Related Experiment Video
Updated: Nov 6, 2025
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Use of Synaptic Zinc Histochemistry to Reveal Different Regions and Laminae in the Developing and Adult Brain
Published on: October 29, 2017
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Synaptic Zinc: An Emerging Player in Parkinson's Disease
Joanna Sikora1,2, Abdel-Mouttalib Ouagazzal1
1CNRS, Laboratoire de Neurosciences Cognitives, (UMR 729), Aix Marseille Université, 13331 Marseille, France.
International Journal of Molecular Sciences
|May 5, 2021
Summary
Altered zinc levels impact Parkinson's disease (PD) by affecting synaptic function. This study explores how synaptic zinc (Zn2+) influences PD, particularly its interaction with glutamate and NMDA receptors.
Area of Science:
- Neuroscience
- Neurochemistry
- Pathophysiology
Background:
- Zinc homeostasis is crucial in Parkinson's disease (PD) pathophysiology.
- Both zinc deficiency and excess contribute to PD.
- Synaptic zinc (Zn2+) acts as a neurotransmitter in the brain, particularly in cortico-striatal pathways.
Purpose of the Study:
- To review recent evidence linking synaptic zinc to PD.
- To discuss the mechanisms by which synaptic zinc contributes to PD.
- To highlight the interaction between zinc and NMDA receptors in PD.
Main Methods:
- Literature review of recent studies on zinc and PD.
- Analysis of the role of synaptic zinc in neuronal function.
- Focus on the interaction between Zn2+ and NMDA receptors.
Main Results:
- Synaptic zinc dysregulation is implicated in PD.
- Overactivation of the cortico-striatal glutamatergic system, involving zinc, is a key feature of PD.
- Zinc interacts functionally with NMDA receptors, influencing glutamatergic neurotransmission.
Conclusions:
- Synaptic zinc plays a significant role in the pathophysiology of Parkinson's disease.
- Understanding the mechanisms of synaptic zinc in PD may offer new therapeutic targets.
- The interaction between zinc and NMDA receptors is a critical area for PD research.
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