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Cell Signaling and Neurotoxicity: 3H-Arachidonic acid release (Phospholipase A2) in cerebellar granule neurons
Citation:
KODAVANTI, PRASADA RAO S. Cell Signaling and Neurotoxicity: 3H-Arachidonic acid release (Phospholipase A2) in cerebellar granule neurons. Chapter 22, In Vitro Neurotoxicity: Methods and Protocols, Methods in Molecular Biology. Springer Science + Business Media, New York, NY, 758:321-328, (2011).
Impact/Purpose:
This book chapter is on the measurement of 3H-arachidonic acid (AA) release in rat neuronal cell cultures. This measurement indicates the activity of several phospholipases including phospholipase A2. AA is abundant in the membrane phospholipids of the brain where its release has been shown to be involved in synaptic plasticity processes, such as long-term potentiation. The release of 3H-AA is often used as a measure of phospholipase A2 activity in cell culture studies. AA is one of the key molecules in cell signaling. Cell signaling is a complex process which controls basic cellular activities and coordinates actions to maintain normal cellular homeostasis. Alterations in signaling processes have been associated with diseases such as neurolocgical], as well as, cancer, autoimmunitiy, and diabetes. Recent evidence also indicates a role for signaling molecules in the adverse effects associated with exposure to environmental chemicals. In our laboratory, we have demonstrated the relationship between stimulation of 3H-AA release by persistent chemicals such as polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDEs), and the associated cytotoxicity following in vitro exposure. Understanding the role of the AA signaling pathway in chemically-induced effects on the nervous system will provide specific mode of action information that can be used in assessing compound risk.
Description:
Cell signaling is a complex process which controls basic cellular activities and coordinates actions to maintain normal cellular homeostasis. Alterations in signaling processes have been associated with neurological diseases such as Alzheimer's and cerebellar ataxia, as well as, cancer, autoimmunitiy, and diabetes. Recent evidence also indicates a role for signaling molecules in the adverse effects associated with exposure to environmental chemicals. One of these signaling molecules is arachidonic acid (AA). AA is abundant in the membrane phospholipids ofthe brain where its release has been shown to be involved in synaptic plasticity processes, such as long-term potentiation. AA release is primarily produced by activation of phospholipases, most commonly by phospholipase Az. The release of 3H-AA is often used as a measure of phospholipase A2 activity in cell culture studies. In our laboratory, we have demonstrated the relationship between stimulation of 3H-AA release by persistent chemicals such as polychlorinated biphenyls (PCBs) and polybrorninated diphenyl ethers (PBDEs), and the associated cytotoxicity following in vitro exposure. Understanding the role of the AA signaling pathway in chemically-induced effects on the nervous system will provide specific mode of action information that can be used in assessing compound risk.