Modes of Calcium Regulation in Ischemic Neuron

Calcium (Ca 2+ ) dysregulation is a major catalytic event. Ca 2+ dysregulation leads to neuronal cell death and brain damage result in cerebral ischemia. Neurons are unable in maintaining calcium homeostasis. Ca 2+ homeostasis imbalance results in increased calcium influx and impaired calcium extrus...

Full description

Saved in:
Bibliographic Details
Published in:Indian journal of clinical biochemistry 2019-07, Vol.34 (3), p.246-253
Main Authors: Singh, Vineeta, Mishra, Vijaya Nath, Chaurasia, Rameshwar Nath, Joshi, Deepika, Pandey, Vibha
Format: Article
Language:English
Subjects:
Amino acids
Apoptosis
Biochemistry
Biomedical and Life Sciences
Brain
Brain damage
Brain injury
Calcium (intracellular)
Calcium buffering
Calcium homeostasis
Calcium influx
Cell death
Chemistry/Food Science
Drug development
Homeostasis
Injuries
Intracellular
Ischemia
Life Sciences
Microbiology
Neurons
Neuroprotection
Neurotoxicity
Pathology
Review
Review Article
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Calcium (Ca 2+ ) dysregulation is a major catalytic event. Ca 2+ dysregulation leads to neuronal cell death and brain damage result in cerebral ischemia. Neurons are unable in maintaining calcium homeostasis. Ca 2+ homeostasis imbalance results in increased calcium influx and impaired calcium extrusion across the plasma membrane. Ca 2+ dysregulation is mediated by different cellular and biochemical mechanism, which leads to neuronal loss resulting stroke/cerebral ischemia. A better understanding of the Ca 2+ dysregulation might help in the development of new treatments in order to reduce ischemic brain injury. An optimal concentration of Ca 2+ does not lead to neurotoxicity in the ischemic neuron. Intracellular Ca 2+ act as a trigger for acute neurotoxicity and this cause induction of long-lasting processes leading to necrotic and/or apoptotic post-ischemic delayed neuronal death or of compensatory, neuroprotective mechanisms has increased considerably. Moreover, routes of ischemic Ca 2+ influx to neurons, involvement of intracellular Ca 2+ stores and Ca 2+ buffers, spatial and temporal relations between ischemia-induced increases in intracellular Ca 2+ concentration and neurotoxicity will further increase our understanding about underlying mechanism and they can act as a target for the development of drugs. Here, in our article we are trying to provide a brief overview of various Ca 2+ influx pathways involve in ischemic neuron and how ischemic neuron attempts to counterbalance this calcium overload.
ISSN:0970-1915
0974-0422
DOI:10.1007/s12291-019-00838-9