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Release of dopamine from striatal synaptosomes
Annali Dell'Istituto Superiore Di Sanita
|January 1, 1978
Summary
Dopamine (DA) release from nerve endings involves both carrier-mediated and calcium-dependent processes. Nomifensine, a DA carrier blocker, distinguished these pathways, revealing distinct mechanisms for DA release.
Area of Science:
- Neuroscience
- Neurochemistry
- Pharmacology
Background:
- Dopamine (DA) is a crucial neurotransmitter involved in various brain functions.
- Understanding the mechanisms of DA release from central nerve endings is vital for neurological research.
Purpose of the Study:
- To investigate the mechanisms of dopamine (DA) release from rat striatal synaptosomes.
- To differentiate between DA release mediated by the DA carrier and release independent of the carrier using nomifensine.
Main Methods:
- Utilized superfused rat striatal synaptosomes prelabeled with 3H-DA.
- Employed nomifensine as a tool to block DA carrier-mediated release.
- Investigated the effects of sodium gradient alterations, amphetamine, high K+, veratridine, and ionophore A23187 on DA release.
Main Results:
- Sodium gradient alterations enhanced carrier-mediated DA release, blocked by nomifensine.
- Amphetamine-induced DA release was nomifensine-sensitive, indicating carrier involvement.
- High K+ depolarization released newly taken up and synthesized DA.
- Calcium-dependent DA release was unaffected by nomifensine, suggesting an exocytic-like process.
- Apomorphine and neuroleptics did not support presynaptic receptor-mediated inhibitory control of DA release.
Conclusions:
- Dopamine release involves both carrier-mediated and calcium-dependent, exocytic-like mechanisms.
- Nomifensine effectively distinguishes between these DA release pathways.
- Evidence does not support a presynaptic receptor-mediated inhibitory control of DA release similar to noradrenaline.