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.

Public Health Relevance

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.

National Institute of Health (NIH)
National Institute of Neurological Disorders and Stroke (NINDS)
Center Core Grants (P30)
Project #
Application #
Study Section
National Institute of Neurological Disorders and Stroke Initial Review Group (NSD)
Program Officer
Talley, Edmund M
Project Start
Project End
Budget Start
Budget End
Support Year
Fiscal Year
Total Cost
Indirect Cost
J. David Gladstone Institutes
San Francisco
United States
Zip Code
Maeda, Sumihiro; Djukic, Biljana; Taneja, Praveen et al. (2016) Expression of A152T human tau causes age-dependent neuronal dysfunction and loss in transgenic mice. EMBO Rep 17:530-51
Tong, Leslie M; Yoon, Seo Yeon; Andrews-Zwilling, Yaisa et al. (2016) Enhancing GABA Signaling during Middle Adulthood Prevents Age-Dependent GABAergic Interneuron Decline and Learning and Memory Deficits in ApoE4 Mice. J Neurosci 36:2316-22
Possin, Katherine L; Sanchez, Pascal E; Anderson-Bergman, Clifford et al. (2016) Cross-species translation of the Morris maze for Alzheimer's disease. J Clin Invest 126:779-83
Oliveira, Ana Osório; Osmand, Alexander; Outeiro, Tiago Fleming et al. (2016) αB-Crystallin overexpression in astrocytes modulates the phenotype of the BACHD mouse model of Huntington's disease. Hum Mol Genet 25:1677-89
Tracy, Tara E; Sohn, Peter Dongmin; Minami, S Sakura et al. (2016) Acetylated Tau Obstructs KIBRA-Mediated Signaling in Synaptic Plasticity and Promotes Tauopathy-Related Memory Loss. Neuron 90:245-60
Dubal, Dena B; Zhu, Lei; Sanchez, Pascal E et al. (2015) Life extension factor klotho prevents mortality and enhances cognition in hAPP transgenic mice. J Neurosci 35:2358-71
Min, Sang-Won; Chen, Xu; Tracy, Tara E et al. (2015) Critical role of acetylation in tau-mediated neurodegeneration and cognitive deficits. Nat Med 21:1154-62
Orr, Anna G; Hsiao, Edward C; Wang, Max M et al. (2015) Astrocytic adenosine receptor A2A and Gs-coupled signaling regulate memory. Nat Neurosci 18:423-34
Minami, S Sakura; Shen, Vivian; Le, David et al. (2015) Reducing inflammation and rescuing FTD-related behavioral deficits in progranulin-deficient mice with α7 nicotinic acetylcholine receptor agonists. Biochem Pharmacol 97:454-62
Shields, L Y; Kim, H; Zhu, L et al. (2015) Dynamin-related protein 1 is required for normal mitochondrial bioenergetic and synaptic function in CA1 hippocampal neurons. Cell Death Dis 6:e1725

Showing the most recent 10 out of 37 publications