Properties of kainate receptor/channels on cultured Bergmann glia.
Following the localization, at the electron microscope level, of the immunoreactivity towards a putative kainate receptor on Bergmann glial cells in the chick cerebellar cortex, cultures of Bergmann glia were used to establish the presence of functional kainate receptor/channels and study their properties. Bergmann glia were identified by their fusiform morphology and their ability to bind an anti-kainate binding protein monoclonal antibody, a kainate receptor high affinity ligand--kainyl-bovine serum albumin--and a glial marker--anti-vimentin monoclonal antibody. Membranes prepared from the culture cells displayed, using 25 nM [3H]kainate, the binding of 4.1 pmol of [3H]kainate/mg protein and showed the presence in Western blots of the two polypeptides of 49 and 93 kDa attributed to the kainate binding protein. Kainate, at concentrations above 0.1 mM, was found to increase the influx into cultured Bergmann glia of 22Na+, 86Rb+, 45Ca2+ and 36Cl- ions. The traffic of 22Na+, induced by kainate and glutamate, observed only in the presence of 1 mM ouabain, was blocked by kainate receptor antagonists and by 0.01 mM quisqualate. Analysis of the kinetics of incorporation of 22Na+ and 45Ca2+ ions showed an initial accumulation of 22Na+ and 45Ca2+ ions followed by their total dissipation. The results indicate that the kainate-induced influx of Na+ ions through the kainate receptor/channel causes the reverse transport of Na+ ions, by activation of the Na+/Ca2+ and Na+/H+ exchangers which remove intracellular Na+ ions. Pre-exposure of the cells to 0.5 mM dibutyryl cAMP was found to greatly enhance the kainate-induced 22Na+ ion influx. We propose that the Bergmann glia kainate receptors modulate the efficacy of the glutamatergic synapses between the parallel fibers and Purkinje cell spines and form part of a glial machinery responsible for plastic changes in synaptic transmission.
Ortega
A
A
Department of Neurobiology, Weizmann Institute of Science, Rehovot, Israel.
Eshhar
N
N
Teichberg
V I
VI
D018750:6-Cyano-7-nitroquinoxaline-2,3-dione; D000818:Animals; D000911:Antibodies, Monoclonal; D002118:Calcium / Q000378:metabolism; D002462:Cell Membrane / Q000502:physiology; D002478:Cells, Cultured; D002525:Cerebellar Cortex / Q000166:cytology / Q000502:physiology*; D002642:Chick Embryo; D002712:Chlorides / Q000378:metabolism; D004151:Dipeptides / Q000494:pharmacology; D007473:Ion Channels / Q000187:drug effects / Q000502:physiology*; D007608:Kainic Acid / Q000378:metabolism / Q000494:pharmacology*; D007700:Kinetics; D007736:Kynurenic Acid / Q000494:pharmacology; D008959:Models, Neurological; D009457:Neuroglia / Q000502:physiology*; D011810:Quinoxalines / Q000494:pharmacology; D016318:Quisqualic Acid / Q000494:pharmacology; D018092:Kainic Acid Receptors; D017981:Receptors, Neurotransmitter / Q000187:drug effects / Q000502:physiology*; D012413:Rubidium / Q000378:metabolism; D012964:Sodium / Q000378:metabolism*
D018750:6-Cyano-7-nitroquinoxaline-2,3-dione; D000911:Antibodies, Monoclonal; D002118:Calcium; D002712:Chlorides; D004151:Dipeptides; D007473:Ion Channels; D007608:Kainic Acid; D007736:Kynurenic Acid; D011810:Quinoxalines; D016318:Quisqualic Acid; D018092:Kainic Acid Receptors; D017981:Receptors, Neurotransmitter; D012413:Rubidium; D012964:Sodium; C028929:gamma-glutamylglycine