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Zinc mediates the neuronal activity-dependent anti-apoptotic effect
Mei Qiu1,2, Yang-Ping Shentu1, Ji Zeng3
1Department of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Plos One
|August 9, 2017
Summary
Synaptic activity protects neurons from apoptosis, a cell death process. This neuroprotection is mediated by zinc released during neuronal signaling, enhancing cell survival.
Area of Science:
- Neuroscience
- Cell Biology
- Biochemistry
Background:
- Synaptic activity enhances neuronal resistance to apoptosis, but mechanisms are unclear.
- Zinc is known to promote cell survival.
- The role of synaptically released zinc in this protective effect is unknown.
Purpose of the Study:
- To investigate the role of synaptically released zinc in activity-dependent neuronal resistance to apoptosis.
Main Methods:
- Cultured hippocampal slices and primary neurons were used.
- Apoptosis was induced using staurosporine (STP).
- Synaptic activity was enhanced using bicuculline (Bic)/4-Aminopyridine (AP).
- Zinc was chelated using Ca-EDTA.
Main Results:
- Enhanced synaptic activity significantly prevented staurosporine-induced neuronal apoptosis.
- Increased neuronal survival and suppressed caspase-3 activity were observed with enhanced activity.
- Chelation of synaptically released zinc with Ca-EDTA completely blocked the anti-apoptotic effect of enhanced synaptic activity.
Conclusions:
- Synaptic activity confers resistance to apoptosis in neurons.
- This neuroprotective effect is mediated by zinc released from synapses.
- Synaptically released zinc plays a crucial role in neuronal survival under apoptotic stress.
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