Browsing by Author "ABARCA, J"
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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.
- ItemEFFECT OF INTRANIGRAL MN-2+ ON STRIATAL AND NIGRAL SYNTHESIS AND LEVELS OF DOPAMINE AND COFACTOR(1991) DANIELS, AJ; ABARCA, JA single injection of manganese chloride into the rat substantia nigra caused a significant and reversible drop in nigral and striatal dopamine and cofactor content ipsilateral to the lesion. Maximal decrease, in both tissues, was observed 60 days after the lesion, and showed complete recovery at 90 days. In vivo striatal tyrosine hydroxylation and GTP cyclohydrolase activities were also decreased maximally at 60 days and were recovered by 90 days after the lesion. No effects were observed on the side contralateral to the injection.
- ItemRAT STRIATAL DOPAMINE AND TETRAHYDROBIOPTERIN CONTENT FOLLOWING AN INTRASTRIATAL INJECTION OF MANGANESE CHLORIDE(1986) LISTA, A; ABARCA, J; RAMOS, C; DANIELS, AJInjection of manganese into the rat corpus striatum causes a rapid fall in the biopterin and dopamine (DA) content ipsilateral to the lesion. Two weeks after the lesion both biopterin and DA are partially recovered. Controls, injected with saline or magnesium, do not show alterations in their DA or cofactor levels. It is proposed that the fall in DA levels results from a rapid displacement of the amine from its storage sites by manganese followed by a decrease in the rate of DA synthesis causes by the drop in cofactor levels.
- ItemRELEASE OF D-[H-3] ASPARTIC ACID FROM THE RAT STRIATUM - EFFECT OF VERATRIDINE-EVOKED DEPOLARIZATION, FRONTO-PARIETAL CORTEX ABLATION, AND STRIATAL LESIONS WITH KAINIC ACID(1985) ARQUEROS, L; ABARCA, J; BUSTOS, GThe spontaneous and depolarization-evoked release of radiolabeled D-aspartic acid, previously taken up by rat striatal slices, was studied by using a superfusion system. Veratridine (10-50 .mu.M), electrical field stimulation (20 Hz, 1.0 V, 60 s), and K (53 mM) markedly potentiated the release of D-[3H]aspartate from striatal slices. The release of L-[3H]glutamate was also increased by veratridine, according to a pattern and time course of release similar to that of D-[3H]aspartate. The ratio of D-[3H]aspartic acid release evoked by veratridine over-spontaneous levels of release was much higher when compared to that of radiolabeled L-glutamate. Omission of Ca from the superfusion medium almost completely suppressed D-[3H]aspartate release evoked by veratridine or by electrical stimulation whereas high K+-evoked release of the [3H]amino acid was only slightly reduced. Increasing Mg2+ concentration of 12 mM in the superfusion medium did substantially block D-[3H]aspartate release induced by K+-depolarization. Tetrodotoxin (1 .mu.M), a blocker of voltage-dependent Na+ channels, totally abolished veratridine-evoked release of D-[3H]aspartate from striatal slices. Lesion studies showed that unilateral ablation of the frontoparietal cortex was accompanied by a significant decrease in the high-affinity uptake of striatal D-[3H]aspartate and by a large and parallel loss from striatal slices in D-[3H]aspartate release evoked by either veratridine or high K+. In contrast, unilateral injection of kainic acid into the striatum did not influence depolarization-evoked release of D-[3H]asparate from striatal slices. D-[3H]aspartic acid may be taken up preferentially and then released, in a Ca2+-dependent manner, by veratridine and electrical stimulation from nerve terminals belonging to the cortico-striatal pathway. Excitatory amino acids may act as neurotransmitters at the cortico-striatal nerve fibers.
- ItemRELEASE OF D-[H-3] ASPARTIC ACID FROM THE RAT SUBSTANTIA NIGRA - EFFECT OF VERATRIDINE-EVOKED DEPOLARIZATION AND CORTICAL ABLATION(1985) ABARCA, J; BUSTOS, GThe spontaneous and veratridine-evoked release of radioactive D-aspartic acid, previously taken up by rat substantia nigra slices, was studied by using a superfusion system. Veratridine (25 .mu.M, 1 min) markedly produced a 14-fold increase in D-[3H]aspartic acid release from nigral slices. Omission of Ca2+ and increasing Mg2+ concentration to 12 mM in the superfusion medium did substantially block D-[3H]aspartate release induced by veratridine depolarization. Veratridine was able to evoke [3H]amino acid release which seemed to be, at least, 30% Ca2+-independent. Tetrodotoxin (0.01-0.1 .mu.M), a blocker of voltage-dependent Na+ channels, totally abolished veratridine-evoked release of D-[3H]aspartate from nigral slices. Lesion studies were performed to learn about the nature of the neuronal compartment in the substantia nigra upon which veratridine-depolarization acted to induce D-[3H]aspartate release. Unilateral ablation of the fronto-parietal cortex was accompanied by a significant decrease in the accumulation of nigral D-[3H]aspartate and by a large loss from ipsilateral nigral slices in D-[3H]aspartate release evoked by veratridine. Both the accumulation and veratridine-evoked release of [3H]dopamine, remained unchanged in the ipsilateral substantia nigra slices to the lesion. D-[3H]aspartic acid may be taken up and then released, in a Ca2+-dependent manner, by nerve terminals located in the substantia nigra. L-glutamate and/or L-aspartate may act as neurotransmitters at the cortico-nigral neuronal pathway.
- 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.