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Grant: Project Grant

Research Institute of the McGill University Health Centre

$833,850.00

Dual-function glutamate transporter/chloride channels in brain physiology and neurological diseases.

FY 2022-23

Summary
The brain has two main cell types, neurons and glia, and interactions between them are crucial for many processes involved in brain development and information processing. For example, their two-way communication regulates the number and types of cells that are produced and influences how neurons communicate chemically with one another at synapses, their sites of contact. There is still much to learn about the interactions between neurons and different types of glia. We are particularly interested in how glial cells use Excitatory Amino Acid Transporters (EAATs) to take up important chemical transmitters like glutamate from synapses and act as channels for the passage of chloride ions in and out of cells. Defects of EAATs are a common feature of a variety of disorders such as ataxia and neurodegenerative diseases. Historically, there has been a dearth of tools to study and manipulate glial subtypes in the laboratory. We have spent several years generating and collecting such tools, and we have launched new approaches to study neuron-glial interactions. We are using a genetically tractable model organism, the fruit fly, because it has a simple yet sophisticated brain and central nervous system (CNS) in which neurons and glia perform many of the same functions they do in humans. In flies, it is also easy to study how the CNS controls behaviors like movement and sleep. In this proposal we are specifically addressing the following questions: How do EAATs control sleep? How might EAATs link sleep and brain energy metabolism? How do mutations of the glutamate transporter EAAT1 cause ataxia?
Program
Project Grant
Location
Quebec, Canada
Type
Grant
Source
CIHR Funding Decisions Database

As published

Id
480399
Name
van Meyel Donald J
Region
Québec
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Neurosciences, Mental Health and Addiction
Theme2
Biomedical
Prcname2
Cell Biology - Disease
Projecttitle
Dual-function glutamate transporter/chloride channels in brain physiology and neurological diseases.
Programtype2
Operating Grants
Orgnameinp2
Research Institute of the McGill University Health Centre
Cihramount2
$833,850
Cihrequipment2
$0
Programname2
Project Grant
Keyworddelim
Astrocyte; Ataxia; Chloride; Drosophila; Ensheathing Glia; Glaucoma; Glia; Glutamate; Neuron-Glial Interactions; Transporter
Abstract
The brain has two main cell types, neurons and glia, and interactions between them are crucial for many processes involved in brain development and information processing. For example, their two-way communication regulates the number and types of cells that are produced and influences how neurons communicate chemically with one another at synapses, their sites of contact. There is still much to learn about the interactions between neurons and different types of glia. We are particularly interested in how glial cells use Excitatory Amino Acid Transporters (EAATs) to take up important chemical transmitters like glutamate from synapses and act as channels for the passage of chloride ions in and out of cells. Defects of EAATs are a common feature of a variety of disorders such as ataxia and neurodegenerative diseases. Historically, there has been a dearth of tools to study and manipulate glial subtypes in the laboratory. We have spent several years generating and collecting such tools, and we have launched new approaches to study neuron-glial interactions. We are using a genetically tractable model organism, the fruit fly, because it has a simple yet sophisticated brain and central nervous system (CNS) in which neurons and glia perform many of the same functions they do in humans. In flies, it is also easy to study how the CNS controls behaviors like movement and sleep. In this proposal we are specifically addressing the following questions: How do EAATs control sleep? How might EAATs link sleep and brain energy metabolism? How do mutations of the glutamate transporter EAAT1 cause ataxia?
Competitiondate
202303
Approvedterm2
5 yrs 0 mth
Pinamesdelim
van Meyel, Donald J
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $833,850~ $0~