan, Donald A et al. (2016) Selective Deletion of the Brain-Specific Isoform of Renin Causes Neurogenic Hypertension. Hypertension 68:1385-1392
Hu, Chunyan; Lu, Ko-Ting; Mukohda, Masashi et al. (2016) Interference with PPARγ in endothelium accelerates angiotensin II-induced endothelial dysfunction. Physiol Genomics 48:124-34
Chapleau, Mark W; Rotella, Diane L; Reho, John J et al. (2016) Chronic vagal nerve stimulation prevents high-salt diet-induced endothelial dysfunction and aortic stiffening in stroke-prone spontaneously hypertensive rats. Am J Physiol Heart Circ Physiol 311:H276-85
Mark, Allyn L; Somers, Virend K (2016) Obesity, Hypoxemia, and Hypertension: Mechanistic Insights and Therapeutic Implications. Hypertension 68:24-6
Bell, Balyssa B; Rahmouni, Kamal (2016) Leptin as a Mediator of Obesity-Induced Hypertension. Curr Obes Rep 5:397-404

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