ParkinsonCanadaV1, Main, Exploration, bibRecord, 000C86

Regulation of adenosine levels during cerebral ischemia.

Identifieur interne : 000C86 ( Main/Exploration ); précédent : 000C85; suivant : 000C87

Regulation of adenosine levels during cerebral ischemia.

Auteurs : Stephanie Chu [Canada] ; Wei Xiong ; Dali Zhang ; Hanifi Soylu ; Chao Sun ; Benedict C. Albensi ; Fiona E. Parkinson

Source :

Acta pharmacologica Sinica [ 1745-7254 ] ; 2013.

RBID : pubmed:23064722

English descriptors

KwdEn :
- Adenosine (metabolism), Adenosine Triphosphate (metabolism), Animals, Brain (blood supply), Brain (metabolism), Brain (pathology), Brain Ischemia (metabolism), Brain Ischemia (pathology), Humans, Neurons (metabolism), Neurons (pathology), Nucleoside Transport Proteins (metabolism).
MESH :
- chemical , metabolism : Adenosine, Adenosine Triphosphate, Nucleoside Transport Proteins.
- blood supply : Brain.
- metabolism : Brain, Brain Ischemia, Neurons.
- pathology : Brain, Brain Ischemia, Neurons.
- Animals, Humans.

Abstract

Adenosine is a neuromodulator with its level increasing up to 100-fold during ischemic events, and attenuates the excitotoxic neuronal injury. Adenosine is produced both intracellularly and extracellularly, and nucleoside transport proteins transfer adenosine across plasma membranes. Adenosine levels and receptor-mediated effects of adenosine are regulated by intracellular ATP consumption, cellular release of ATP, metabolism of extracellular ATP (and other adenine nucleotides), adenosine influx, adenosine efflux and adenosine metabolism. Recent studies have used genetically modified mice to investigate the relative contributions of intra- and extracellular pathways for adenosine formation. The importance of cortical or hippocampal neurons as a source or a sink of adenosine under basal and hypoxic/ischemic conditions was addressed through the use of transgenic mice expressing human equilibrative nucleoside transporter 1 (hENT1) under the control of a promoter for neuron-specific enolase. From these studies, we conclude that ATP consumption within neurons is the primary source of adenosine in neuronal cultures, but not in hippocampal slices or in vivo mice exposed to ischemic conditions.

DOI: 10.1038/aps.2012.127
PubMed: 23064722

Affiliations:

Le document en format XML

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<front><div type="abstract" xml:lang="en">Adenosine is a neuromodulator with its level increasing up to 100-fold during ischemic events, and attenuates the excitotoxic neuronal injury. Adenosine is produced both intracellularly and extracellularly, and nucleoside transport proteins transfer adenosine across plasma membranes. Adenosine levels and receptor-mediated effects of adenosine are regulated by intracellular ATP consumption, cellular release of ATP, metabolism of extracellular ATP (and other adenine nucleotides), adenosine influx, adenosine efflux and adenosine metabolism. Recent studies have used genetically modified mice to investigate the relative contributions of intra- and extracellular pathways for adenosine formation. The importance of cortical or hippocampal neurons as a source or a sink of adenosine under basal and hypoxic/ischemic conditions was addressed through the use of transgenic mice expressing human equilibrative nucleoside transporter 1 (hENT1) under the control of a promoter for neuron-specific enolase. From these studies, we conclude that ATP consumption within neurons is the primary source of adenosine in neuronal cultures, but not in hippocampal slices or in vivo mice exposed to ischemic conditions.</div>
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La maladie de Parkinson au Canada (serveur d'exploration)

Regulation of adenosine levels during cerebral ischemia.

Regulation of adenosine levels during cerebral ischemia.

Source :

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

Pour générer des pages wiki

	La maladie de Parkinson au Canada (serveur d'exploration)
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