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Lipid signaling in experimental epilepsy.

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.
AuthorsKasie K Cole-Edwards, Nicolas G Bazan
JournalNeurochemical research (Neurochem Res) 2005 Jun-Jul Vol. 30 Issue 6-7 Pg. 847-53 ISSN: 0364-3190 [Print] United States
PMID16187219 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, U.S. Gov't, P.H.S., Review)
Topics
  • Animals
  • Epilepsy (metabolism, physiopathology)
  • Lipid Metabolism
  • Neuronal Plasticity
  • Signal Transduction

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