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Measurement of Total Calcium in Neurons by Electron Probe X-ray Microanalysis
Published on: November 20, 2013
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Calcium ion--the key player in cerebral ischemia
V S Suvanish Kumar, A Gopalakrishnan, M Naziroğlu
1School of Biotechnology, Coordinator, DBT -Centre for Bioinformatics, National Institute of Technology Calicut, Calicut 673601, India. rajanikant@nitc.ac.in.
Current Medicinal Chemistry
|December 31, 2013
Summary
Calcium ion (Ca2+) is crucial for neuron function and development. Dysregulation of Ca2+ homeostasis leads to neuronal death and brain damage, particularly in cerebral ischemia.
Area of Science:
- Neuroscience
- Cell Biology
- Biochemistry
Background:
- Calcium ion (Ca2+) plays a critical role in neuronal function, including ATP production and central nervous system development.
- Disruptions in Ca2+ homeostasis can trigger cell death pathways, leading to neuronal demise and potential brain damage.
- Cerebral ischemia involves complex signaling cascades where endoplasmic reticulum and ion channels mediate cellular damage.
Purpose of the Study:
- To elucidate the multifaceted role of calcium ion (Ca2+) in neuronal functioning and death.
- To examine the mechanisms underlying Ca2+ homeostasis failure in the context of neuronal health.
- To highlight Ca2+ as a key factor in cerebral damage following ischemic events.
Main Methods:
- Review and synthesis of existing literature on calcium ion (Ca2+) roles in neuronal physiology and pathology.
- Analysis of studies investigating the involvement of endoplasmic reticulum and specific ion channels (CaVs, TRP, NMDAR) in neuronal damage.
- Evaluation of the impact of Ca2+ dysregulation on neuronal survival and brain injury.
Main Results:
- Calcium ion (Ca2+) is essential for normal neuronal operations from early development to maturity.
- Impaired Ca2+ regulation results in excessive intracellular Ca2+ accumulation, initiating detrimental signaling cascades.
- These cascades overwhelm neuronal defense mechanisms, culminating in cell death and exacerbating brain damage, especially in ischemic conditions.
Conclusions:
- Calcium ion (Ca2+) is a significant contributor to neuronal death and cerebral damage post-ischemia.
- Understanding Ca2+ regulatory mechanisms and the consequences of their failure is vital for addressing neurological disorders.
- Targeting Ca2+ pathways presents a potential therapeutic strategy for mitigating ischemic brain injury.
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