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Regulation of neuronal connectivity and plasticity by activity dependent mitocho...

Regulation of neuronal connectivity and plasticity by activity dependent mitochondrial trafficking to synapses Regulated trafficking of mitochondria is essential for providing ATP at the correct spatial location to power neural computation, and for providing calcium buffering at sites of calcium entry or release. In neurons, the concentrat... ver más

31/01/2018

UNIVERSITY COLLEGE...

2M€

Presupuesto del proyecto: 2M€

Líder del proyecto

UNIVERSITY COLLEGE LONDON No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Fecha límite participación Sin fecha límite de participación.

Financiación concedida El organismo FP7 notifico la concesión del proyecto el día 2018-01-31 No tenemos la información de la convocatoria

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1 Participantes

UNIVERSITY COLLEGE LONDON

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Líder del proyecto

UNIVERSITY COLLEGE LONDON No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 2M€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto Regulated trafficking of mitochondria is essential for providing ATP at the correct spatial location to power neural computation, and for providing calcium buffering at sites of calcium entry or release. In neurons, the concentration of mitochondria in specific regions such as growth cones and synapses is important for correct neuronal function and development. Moreover mutations in proteins regulating mitochondrial trafficking compromise neuronal development and the formation, function and plasticity of synapses, and defective mitochondrial trafficking is increasingly implicated in neurological diseases. Understanding the molecular mechanisms that allow neurons to tailor the distribution of mitochondria to changes in neuronal activity therefore has important implications for our understanding of neuronal function and communication. This proposal will study the mechanisms that control the trafficking of the energy providing mitochondria within neurons, and how this relates to neuronal connectivity and plasticity. Using imaging, electrophysiological, molecular and cell biological techniques, combined with viral transduction and mouse transgenic approaches we will determine the molecular mechanisms underlying the activity-dependent subcellular positioning of mitochondria in neurons. We will examine how the mitochondrial Ca2+-sensing GTPases Miro1 and Miro2 act to regulate mitochondrial movement, distribution and function and how this contributes to neuronal development, synaptogenesis and synaptic plasticity. A key goal will be to determine if different roles exist for constitutive versus activity-dependent control of mitochondrial transport by Miro1 and Miro2 in these processes. These studies will significantly advance our understanding of the molecular mechanisms that control mitochondrial localisation in neurons and the role that activity-dependent mitochondrial trafficking plays in regulating neuronal development, morphogenesis, connectivity and function.

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