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In vivo effects of phosphodiesterase inhibition on basal cGMP levels in the pre-frontal cortex, hippocampus and cerebellum of freely moving rats.
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GABAA, but not NMDA, receptors modulate in vivo NO-mediated cGMP synthesis in the rat cerebral cortex
No full textEffects of dopamine receptor agonists on the efflux of excitatory and inhibitory amino acids in Parkinson's disease patients: A microdialysis approach
No full textIn vivo activation of N-methyl-D-aspartate receptors in the rat hippocampus increases prostaglandin E2 extracellular levels and triggers lipid peroxidation through cyclooxygenase-mediated mechanisms
No full textCyclooxygenase-1 and -2 differently contribute to prostaglandin E2 synthesis and lipid peroxidation after in vivo activation of N-methyl-D-aspartate receptors in rat hippocampus.
No full textUsing intracerebral microdialysis, we reported previously that acute in vivo activation of NMDA glutamate receptors triggers rapid and transient releases of prostaglandin E2 (PGE2) and F2-isoprostane 15-F2t-IsoP in the hippocampus of freely moving rats. The formation of the two metabolites – produced through cyclo-oxygenase (COX) enzymatic activity and free radical-mediated peroxidation of arachidonic acid (AA), respectively, – was prevented by the specific NMDA antagonist MK-801, and was largely dependent on COX-2 activity. Here, we demonstrate that besides COX-2, which is the prominent COX isoform in the brain and particularly in the hippocampus, the constitutive isoform, COX-1 also contributes to prostaglandin (PG) synthesis and oxidative damage following in vivo acute activation of hippocampal NMDA glutamate receptors. The relative contribution of the two isoforms is dynamically regulated, as the COX-2 selective inhibitor NS398 immediately prevented PGE2 and 15-F2t-IsoP formation during the application of NMDA, whereas the COX-1 selective inhibitor SC560 was effective only 1 h after agonist infusion. Our data suggest that, although COX-2 is the prominent isoform, COX-1 activity may significantly contribute to excitotoxicity, particularly when considering the amount of lipid peroxidation associated with its catalytic cycle. We suggest that both isoforms should be considered as possible therapeutic targets to prevent brain damage caused by excitotoxicity
Clinical and electrophysiological effects of apomorphine in Parkinson's disease are not paralleled by aminoacid release changes: a microdialysis study
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