Abstract |
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 (DGKepsilon)-knockout mice.
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Authors | Kasie K Cole-Edwards, Nicolas G Bazan |
Journal | Neurochemical research
(Neurochem Res)
2005 Jun-Jul
Vol. 30
Issue 6-7
Pg. 847-53
ISSN: 0364-3190 [Print] United States |
PMID | 16187219
(Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, U.S. Gov't, P.H.S., Review)
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Topics |
- Animals
- Epilepsy
(metabolism, physiopathology)
- Lipid Metabolism
- Neuronal Plasticity
- Signal Transduction
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