Khodakhah, Kamran To understand brain function in health and disease one needs to elucidate how it processes sensory inputs, how it encodes information, and how it computes. Exploration of these facets requires tools which enable us eavesdrop on the activity of neurons in the intact brain, and tools for manipulating their function. A powerful approach has been in vivo single unit recordings from populations of neurons in awake animals during behavior. A group of neuroscientists at Albert Einstein College of Medicine (AECOM) seek the opportunity to expand their in vivo recording capabilities to include wireless telemetry in rodents and birds, and the ability to simultaneously monitor the activity of large populations of neurons in discrete brain regions. Moreover, the AECOM group wishes to attain the possibility of modulating the activity of discrete set of neurons by photorelease of bioactive neurotransmitters and neuromodulators. Acquisition of such a system will significantly advance the research programs of these neuroscientists and will enable, for the first time, this group to test hypotheses and address important questions that their respective fields have been longing to tackle.

Agency
National Institute of Health (NIH)
Institute
National Center for Research Resources (NCRR)
Type
Biomedical Research Support Shared Instrumentation Grants (S10)
Project #
1S10RR027888-01
Application #
7795303
Study Section
Special Emphasis Panel (ZRG1-ETTN-K (30))
Program Officer
Levy, Abraham
Project Start
2010-05-13
Project End
2012-05-12
Budget Start
2010-05-13
Budget End
2012-05-12
Support Year
1
Fiscal Year
2010
Total Cost
$500,000
Indirect Cost
Name
Albert Einstein College of Medicine
Department
Neurosciences
Type
Schools of Medicine
DUNS #
110521739
City
Bronx
State
NY
Country
United States
Zip Code
10461
Fremont, Rachel; Tewari, Ambika; Angueyra, Chantal et al. (2017) A role for cerebellum in the hereditary dystonia DYT1. Elife 6:
Isaksen, Toke Jost; Kros, Lieke; Vedovato, Natascia et al. (2017) Hypothermia-induced dystonia and abnormal cerebellar activity in a mouse model with a single disease-mutation in the sodium-potassium pump. PLoS Genet 13:e1006763
Alviña, K; Tara, E; Khodakhah, K (2016) Developmental change in the contribution of voltage-gated Ca(2+) channels to the pacemaking of deep cerebellar nuclei neurons. Neuroscience 322:171-7
Person, Abigail L; Khodakhah, Kamran (2016) Recurrent Feedback Loops in Associative Learning. Neuron 89:427-30
Molero, Aldrin E; Arteaga-Bracho, Eduardo E; Chen, Christopher H et al. (2016) Selective expression of mutant huntingtin during development recapitulates characteristic features of Huntington's disease. Proc Natl Acad Sci U S A 113:5736-41
Fremont, Rachel; Tewari, Ambika; Khodakhah, Kamran (2015) Aberrant Purkinje cell activity is the cause of dystonia in a shRNA-based mouse model of Rapid Onset Dystonia-Parkinsonism. Neurobiol Dis 82:200-212
Cao, Yumei; Bartolomé-Martín, David; Rotem, Naama et al. (2015) Rescue of homeostatic regulation of striatal excitability and locomotor activity in a mouse model of Huntington's disease. Proc Natl Acad Sci U S A 112:2239-44
Chen, Christopher H; Fremont, Rachel; Arteaga-Bracho, Eduardo E et al. (2014) Short latency cerebellar modulation of the basal ganglia. Nat Neurosci 17:1767-75
Fremont, Rachel; Calderon, D Paola; Maleki, Sara et al. (2014) Abnormal high-frequency burst firing of cerebellar neurons in rapid-onset dystonia-parkinsonism. J Neurosci 34:11723-32
Calderon, D Paola; Fremont, Rachel; Kraenzlin, Franca et al. (2011) The neural substrates of rapid-onset Dystonia-Parkinsonism. Nat Neurosci 14:357-65