Premium
Intracellular ascorbic acid inhibits transport of glucose by neurons, but not by astrocytes
Author(s) -
Castro Maite A.,
Pozo Miguel,
Cortés Christian,
García María de los Angeles,
Concha Ilona I.,
Nualart Francisco
Publication year - 2007
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2007.04631.x
Subject(s) - ascorbic acid , glut3 , astrocyte , glucose transporter , glutamatergic , hippocampal formation , glutamate receptor , cotransporter , biochemistry , glucose uptake , intracellular , biology , chemistry , neuron , neuroglia , premovement neuronal activity , microbiology and biotechnology , endocrinology , neuroscience , glut1 , central nervous system , sodium , insulin , receptor , food science , organic chemistry
It has been demonstrated that glutamatergic activity induces ascorbic acid (AA) depletion in astrocytes. Additionally, different data indicate that AA may inhibit glucose accumulation in primary cultures of rat hippocampal neurons. Thus, our hypothesis postulates that AA released from the astrocytes during glutamatergic synaptic activity may inhibit glucose uptake by neurons. We observed that cultured neurons express the sodium‐vitamin C cotransporter 2 and the facilitative glucose transporters (GLUT) 1 and 3, however, in hippocampal brain slices GLUT3 was the main transporter detected. Functional activity of GLUTs was confirmed by means of kinetic analysis using 2‐deoxy‐ d ‐glucose. Therefore, we showed that AA, once accumulated inside the cell, inhibits glucose transport in both cortical and hippocampal neurons in culture. Additionally, we showed that astrocytes are not affected by AA. Using hippocampal slices, we observed that upon blockade of monocarboxylate utilization by α‐cyano‐4‐hydroxycinnamate and after glucose deprivation, glucose could rescue neuronal response to electrical stimulation only if AA uptake is prevented. Finally, using a transwell system of separated neuronal and astrocytic cultures, we observed that glutamate can reduce glucose transport in neurons only in presence of AA‐loaded astrocytes, suggesting the essential role of astrocyte‐released AA in this effect.