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Modulation of Dopamine Uptake and Release in Rat Striatal Synaptosomes by Glycine and Glutamate Publisher Pubmed



Messripour M1 ; Alibabaie Z1
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Authors Affiliations
  1. 1. Department of Biochemistgry Faculty of Pharmacy, Isfahan Medical Sciences University, Isfahan, Iran

Source: Molecular and Chemical Neuropathology Published:1994


Abstract

The uptake and release of dopamine (DA) by rat brain striatal synaptosomes were studied in presence of glycine or glutamate (0.5-20 m M) in incubation media containing 5 or 55 m M KCl. In low K+ medium glycine, up to 5 m M had little effect on DA uptake, but higher concentrations of the amino acid inhibited the uptake. High K+ medium resulted in a decrease in DA uptake as compared to that of basal K+ medium. Glycine at 1 μM, but not at higher concentrations, prevented the inhibition induced by high K+ depolarization. However, glutamate in the low K+ medium and at a 0.5 m M concentration, stimulated DA uptake, but at higher concentrations it inhibited the uptake. In the high K+ medium, glutamate in all concentrations potentiated the inhibition of DA uptake induced by K+ depolarization. The DA release response of the synaptosomes to glycine concentrations (1-20 m M) in low K+ medium was a biphasic pattern, with a stimulation at 1 m M and an inhibition at higher concentrations. This pattern was reversed when DA release was measured in the high K+ medium. The pattern of DA release in the presence of glutamate concentrations (1-20 m M) was a triphasic one, with an inhibition at 1 m M, stimulation at 5 m M, and a less effective inhibition at higher concentrations. In the high K+ medium, glutamate at 1 m M concentration prevented the stimulation induced by K+ depolarization, but at 5 m M reversed the rate of release to the depolarization state. Results of this study suggest that glycine and glutamate have more than a simple inhibitory or excitatory transmitter role in the striatum, respectively. The identical effects of glycine with that of glutamate in certain concentrations is consistent with previous reports that glycine and N-methyl d-aspartate (NMDA) act as coagonists of a common excitatory amino acid receptor. © 1994 Humana Press Inc.
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