Journal
NEUROCHEMICAL RESEARCH
Volume 30, Issue 6-7, Pages 847-853Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-005-6878-4
Keywords
cyclooxygenase-2; diacylglycerol; epilepsy; phospholipids; prostaglandins; synaptic plasticity
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Funding
- NCRR NIH HHS [P20RR16816] Funding Source: Medline
- NEI NIH HHS [EY05121] Funding Source: Medline
- NINDS NIH HHS [NS23002, NS46741] Funding Source: Medline
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Glutamate release activates signaling pathways important for learning and memory, and over-stimulation of these pathways during seizures leads to aberrant synaptic plasticity associated with hyper-excitable, seizure-prone states. Seizures induce rapid accumulation of membrane lipid-derived fatty acids at the synapses which, evidence suggests, regulate maladaptive connectivity. Here we give an overview of the significance of the arachidonyl- and inositol-derived messengers, prostaglandins (PGs) and diacylglycerol (DAG), in experimental models of epilepsy. We use studies conducted in our own laboratory to highlight the pro-epileptogenic role of cyclooxygenase-2 (COX-2) and its products, the PGs, and we discuss the possible mechanisms by which PGs may regulate membrane excitability and synaptic transmission at the cellular level. We conclude with a discussion of AA-DAG signaling in synaptic plasticity and seizure susceptibility with an emphasis on recent studies in our laboratory involving DAG kinase epsilon (DGK epsilon)-knockout mice.
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