Article: article from journal or magazin.
Glutamate-induced homocysteic acid release from astrocytes: possible implication in glia-neuron signaling
DA - 20040224 IS - 0306-4522 LA - eng PT - Journal Article RN - 0 (Excitatory Amino Acid Agonists) RN - 0 (Excitatory Amino Acid Antagonists) RN - 0 (Sulfur Isotopes) RN - 1001-13-4 (homocysteic acid) RN - 115066-14-3 (6-Cyano-7-nitroquinoxaline-2,3-dione) RN - 2609-46-3 (Amiloride) RN - 2898-76-2 (benzamil) RN - 454-28-4 (Homocysteine) RN - 56-86-0 (Glutamic Acid) RN - 7440-70-2 (Calcium) SB - IM Institution : Centre for Research in Psychiatric Neuroscience, Department of Psychiatry, University of Lausanne, Route de Cery, CH-1008 Prilly-Lausanne, Switzerland Mention de responsabiblité : Benz,B.;Grima,G.;Do,K.Q. SAPHIRID:48063
Glial cells synthesise neuroactive substances and release them upon neurotransmitter receptor activation. Homocysteic acid (HCA), an endogenous agonist for glutamatergic N-methyl-D-aspartate (NMDA) receptors, is predominantly localised in glial cells. We have previously demonstrated the release of HCA from mouse astrocytes in culture following activation of beta-adrenergic receptors. Moreover, a release of HCA has also been observed in vivo upon physiological stimulation of sensory afferents in the thalamus. Here we report the glutamate-induced release of HCA from astrocytes. The effect of glutamate was mediated by the activation of ionotropic (NMDA and non-NMDA) as well as by metabotropic receptors. In addition, the release of HCA was Ca(2+)- and Na(+)-dependent, and its mechanism involved the activation of the Na+/Ca(2+)-exchanger. Furthermore, we provide evidence for the presence of functional NMDA receptors on astrocytes, which are coupled to an intracellular Ca2+ increase via stimulation of the Na+/Ca(2+)-exchanger. Our data thus favour a participation of glial cells in excitatory neurotransmission and corroborate the role of HCA as a "gliotransmitter."
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