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Cav2.3 channel function and Zn2+-induced modulation: potential mechanisms and (patho)physiological relevance
Felix Neumaier1,2, Toni Schneider3, Walid Albanna4
1Forschungszentrum Jülich GmbH, Institute of Neuroscience and Medicine, Nuclear Chemistry (INM-5) , Jülich, Germany.
Channels (Austin, Tex.)
|October 20, 2020
Summary
Voltage-gated calcium channels (VGCCs) are crucial for calcium influx. This review explores Cav2.3 VGCCs, their structure, function, and zinc modulation, suggesting a role in translating zinc signals in tissues.
Area of Science:
- Molecular and Cellular Biology
- Neuroscience
- Biophysics
Background:
- Voltage-gated calcium channels (VGCCs) regulate calcium ion (Ca²⁺) influx in excitable cells, yet their precise functions remain incompletely understood.
- Atomic-resolution homology models of human VGCCs offer a structural basis for investigating Ca²⁺ flux mechanisms.
Purpose of the Study:
- To review the structure, function, and zinc (Zn²⁺)-induced modulation of Cav2.3 VGCCs, known for mediating R-type currents.
- To explore the physiological relevance of Cav2.3 channel activity in response to endogenous Zn²⁺ signals.
Main Methods:
- Utilizes recent atomic-resolution homology models of human VGCCs for structural analysis.
- Reviews existing literature on Cav2.3 channel function, Zn²⁺ modulation mechanisms, and physiological Zn²⁺ signaling.
Main Results:
- Cav2.3 VGCCs exhibit unique sensitivity to Zn²⁺, with multiple mechanisms of action.
- Zn²⁺'s modulatory role is supported by its presence in neuronal, endocrine, and reproductive tissues where Cav2.3 channels are expressed.
Conclusions:
- Cav2.3 channel expression correlates with endogenous Zn²⁺ pools, suggesting a role in physiological Zn²⁺ signaling.
- These channels may act as a critical link, translating extracellular Zn²⁺ signals into cellular electrical activity and intracellular Ca²⁺ level changes.
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