An organism's behavior can be considered the final output of its nervous system. Therefore, careful evaluation of behavior and of the factors that perturb it is essential to any comprehensive effort to understand the function or dysfunction of the nervous system. Many investigators at Gladstone/UCSF have developed complex rodent models to assess fundamental neuroscientific processes or major neurological diseases, but lack the expertise and equipment necessary for the careful behavioral and electrophysiological phenotyping of these valuable models. It would be expensive and inefficient for each of these investigators to hire trained behavioral neuroscientists and to purchase highly specialized equipment whenever they wished to evaluate a transgenic phenotype or assess the effects of a drug, surgical treatment or genetic intervention. The use of a core facility for such experiments is practical and highly in demand. To address this need, we propose to establish a Behavioral Core to achieve the following specific aims: 1) enable and support diverse behavioral studies ranging in focus from basic to disease-oriented neuroscience;2) encourage collaborations among core users around common themes and potentially related findings observed in different projects;3) provide specialized expertise in the phenotypical characterization of mouse models of human neurological disorders;and 4) assist in the design and execution of pharmacological interventions and preclinical drug trials aimed at distinct behavioral domains or abnormalities. The proposed core would support at least 26 NINDS-sponsored qualifying projects, as well as a variety of projects that are sponsored by Other NIH institutes. In addition, the core would help junior scientists to obtain preliminary data for their first NIH grant applications. By promoting interactions among its users, the core would also promote interdisciplinary research in behavioral neuroscience on a broader scale, linking investigations into the molecular, cellular, anatomical, genetic, and neurophysiological substrates of behavior and behavioral disorders. Because in neurology and psychiatry improvements in behavioral alterations often represent the most relevant outcome measures of therapeutic interventions, the core would also play a key role in advancing translational efforts at Gladstone and UCSF.
The development of a Behavioral Core would give many investigators the tools, expertise and collaborations they need to evaluate an organism's behavior. The evaluation of behavior and of the factors that perturb it is essential to any comprehensive effort to understand the function or dysfunction of the nervous system.
|Gheyara, Ania L; Ponnusamy, Ravikumar; Djukic, Biljana et al. (2014) Tau reduction prevents disease in a mouse model of Dravet syndrome. Ann Neurol 76:443-56|
|Minami, S Sakura; Min, Sang-Won; Krabbe, Grietje et al. (2014) Progranulin protects against amyloid ? deposition and toxicity in Alzheimer's disease mouse models. Nat Med 20:1157-64|
|Knoferle, Johanna; Yoon, Seo Yeon; Walker, David et al. (2014) Apolipoprotein E4 produced in GABAergic interneurons causes learning and memory deficits in mice. J Neurosci 34:14069-78|
|Berthet, Amandine; Margolis, Elyssa B; Zhang, Jue et al. (2014) Loss of mitochondrial fission depletes axonal mitochondria in midbrain dopamine neurons. J Neurosci 34:14304-17|
|Dubal, Dena B; Yokoyama, Jennifer S; Zhu, Lei et al. (2014) Life extension factor klotho enhances cognition. Cell Rep 7:1065-76|
|Tong, Leslie M; Djukic, Biljana; Arnold, Christine et al. (2014) Inhibitory interneuron progenitor transplantation restores normal learning and memory in ApoE4 knock-in mice without or with A? accumulation. J Neurosci 34:9506-15|
|Suberbielle, Elsa; Sanchez, Pascal E; Kravitz, Alexxai V et al. (2013) Physiologic brain activity causes DNA double-strand breaks in neurons, with exacerbation by amyloid-ýý. Nat Neurosci 16:613-21|
|Morris, Meaghan; Hamto, Patricia; Adame, Anthony et al. (2013) Age-appropriate cognition and subtle dopamine-independent motor deficits in aged tau knockout mice. Neurobiol Aging 34:1523-9|
|Bien-Ly, Nga; Gillespie, Anna K; Walker, David et al. (2012) Reducing human apolipoprotein E levels attenuates age-dependent Aýý accumulation in mutant human amyloid precursor protein transgenic mice. J Neurosci 32:4803-11|
|Kwan, Wanda; Magnusson, Anna; Chou, Austin et al. (2012) Bone marrow transplantation confers modest benefits in mouse models of Huntington's disease. J Neurosci 32:133-42|
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