+ Site Statistics
+ Search Articles
+ Subscribe to Site Feeds
EurekaMag Most Shared ContentMost Shared
EurekaMag PDF Full Text ContentPDF Full Text
+ PDF Full Text
Request PDF Full TextRequest PDF Full Text
+ Follow Us
Follow on FacebookFollow on Facebook
Follow on TwitterFollow on Twitter
Follow on LinkedInFollow on LinkedIn

+ Translate

Release of tritiated d aspartic acid from the rat striatum effect of veratridine evoked depolarization frontoparietal cortex ablation and striatal lesions with kainic acid

Release of tritiated d aspartic acid from the rat striatum effect of veratridine evoked depolarization frontoparietal cortex ablation and striatal lesions with kainic acid

Biochemical Pharmacology 34(8): 1217-1224

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 .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.

(PDF emailed within 1 workday: $29.90)

Accession: 006306540

Download citation: RISBibTeXText

Related references

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. Biochemical Pharmacology 34(8): 1217-1224, 1985

Release of tritiated d aspartic acid from the rat substantia nigra effect of veratridine evoked depolarization and cortical ablation. Neurochemistry International 7(2): 229-236, 1985

Release of d-[(3)H]aspartic acid from the rat substantia nigra: effect of veratridine-evoked depolarization and cortical ablation. Neurochemistry International 7(2): 229-236, 1985

Tritiated kainic acid binding alterations after striatal kainic acid lesions. Pharmacologist 20(3): 239, 1978

Effects of acromelic acid a on the binding of tritiated glutamic acid and tritiated kainic acid to synaptic membranes and on the depolarization at the frog spinal cord. Brain Research 504(2): 328-331, 1989

Effect of psychotropic drugs and gamma amino butyric acid analogues and derivatives on tritiated d aspartic acid release from perfused synaptosomes of rat brain cortex. Farmakologiya i Toksikologiya (Moscow) 50(1): 10-14, 1987

L glutamate specific tritiated kainic acid binding in the rat neo striatum after degeneration of the cortico striatal pathway. Neuroscience Letters 11(3): 341-346, 1979

Effects of glutamic acid, kainic acid and aspartic acid on GABA release from rat retina degenerated by kainic acid. Japanese Journal of Ophthalmology 28(1): 57-61, 1984

Picolinic acid modulates kainic acid-evoked glutamate release from the striatum in vitro. Brain Research. 627(2): 198, 1993

Excitatory amino acid receptors in the human cerebral cortex a quantitative autoradiographic study comparing the distributions of tritiated tcp tritiated glycine tritiated l glutamate tritiated ampa and tritiated kainic acid binding sites. Neuroscience 32(3): 587-608, 1989

Change in the distribution of acetylcholinesterase molecular forms in frontoparietal cortex of the rat following nucleus basalis lesions with kainic acid. Brain Research 449(1-2): 391-394, 1988

Release of radio labeled dopamine serotonin acetyl choline and gamma amino butyric acid from slices of rat striatum after intra striatal kainic acid injections. Brain Research 135(2): 368-373, 1977

Serotonin stimulated release of tritiated dopamine via reversal of the dopamine transporter in rat striatum and nucleus accumbens a comparison with release elicited by potassium n methyl d aspartic acid glutamic acid and d amphetamine. Journal of Pharmacology & Experimental Therapeutics 262(1): 356-364, 1992

Changes of tritiated colchicine binding and protein synthesis in the rat striatum following kainic acid lesions. Brain Research 146(1): 195-199, 1978

Excitatory amino acid evoked release of tritiated gamma aminobutyric acid from striatal neurons in primary culture. Journal of Neurochemistry 51(2): 435-441, 1988