NDLI: Changes in Brain Cholesterol Metabolome After Excitotoxicity

Content Provider	Springer Nature Link
Author	Ong, Wei Yi Kim, Ji Hyun He, Xin Chen, Peng Farooqui, Akhlaq A. Jenner, Andrew M.
Copyright Year	2010
Abstract	Excitotoxicity due to excess stimulation of glutamate receptors in neurons is accompanied by increased Ca$^{2+}$ influx, stimulation of Ca$^{2+}$-dependent enzymes, ATP depletion, increase in lipid peroxidation products, and loss of glutathione. These changes resemble neurochemical alterations in acute neuronal injury (stroke, spinal cord injury, and traumatic brain injury) and chronic neurodegenerative diseases such as Alzheimer’s disease. Intracerebroventricular injection of the potent glutamate analog kainate in rats results in increased cholesterol concentration in the hippocampus at short to medium time intervals, i.e., 3 days–1 week post-injection, as detected by gas chromatography–mass spectrometry in the lesioned hippocampus. This is accompanied by an early increase in levels of cholesterol biosynthetic precursors and increases in both enzymatically derived oxysterols such as 24-hydroxycholesterol and cholesterol oxidation products (COPs) generated by reactive oxygen species, including cholesterol epoxides and 7-ketocholesterol. In contrast to COPs, no change in concentration of the neurosteroid pregnenolone was found after KA injury. Cholesterol and COPs significantly increase exocytosis in cultured PC12 cells and neurons, and both oxysterols and COPs are able to induce cytotoxic and apoptotic injuries in different cell types, including neurons. Together, the findings suggest that increased cholesterol and COPs after KA excitotoxicity could themselves lead to disturbed neuronal ion homeostasis, increased neurotransmitter release, and propagation of excitotoxicity.
Starting Page	299
Ending Page	313
Page Count	15
File Format	PDF
ISSN	08937648
Journal	Molecular Neurobiology
Volume Number	41
Issue Number	2-3
e-ISSN	15591182
Language	English
Publisher	Humana Press Inc
Publisher Date	2010-02-06
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Cholesterol Oxysterols Cholesterol oxidation products Brain injury Kainate Excitotoxicity Neurology Cell Biology Neurobiology Neurosciences
Content Type	Text
Resource Type	Article
Subject	Neurology Cellular and Molecular Neuroscience

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