Browsing by Author "GYSLING, K"
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- ItemCHANGES IN EXTRACELLULAR LEVELS OF GLUTAMATE AND ASPARTATE IN RAT SUBSTANTIA-NIGRA INDUCED BY DOPAMINE-RECEPTOR LIGANDS - IN-VIVO MICRODIALYSIS STUDIES(1995) ABARCA, J; GYSLING, K; ROTH, RH; BUSTOS, GThe microdialysis technique was utilized to study the local effects of D-1 and D-2 family type dopamine (DA) receptor (R) ligands on the in vivo release of endogenous glutamate (GLU) and aspartate (ASP) from rat substantia nigra (SN). Addition to the dialysis perfusion solution of either D-1-R and D-2-R agonists, such as SKF-38393 (50 and 100 mu M) and Quinpirole (5 and 10 mu M), resulted in dose-dependent increases in extracellular concentrations of GLU and ASP, respectively. The SKF-38393 and Quinpirole-induced effects were reduced by SCH-23390 (0.5 mu M), a D-1-R antagonist, and by Spiperone (1.0 mu M), a D-2-R antagonist, respectively. However, SCH-23390 and Spiperone did increase GLU and ASP extracellular concentrations. Local infusion with Tetrodotoxin (TTX) (1.0 mu M), a blocker of voltage-dependent Na+ channels, increased basal extracellular levels of GLU. In addition, co-infusion of TTX and SKF-38393 evoked increases in extracellular GLU levels higher than those observed after SKF-38393 alone. Finally, chemical lesions of nigral DA cells with 6-OH-DA. increased the basal extracellular levels of GLU. It is proposed that the release of GLU and ASP from SN may be regulated by D-1- and D-2- receptors present in this basal ganglia structure. In addition, part of the D-1 receptors present in SN might be located presynaptically on GLU-containing nerve endings.
- ItemREGULATION OF [H-3] NOREPINEPHRINE RELEASE BY N-METHYL-D-ASPARTATE RECEPTORS IN MINISLICES FROM THE DENTATE GYRUS AND THE CA(1)-CA(3) AREA OF THE RAT HIPPOCAMPUS(1993) ANDRES, ME; BUSTOS, G; GYSLING, KIt has been reported previously that N-methyl-D-aspartic acid induces a significant release of [H-3] norepinephrine preaccumulated in slices from the hippocampus. In the present study, we investigated whether there are regional differences in the hippocampus regarding this N-methyl-D-aspartate effect. In the absence of Mg2+, N-methyl-D-aspartate (10-200 mu M) induced the release of [H-3]norepinephrine from superfused minislices containing the dentate gyrus area or the CA(1)-CA(3) region of the hippocampus. Such N-methyl-D-aspartate effects on [H-3]norepinephrine release were significantly higher in the dentate gyrus than in the CA(1)-CA(3) area. The N-methyl-D-aspartate effects in both hippocampal areas were also reduced significantly by D-2-amino-5-phosphonovaleric acid (50 mu M), an antagonist of the N-methyl-D-aspartate receptor, and by tetrodotoxin, a blocker of the voltage-dependent Na+ channels. The extent of this reduction was the same in the dentate gyrus and the CA(1)-CA(3) area. Further experiments, conducted in the presence of Mg2+, demonstrated that N-methyl-D-aspartic acid increased K+-induced release of [H-3]norepinephrine from dentate gyrus minislices but not from the CA(1)-CA(3) area. The results are consistent with the existence of a higher density and/or different subtypes of N-methyl-D-aspartate receptors modulating [H-3]norepinephrine release in the dentate gyrus as compared with the CA(1)-CA(3) hippocampal area.
