AMPA-type glutamate receptors in glial precursor cells of the rat corpus callosum: ionic and pharmacological properties.
Glial cells in fiber tracts express various functional transmitter receptors, e.g., got glutamate. However, little is known about their biophysical and pharmacological profile. Using the in situ patch-clamp technique, kainate- and AMPA-induced conductance changes of glial precursor cells in the rat corpus callosum were investigated to study these aspects. Precursor cells were identified by their voltage-gated currents and were easily discernable from astrocytes and oligodendrocytes. Kainate induced two overlying effects in these cells: the activation of a cationic current and the block of potassium conductances. Cesium in the pipette solution blocked potassium conductances nearly completely and the ionic profile of the kainate-induced cationic current could be studied in detail. Full replacement of the sodium in the bath by calcium resulted only in a small kainate-induced (calcium) inward current flow, but the kainate-induced outward current carried by Cs+ was less affected reflecting a weak calcium permeability. The kainate response could be blocked by 6,7-dinitroquinoxaline-2,3-dione (DNQX) and millimolar zinc concentrations. Co-application of micromolar concentrations of zinc slightly enhanced the kainate-induced current, while Evans Blue was without any significant effect. Cyclothiazide increased the kainate response by a factor of x6 while concanavalin A did not enlarge it. The AMPA-induced current was amplified by a factor of x39 by cyclothiazide. The present data suggested the expression of weakly calcium-permeable AMPA receptors on glial precursor cells in the rat corpus callosum. Only a small fraction of the agonist-induced current could be seen without the appropriate blockers of receptor desensitization. An additional expression of kainate-preferring glutamate receptors could not be shown.
Berger
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Institute of Anatomy, University of Freiburg, Germany.
D000818:Animals; D001581:Benzothiadiazines / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D002712:Chlorides / Q000494:pharmacology; D003208:Concanavalin A / Q000494:pharmacology; D003337:Corpus Callosum / Q000166:cytology*; D004232:Diuretics; D005070:Evans Blue / Q000494:pharmacology; D007608:Kainic Acid / Q000494:pharmacology; D009457:Neuroglia / Q000378:metabolism* / Q000648:ultrastructure; D018408:Patch-Clamp Techniques; D011810:Quinoxalines / Q000494:pharmacology; D051381:Rats; D018091:Receptors, AMPA / Q000502:physiology*; D018092:Kainic Acid Receptors / Q000502:physiology; D049993:Sodium Chloride Symporter Inhibitors / Q000494:pharmacology; D017967:Zinc Compounds / Q000494:pharmacology
D001581:Benzothiadiazines; D002118:Calcium; D002712:Chlorides; D003208:Concanavalin A; D004232:Diuretics; D005070:Evans Blue; D007608:Kainic Acid; D011810:Quinoxalines; D018091:Receptors, AMPA; D018092:Kainic Acid Receptors; D049993:Sodium Chloride Symporter Inhibitors; D017967:Zinc Compounds; C056723:FG 9041; C016837:zinc chloride; C004639:cyclothiazide