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Identifying mechanisms of information encoding in myelinated single axons

Cel

A major challenge in neuroscience is to understand how information is stored and coded within single nerve cells (neurons) and across neuron populations in the brain. Nerve cell fibres (axons) are thought to provide the wiring to connect neurons and conduct the electrical nerve impulse (action potential; AP). Recent discoveries, however, show that the initial part of axons actively participates in modulating APs and providing a means to enhance the computational repertoire of neurons in the central nervous system. To decrease the temporal delay in information transmission over long distances most axons are myelinated. Here, we will test the hypothesis that the degree of myelination of single axons directly and indirectly influences the mechanisms of AP generation and neural coding. We will use a novel approach of patch-clamp recording combined with immunohistochemical and ultrastructural identification to develop a detailed model of single myelinated neocortical axons. We also will investigate the neuron-glia interactions responsible for the myelination process and measure whether their development follows an activity-dependent process. Finally, we will elucidate the physiological and molecular similarities and discrepancies between myelinated and experimentally demyelinated single neocortical axons. These studies will provide a novel methodological framework to study central nervous system axons and yield basic insights into myelin physiology and pathophysiology.

Zaproszenie do składania wniosków

ERC-2010-StG_20091118
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System finansowania

ERC-SG - ERC Starting Grant

Instytucja przyjmująca

KONINKLIJKE NEDERLANDSE AKADEMIE VAN WETENSCHAPPEN - KNAW
Wkład UE
€ 1 994 640,00
Adres
KLOVENIERSBURGWAL 29 HET TRIPPENHUIS
1011 JV AMSTERDAM
Niderlandy

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Region
West-Nederland Noord-Holland Groot-Amsterdam
Rodzaj działalności
Research Organisations
Kontakt administracyjny
Ronald Van Der Neut (Dr.)
Kierownik naukowy
Maarten Kole (Dr.)
Linki
Koszt całkowity
Brak danych

Beneficjenci (1)