Bloodgood, Brenda - University of California, San Diego

研究领域

The goal of our lab is to understand how neuronal computations change in response to an animal’s interactions with the environment. From the moment an animal is born, its brain is working to extract information from its surroundings and initiate appropriate behavioral responses. This is done through the activity of excitatory and inhibitory neurons that are organized into synaptically connected circuits. Our lab is interested in understanding how experience, via the execution of activity-dependent gene expression, regulates the connectivity of inhibitory and excitatory neurons and how these processes relate to animal behavior and disease states. We focus on addressing three main questions: Which components of the inhibitory microcircuitry change their strength in response to activity-dependent changes in gene expression? What are the cellular and molecular mechanisms that underlie these changes in connectivity? How do changes in inhibition affect excitatory synaptic signaling, synaptic integration, and the propagation of information to downstream neurons? Our studies are performed in the mouse hippocampus to take advantage of its role in spatial learning and memory and the thoroughly characterized circuit architecture. Our experimental approaches are multidisciplinary – we manipulate gene expression and molecular function in specific cell types while probing synaptic connectivity with optogenetics, viral circuit tracing, two-photon uncaging of neurotransmitters, and electrophysiology.

近期论文

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Bloodgood, B.L.*, Sharma, N.*, Browne, H.A., Trepman, A.Z., Greenberg, M.E., Domain-specific regulation of inhibitory synapses by the activity-dependent transcription factor Npas4, Nature, 2013 Nov 7. 503(7474):121-5. Greer, P. L., Hanayama, R., Bloodgood, B. L., Flavell, S.W., Mardinly, A.R., Lipton, D.M., Kim, TK., Griffith, E.C., Waldon, Z., Maehr, R., Ploegh, H. L., Chowdhury, S., Worley, P. F., Steen, J., Greenberg, M. E. (2010). The AngelmanSyndrome-associated ubiquitin ligase Ube3a regulates synapse development and function through the ubiquination of Arc. Cell 140:704-716. Bloodgood B. L., Giessel A. J., Sabatini B. L. (2009). Biphasic synaptic Ca influx arising from compartmentalized electrical signals in dendritic spines. PLoS Biol. 7:e1000190. Lin Y., Bloodgood B.L., Hauser J.L., Lapan A.D., Koon A.C., Kim T.K., Hu L.S., Malik A.N., Greenberg M.E. (2008). Activity-dependent regulation of inhibitory synapse development by Npas4. Nature 455:1198-1204. Bloodgood, B.L., and Sabatini B.L. (2008). Regulation of synaptic signaling by postsynaptic, non-glutamate receptor ion channels. J. Physiol. 586:1475-1480. PMC2375695 Shankar G. M, Bloodgood B. L., Townsend M., Walsh D. M., Dennis J. Selkoe D. J., Sabatini B. L. (2007). Natural oligomers of the Alzheimer amyloid-beta protein induce reversible synapse loss by modulation of an NMDAR dependent signaling pathway. J. Neurosci. 27:2866-2875. Bloodgood, B.L., Sabatini B.L. (2007). Ca2+ signaling in dendritic spines. Curr.t Opin. Neurobiol. 17: 345-351. PMID: 17451936 Bloodgood B.L., Sabatini B.L. (2007). Nonlinear regulation of unitary synaptic signals by CaV2.3 voltage-sensitive calcium channels located in dendritic spines. Neuron 53: 249-260. Bloodgood B.L., Sabatini B.L. (2005). Neuronal activity regulates diffusion across the neck of dendritic spines. Science 310:866-869. Ngo-Anh T.J., Bloodgood B.L., Lin M., Sabatini B.L., Maylie J., and Adelman J.P. (2005). SK channels and NMDA receptors form a Ca2+-mediated feedback loop in dendritic spines. Nat. Neurosci. 8:642-649.