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dc.contributor.authorGilles Bonveto
dc.contributor.authorCarole Escartin
dc.creatorBarros- Felipe
dc.date.accessioned2017-05-03T17:57:41Z
dc.date.available2017-05-03T17:57:41Z
dc.date.issued2010
dc.identifier.urihttp://hdl.handle.net/10533/198103
dc.description.abstractProcessing of information in the brain is metabolically expensive. The brain represents only 2% of our body mass, but consumes 20% of its oxygen and glucose. Glucose, transported by the blood, is the major source of energy used by the brain for neuronal activity. Astrocytes provide by their perivascular endfeet (Kacem et al., 1998) a physical link between the vasculature and the synaptic terminals, supporting the concept of metabolic coupling between astrocytes and neurons. It has been proposed that neurons obtain most of their energy from extracellular lactate, a glucose metabolite produced by astrocytes (Pellerin and Magistretti, 1994). This hypothesis is termed the Astrocyte-to-Neuron Lactate Shuttle (ANLSH). 15 years later the existence of the Lactate Shuttle is still debated because we do not know the behavior of glucose and lactate in brain tissue with sufficient spatialresolution to discriminate the contribution of individual cell types (Bonvento et al., 2006; Barros andDeitmer, 2010). Nor do we have enough temporal resolution to tell how glucose and lactate fluxesmay oscillate in the rapid time frames typical of neural signaling. This is a critical issue both in basicphysiology, because this metabolic dialogue between neurons and astrocytes is now recognized of critical importance to support synaptic function but also in the field of neurodegenerative diseases. Indeed, there is now powerful evidence that the neurodegenerative process is not mediated solely by damage from the mutant protein within the target neurons but is strongly influenced by toxicity or mutant protein expression in non-neuronal cells such as astrocytes (Lobsiger and Cleveland, 2007). Ample clinical and experimental evidence indicates that metabolic dysfunction occurs in many, if not all, neurodegenerative disorders. Since these brain diseases are also characterized by a change in the status of astrocytes called reactive astrocytosis (Escartin and Bonvento, 2008) a fundamental question arises about the functional status of the metabolic dialogue between astrocytes and neurons in the course of these disorders. Definitive answer might have important consequences for the development of new therapeutic strategies and the identification of alternative therapeutic targets. Processing of information in the brain is metabolically expensive. The brain represents only 2% of our body mass, but consumes 20% of its oxygen and glucose. Glucose, transported by the blood, is the major source of energy used by the brain for neuronal activity. Astrocytes provide by their perivascular endfeet (Kacem et al., 1998) a physical link between the vasculature and the synaptic terminals, supporting the concept of metabolic coupling between astrocytes and neurons. It has been proposed that neurons obtain most of their energy from extracellular lactate, a glucose metabolite produced by astrocytes (Pellerin and Magistretti, 1994). This hypothesis is termed the Astrocyte-to-Neuron Lactate Shuttle (ANLSH). 15 years later the existence of the Lactate Shuttle is still debated because we do not know the behavior of glucose and lactate in brain tissue with sufficient spatialresolution to discriminate the contribution of individual cell types (Bonvento et al., 2006; Barros andDeitmer, 2010). Nor do we have enough temporal resolution to tell how glucose and lactate fluxesmay oscillate in the rapid time frames typical of neural signaling. This is a critical issue both in basicphysiology, because this metabolic dialogue between neurons and astrocytes is now recognized of critical importance to support synaptic function but also in the field of neurodegenerative diseases. Indeed, there is now powerful evidence that the neurodegenerative process is not mediated solely by damage from the mutant protein within the target neurons but is strongly influenced by toxicity or mutant protein expression in non-neuronal cells such as astrocytes (Lobsiger and Cleveland, 2007). Ample clinical and experimental evidence indicates that metabolic dysfunction occurs in many, if not all, neurodegenerative disorders. Since these brain diseases are also characterized by a change in the status of astrocytes called reactive astrocytosis (Escartin and Bonvento, 2008) a fundamental question arises about the functional status of the metabolic dialogue between astrocytes and neurons in the course of these disorders. Definitive answer might have important consequences for the development of new therapeutic strategies and the identification of alternative therapeutic targets. Processing of information in the brain is metabolically expensive. The brain represents only 2% of our body mass, but consumes 20% of its oxygen and glucose. Glucose, transported by the blood, is the major source of energy used by the brain for neuronal activity. Astrocytes provide by their perivascular endfeet (Kacem et al., 1998) a physical link between the vasculature and the synaptic terminals, supporting the concept of metabolic coupling between astrocytes and neurons. It has been proposed that neurons obtain most of their energy from extracellular lactate, a glucose metabolite produced by astrocytes (Pellerin and Magistretti, 1994). This hypothesis is termed the Astrocyte-to-Neuron Lactate Shuttle (ANLSH). 15 years later the existence of the Lactate Shuttle is still debated because we do not know the behavior of glucose and lactate in brain tissue with sufficient spatialresolution to discriminate the contribution of individual cell types (Bonvento et al., 2006; Barros andDeitmer, 2010). Nor do we have enough temporal resolution to tell how glucose and lactate fluxesmay oscillate in the rapid time frames typical of neural signaling. This is a critical issue both in basicphysiology, because this metabolic dialogue between neurons and astrocytes is now recognized of critical importance to support synaptic function but also in the field of neurodegenerative diseases. Indeed, there is now powerful evidence that the neurodegenerative process is not mediated solely by damage from the mutant protein within the target neurons but is strongly influenced by toxicity or mutant protein expression in non-neuronal cells such as astrocytes (Lobsiger and Cleveland, 2007). Ample clinical and experimental evidence indicates that metabolic dysfunction occurs in many, if not all, neurodegenerative disorders. Since these brain diseases are also characterized by a change in the status of astrocytes called reactive astrocytosis (Escartin and Bonvento, 2008) a fundamental question arises about the functional status of the metabolic dialogue between astrocytes and neurons in the course of these disorders. Definitive answer might have important consequences for the development of new therapeutic strategies and the identification of alternative therapeutic targets.
dc.titleReal-Time Measurement of Glycolytic Fluxes In Brain Cells In Situ
dc.typeProyecto
dc.contributor.corporatenameCentro de Estudios Científicos Cecs
dc.contributor.institutionCPT
dc.contributor.institutionCNRS.Ec.Sup. Ing. de Rennes
dc.identifier.folioC10S04
dc.description.conicytinstrumentcontestECOS
dc.description.conicytprogramPrograma de Cooperación Internacional
dc.relation.contestHandle/10533/198095
dc.identifier.generoM
dc.relation.instrumentHandle/10533/108080
dc.relation.programhandle/10533/108039
dc.description.shortconicytprogramPrograma de Cooperación Internacional
dc.date.annoconcurso2010
dc.description.corporaterolIP
dc.subject.fondecyt1nCiencias de la Salud


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