Release of D-[3H]aspartic acid from the rat striatum. Effect of veratridine-evoked depolarization, fronto-parietal cortex ablation, and striatal lesions with kainic acid.
The 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 microM), electrical field stimulation (20 Hz, 1.0 V, 60 sec), and potassium (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. However, 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 calcium 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. However, increasing Mg2+ concentration to 12 mM in the superfusion medium did substantially block D-[3H]aspartate release induced by K+-depolarization. Additional experiments showed that tetrodotoxin (1 microM), a blocker of voltage-dependent Na+ channels, totally abolished veratridine-evoked release of D-[3H]aspartate from striatal slices. Finally, 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]aspartate from striatal slices. The findings reported suggest that 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. In addition, the results provide further support for the view that excitatory amino acids may act as neurotransmitters at the cortico-striatal nerve fibers.
Arqueros
L
L
Abarca
J
J
Bustos
G
G
D000818:Animals; D001224:Aspartic Acid / Q000378:metabolism*; D002118:Calcium / Q000502:physiology; D002540:Cerebral Cortex / Q000502:physiology; D003342:Corpus Striatum / Q000187:drug effects / Q000378:metabolism* / Q000502:physiology; D005625:Frontal Lobe; D005971:Glutamates / Q000378:metabolism; D018698:Glutamic Acid; D007473:Ion Channels / Q000187:drug effects; D007608:Kainic Acid / Q000494:pharmacology; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D009434:Neural Pathways / Q000502:physiology; D018377:Neurotransmitter Agents / Q000378:metabolism*; D010296:Parietal Lobe; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D013779:Tetrodotoxin / Q000494:pharmacology; D014701:Veratridine / Q000494:pharmacology
D005971:Glutamates; D007473:Ion Channels; D018377:Neurotransmitter Agents; D001224:Aspartic Acid; D018698:Glutamic Acid; D013779:Tetrodotoxin; D014701:Veratridine; D011188:Potassium; D007608:Kainic Acid; D002118:Calcium