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Glial regulation of nonsynaptic extracellular glutamate in the substantia nigra
Author(s) -
Rodríguez Díaz Manuel,
Alonso Teofilo Jorge,
Perdomo Diaz Juan,
Gonzalez Hernández Tomás,
Castro Fuentes Rafael,
Sabate Magdalena,
Garcia Dopico Jose
Publication year - 2004
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.20100
Subject(s) - substantia nigra , biology , glutamate receptor , neuroscience , extracellular , dopamine , microbiology and biotechnology , biochemistry , dopaminergic , receptor
Abstract GLU is the main neurotransmitter in the brain, where it induces a synaptic excitatory action. There is recent evidence for an extracellular nonsynaptic GLU (EnS‐GLU) pool in different brain nuclei that, released from glial cells, may act on extrasynaptic GLU receptors of cells located far from the position in which it was released. In the present work, the EnS‐GLU pool was studied with microdialysis in the rat substantia nigra (SN). We observed an EnS‐GLU pool that increased in a Ca 2+ ‐dependent manner during cell depolarization. The selective alteration of with methionine sulfoximide (MSO) and fluorocitrate induced marked modifications in EnS‐GLU suggesting that EnS‐GLU is dependent on glial cells. Glutamine administration increased GLU, suggesting that neurons are also involved in EnS‐GLU modulation. GLU administered in the rostral SN showed a long‐distance diffusion to the caudal SN. The ionotropic GLU receptors agonist N‐methyl‐ D ‐aspartate and kainate and the metabotropic GLU receptors agonist ACPD increased EnS‐GLU and decreased extracellular glutamine. Taken together, these data indicate that nigral glia releases GLU, which probably performs a volume transmitter role. © 2004 Wiley‐Liss, Inc.