M1SYNC
Circuit mechanisms underlying dynamic spike time synchronization in mouse motor cortex
| Coordinatore | THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF OXFORD
Organization address
address: University Offices, Wellington Square contact info |
| Nazionalità Coordinatore | United Kingdom [UK] |
| Totale costo | 100˙000 € |
| EC contributo | 100˙000 € |
| Programma | FP7-PEOPLE
Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013) |
| Code Call | FP7-PEOPLE-2011-CIG |
| Funding Scheme | MC-CIG |
| Anno di inizio | 2012 |
| Periodo (anno-mese-giorno) | 2012-03-01 - 2016-02-29 |
Partecipanti
| # | ||||
|---|---|---|---|---|
| 1 |
THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF OXFORD
Organization address
address: University Offices, Wellington Square contact info |
UK (OXFORD) | coordinator | 100˙000.00 |
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Obiettivo del progetto (Objective)
'Direct electrical stimulation of the motor cortex is sufficient to trigger movement, but the mechanisms by which neurons in this cortical region intrinsically encode motor output continue to be resolved. Spontaneous activity in the motor cortex is surprisingly sparse, and the precise temporal synchronization of this weak and distributed activity may be critical for efficient cortical communication. The fact that spiking within cortical motor circuits naturally reverberates within rhythmic oscillations demonstrates that exquisite mechanisms for controlling spike timing do exist. Moreover, these brain rhythms display a transition from beta- (15-30 Hz) to gamma-frequency oscillations (30-120 Hz) during movement planning and initiation, and even during motor imagery, suggesting further that flexible control of spike time synchronization may be an important feature of cortical coding. This project will use optogentic control of neuronal activity in order to elucidate the circuit mechanisms and function of beta/gamma-frequency oscillations in the mouse motor cortex. The objectives are to (i) determine how the pattern of network synchronization reflects the spatial profile and intensity of light-induced neuronal activity in acute cortical slices, (ii) resolve the synaptic and circuit mechanisms underlying the activity-dependent tuning of these cortical networks, and (iii) determine how fast network oscillations influence sensorimotor integration of sensory-evoked responses in vivo. The synchronization of brain activity is disrupted in numerous neurological and mental disorders, and thus resolving its role in cortical circuit processing could be key to understanding both brain function and dysfunction.'