RELEASE 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

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dc.contributor.authorARQUEROS, L
dc.contributor.authorABARCA, J
dc.contributor.authorBUSTOS, G
dc.date.accessioned2025-01-23T19:27:22Z
dc.date.available2025-01-23T19:27:22Z
dc.date.issued1985
dc.description.abstractThe 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.
dc.fuente.origenWOS
dc.identifier.eissn1873-2968
dc.identifier.issn0006-2952
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/99718
dc.identifier.wosidWOS:A1985AGW5400015
dc.issue.numero8
dc.language.isoen
dc.pagina.final1224
dc.pagina.inicio1217
dc.revistaBiochemical pharmacology
dc.rightsacceso restringido
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleRELEASE 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
dc.typeartículo
dc.volumen34
sipa.indexWOS
sipa.trazabilidadWOS;2025-01-12
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