- ItemREGULATION OF TRANSMITTER SYNTHESIS AND RELEASE IN MESOLIMBIC DOPAMINERGIC NERVE-TERMINALS - EFFECT OF ETHANOL(1981) BUSTOS, G; LIBERONA, JL; GYSLING, KSlices from rat olfactory tubercle were incubated in freshly oxygenated Krebs-Ringer phosphate (KRP) and in the presence of L-tyrosine[14C-U [uniformly 14C-labeled]] as dopamine (DA) precursor. The newly synthesized [14C]DA and the [14C]DA released into the incubation media were isolated by Alumina column and ion-exchange chromatography. The presence of K+ depolarizing concentrations (25-70 mM) in the incubation media markedly increased the formation of [14C]DA from [14C]tyrosine, following a rather complex and biphasic pattern. Dibutyryl cAMP (dB-cAMP) and theophylline increased the formation of newly synthesized [14C]DA. Ethanol (0.2 to 0.4%, wt/vol) significantly blocked the stimulation of [14C]DA biosynthesis that was induced by low K+ depolarizing concentrations (25 mM) and by dB-cAMP (5 .times. 10-4 M) or theophylline (1 .times. 10-3 M. Only higher ethanol concentrations (0.8 to 1.1%, wt/vol) blocked the increase in DA formation induced by high K+ depolarizing concentrations (40 and 55 mM). K depolarization (40 mM) markedly evoked the release of newly synthesized [3H]DA or [3H]DA previously taken up by the slices. The release was dependent upon the presence of Ca2+ and inhibited by an excess of Mg2+ (12 mM). Ethanol (0.8-1.1%, wt/vol) produced no effect on K+-induced release of [3H]DA. The model described can be used as a simple experimental tool to study neurotransmitter synthesis and release from nerve terminals belonging to the mesolimbic dopaminergic system. At least 2 mechanisms exist by which neuronal depolarization increases transmitter formation in mesolimbic dopaminergic terminals. Ethanol, at relatively low concentrations, seems to produce a specific inhibitory effect upon the mechanism that predominates under low depolarizing conditions. The possibility is raised that the effects described for ethanol may play a role in the neuropharmacological responses induced by this agent in vivo.
- ItemRELEASE OF ENDOGENOUS CATECHOLAMINES FROM THE STRIATUM AND BED NUCLEUS OF STRIA TERMINALIS EVOKED BY POTASSIUM AND N-METHYL-D-ASPARTATE - IN-VITRO MICRODIALYSIS STUDIES(1995) ALIAGA, E; BUSTOS, G; GYSLING, KInduced release of endogenous dopamine and noradrenaline from coronal slices containing the striatum and the bed nucleus of the stria terminalis, respectively, was studied by means of in vitro microdialysis, A Ca+2-dependent and reserpine-sensitive K+-induced release of catecholamines was detected in both nuclei, We confirmed that N-methyl-D-aspartate (2.5 and 5.0 mM in the dialysis perfusion solution) induces the release of dopamine from the striatum, and this effect was blocked by prior dialysis perfusion with 500 mu M MK-801, a noncompetitive N-methyl-D-aspartate receptor antagonist, Infusion of N-methyl-D-aspartate (1-10 mM) or glutamate through the dialysis probe did not produce any detectable modification in the extracellular levels of noradrenaline in the bed nucleus of the stria terminalis, In addition, perfusion with D-serine (100 mu M) alone or in the presence of desipramine (10 mu M), resulted in a slight increase in extracellular noradrenaline in the bed nucleus of the stria terminalis. However, N-methyl-D-aspartate in the presence of D-serine and desipramine produced a marked increase in extracellular noradrenaline from the bed nucleus of the stria terminalis. These results indicate that N-methyl-D-aspartate receptors might regulate the release of noradrenaline from the bed nucleus of the stria terminalis as is the case of dopamine release in the striatum, The in vitro microdialysis seems to be a suitable complement to the in vivo microdialysis for the study of catecholamine release in discrete regions of the central nervous system and its local regulation by excitatory amino acid receptors. (C) 1995 Wiley Liss, Inc.
- ItemUPTAKE AND RELEASE OF MANGANESE BY RAT STRIATAL SLICES(1981) DANIELS, AJ; GYSLING, K; ABARCA, JAccumulation of Mn in rat corpus striatum slices was non-saturable, although relatively strongly temperature dependent and inhibited by 2,4-dinitrophenol (2,4-DNP). Once incorporated, the metal ion was released by K+ (55 mM) depolarization in the presence of Ca ions, following a time course of efflux parallel to that of [3H]dopamine ([3H]DA). The release of the metal ion was not induced by tyramine. [3H]DA release was also induced by low concentrations of MnCl2. The possibility exists that these findings may be related in some way to the functional deficiency of the nigro-striatal dopaminergic system found after Mn poisoning.