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J Neurophysiol 87: 2851-2857, 2002;
0022-3077/02 $5.00
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The Journal of Neurophysiology Vol. 87 No. 6 June 2002, pp. 2851-2857
Copyright ©2002 by the American Physiological Society

Cyclooxygenase-2 Regulates Prostaglandin E2 Signaling in Hippocampal Long-Term Synaptic Plasticity

Chu Chen, Jeffery C. Magee, and Nicolas G. Bazan

Neuroscience Center, School of Medicine, Louisiana State University Health Sciences Center, New Orleans, Louisiana 70112

Chen, Chu, Jeffery C. Magee, and Nicolas G. Bazan. Cyclooxygenase-2 Regulates Prostaglandin E2 Signaling in Hippocampal Long-Term Synaptic Plasticity. J. Neurophysiol. 87: 2851-2857, 2002. The functional significance of cyclooxygenases (COX-1 and -2), the key enzymes that convert arachidonic acid (AA) to prostaglandins (PGs) in brain, is unclear, although they have been implicated in cellular functions and in some neurologic disorders, including stroke, epilepsy, and Alzheimer's disease. Recent evidence that COX-2 is expressed in postsynaptic dendritic spines (which are specialized structures involved in synaptic signaling) and is regulated by synaptic activity implies participation of COX-2 in neuronal plasticity. However, direct evidence is lacking. Here we demonstrate that selective COX-2 inhibitors significantly reduced postsynaptic membrane excitability, back-propagating dendritic action potential-associated Ca2+ influx, and long-term potentiation (LTP) induction in hippocampal dentate granule neurons, while a COX-1 inhibitor is ineffective. All of these actions were effectively reversed by exogenous application of PGE2 but not of PGD2 or PGF2alpha . Our results indicate that COX-2-generated PGE2 regulates membrane excitability and long-term synaptic plasticity in hippocampal perforant path-dentate gyrus synapses.




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