Glucose Tightly Controls Morphological and Functional Properties of Astrocytes

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378041%3A_____%2F16%3A00459489" target="_blank" >RIV/68378041:_____/16:00459489 - isvavai.cz</a>

Alternative codes found

RIV/00216208:11130/16:10323451

Result on the web

<a href="http://dx.doi.org/10.3389/fnagi.2016.00082" target="_blank" >http://dx.doi.org/10.3389/fnagi.2016.00082</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.3389/fnagi.2016.00082" target="_blank" >10.3389/fnagi.2016.00082</a>

Result language

angličtina

Original language name

Glucose Tightly Controls Morphological and Functional Properties of Astrocytes

Original language description

The main energy source powering the brain is glucose. Strong energy needs of our nervous system are fulfilled by conveying this essential metabolite through blood via an extensive vascular network. Glucose then reaches brain tissues by cell uptake, diffusion and metabolization, processes primarily undertaken by astrocytes. Deprivation of glucose can however occur in various circumstances. In particular, ageing is associated with cognitive disturbances that are partly attributable to metabolic deficiency leading to brain glycopenia. Despite the crucial role of glucose and its metabolites in sustaining neuronal activity, little is known about its moment-to-moment contribution to astroglial physiology. We thus here investigated the early structural and functional alterations induced in astrocytes by a transient metabolic challenge consisting in glucose deprivation. Electrophysiological recordings of hippocampal astroglial cells of the stratum radiaturn in situ revealed that shortage of glucose specifically increases astrocyte membrane capacitance, whilst it has no impact on other passive membrane properties. Consistent with this change, morphometric analysis unraveled a prompt increase in astrocyte volume upon glucose deprivation. Furthermore, characteristic functional properties of astrocytes are also affected by transient glucose deficiency. We indeed found that glucoprivation decreases their gap junction-mediated coupling, while it progressively and reversibly increases their intracellular calcium levels during the slow depression of synaptic transmission occurring simultaneously, as assessed by dual electrophysiological and calcium imaging recordings. Together, these data indicate that astrocytes rapidly respond to metabolic dysfunctions, and are therefore central to the neuroglial dialog at play in brain adaptation to glycopenia.

Czech name

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Czech description

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Type

J_x - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)

CEP classification

ED - Physiology

OECD FORD branch

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Project

<a href="/en/project/GBP304%2F12%2FG069" target="_blank" >GBP304/12/G069: Project of excellence in the field of neuroscience</a><br>

Continuities

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Publication year

2016

Confidentiality

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Name of the periodical

Frontiers in Aging Neuroscience

ISSN

1663-4365

e-ISSN

—

Volume of the periodical

8

Issue of the periodical within the volume

85

Country of publishing house

CH - SWITZERLAND

Number of pages

12

Pages from-to

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UT code for WoS article

000374135300001

EID of the result in the Scopus database

2-s2.0-84974535003