The formation and regional distribution of prostaglandins D2 and F2α in the brain of spontaneously convulsing gerbils

Seregi, András; ̈rstermann, Ulrich Fo; Heldt, Renate; Hertting, G.

doi:10.1016/0006-8993(85)91626-9

Cited by 27 publications

(12 citation statements)

References 21 publications

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“…The authors concluded that, during convulsions, there is a selective formation of potentially anticonvulsant prostaglandins (mainly PGD 2 ), especially in areas functionally involved in epilepsy. This finding is compatible with the hypothesis that endogenously formed prostaglandins may play a role in the regulation of seizure activity 19 . We conclude that elevated PGD 2 levels following FC may be responsible for the restriction of the duration and severity of the seizures.…”

Section: Discussionsupporting

confidence: 90%

“…However, we did find significantly elevated PGD 2 levels in the CSF in FC patients. Seregi et al have studied the distribution of PGF 2α and PGD 2 in different regions of the brain in convulsion‐prone gerbils 19 . Following convulsions elicited by environmental stress, prostaglandin concentrations increased in all areas, with the largest increases being observed in the hippocampus and cortex.…”

Section: Discussionmentioning

confidence: 99%

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Proinflammatory cytokines, prostaglandins and zinc in febrile convulsions

Tütüncüoğlu¹,

Kütükçüler²,

Kepe³

et al. 2001

Pediatrics International

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Proinflammatory cytokines, prostaglandins and zinc in febrile convulsions

Tütüncüoğlu¹,

Kütükçüler²,

Kepe³

et al. 2001

Pediatrics International

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“…PG receptor subtypes that are not positively coupled to cAMP could mediate toxic effects, for example the EP3 or the EP1 receptor, or other prostanoids such as the FP receptor, which promotes neuronal death in spinal cord injury (Kitanaka et al, 1993;Liu et al, 2001) and is coupled to increased PI turnover and elevation of intracellular Ca 2ϩ . PGF 2 ␣ levels increase in models of excitotoxicity (Seregi et al, 1985;Ogawa et al, between groups at any flow increment, suggesting that the loss of the EP2 receptor does not alter the distribution of tissue volume with low to near-zero perfusion during middle cerebral artery occlusion. H, Colorized autoradiograms from a pair of representative WT and EP2Ϫ/Ϫ brains are shown with sections taken at -2, Ϫ1, 0, ϩ1, and ϩ 2 mm from the bregma showing changes in CBF at 90 min of MCAO.…”

Section: Discussionmentioning

confidence: 92%

Neuroprotective Function of the PGE₂EP2 Receptor in Cerebral Ischemia

McCullough¹,

Wu²,

Haughey³

et al. 2004

J. Neurosci.

338

375

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The cyclooxygenases COX-1 and COX-2 catalyze the first committed step of prostaglandin synthesis from arachidonic acid. Previous studies in rodent stroke models have shown that the inducible COX-2 isoform promotes neuronal injury, and the administration of COX-2 inhibitors reduces infarct volume. We investigated the function of PGE 2 , a principal prostaglandin product of COX-2 enzymatic activity, in neuronal survival in cerebral ischemia. PGE 2 exerts its downstream effects by signaling through a class of four distinct G-proteincoupled EP receptors (for E-prostanoid: EP1, EP2, EP3, and EP4) that have divergent effects on cAMP and phosphoinositol turnover and different anatomical distributions in brain. The EP2 receptor subtype is abundantly expressed in cerebral cortex, striatum, and hippocampus, and is positively coupled to cAMP production. In vitro studies of dispersed neurons and organotypic hippocampal cultures demonstrated that activation of the EP2 receptor was neuroprotective in paradigms of NMDA toxicity and oxygen glucose deprivation. Pharmacologic blockade of EP2 signaling by inhibition of protein kinase A activation reversed this protective effect, suggesting that EP2-mediated neuroprotection is dependent on cAMP signaling. In the middle cerebral artery occlusion-reperfusion model of transient forebrain ischemia, genetic deletion of the EP2 receptor significantly increased cerebral infarction in cerebral cortex and subcortical structures. These studies indicate that activation of the PGE 2 EP2 receptor can protect against excitotoxic and anoxic injury in a cAMPdependent manner. Taken together, these data suggest a novel mechanism of neuroprotection mediated by a dominant PGE 2 receptor subtype in brain that may provide a target for therapeutic intervention.

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“…Determination of immunoreactive PGF2, was performed as described previously by Seregi et al (1985). For the radioimmunoassay of cysteinyl-LT the resuspended residue was extracted using CIB Sep-Pak as described by Juan et al (1987).…”

Section: Analytical Techniquesmentioning

confidence: 99%

Characterization of Seizure‐Induced Cysteinyl‐Leukotriene Formation in Brain Tissue of Convulsion‐Prone Gerbils

Simmet

Seregi

Hertting

1988

Journal of Neurochemistry

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Tonic-clonic seizures elicited in convulsion-prone gerbils resulted in a large increase in immunoreactive prostaglandin (PG) F2 alpha and in a smaller increase in immunoreactive leukotriene (LT) C4-like material in brain tissue. Brain tissue contents of both eicosanoids were found to reach a maximum at 6 min after the onset of seizures and were still elevated at 54 min after the beginning of convulsions. By reversed phase HPLC the immunoreactive LTC4-like material was identified as LTC4 and LTD4 at 6 min after the onset of convulsions, whereas at 54 min after the onset, transformation of LTD4 to LTE4 could be detected as well. In gerbils showing only weak seizure activity a small increase in PGF2 alpha but no increase in immunoreactive LTC4-like material could be detected at 6 min after the onset of convulsions. Pretreatment with indomethacin abolished the formation of PGF2 alpha but significantly enhanced the biosynthesis of immunoreactive LTC4-like material at 18 min after the beginning of seizures. The results demonstrate formation of cysteinyl-LT following tonic-clonic convulsions in spontaneously convulsing gerbils which could be enhanced by inhibition of the cyclooxygenase pathway of arachidonic acid metabolism. Since cysteinyl-LT have potent biological actions in various organs this finding warrants further investigations on the potential role of cysteinyl-LT in the CNS.

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The formation and regional distribution of prostaglandins D2 and F2α in the brain of spontaneously convulsing gerbils

Cited by 27 publications

References 21 publications

Proinflammatory cytokines, prostaglandins and zinc in febrile convulsions

Proinflammatory cytokines, prostaglandins and zinc in febrile convulsions

Neuroprotective Function of the PGE₂EP2 Receptor in Cerebral Ischemia

Characterization of Seizure‐Induced Cysteinyl‐Leukotriene Formation in Brain Tissue of Convulsion‐Prone Gerbils

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The formation and regional distribution of prostaglandins D2 and F2α in the brain of spontaneously convulsing gerbils

Cited by 27 publications

References 21 publications

Proinflammatory cytokines, prostaglandins and zinc in febrile convulsions

Proinflammatory cytokines, prostaglandins and zinc in febrile convulsions

Neuroprotective Function of the PGE2EP2 Receptor in Cerebral Ischemia

Characterization of Seizure‐Induced Cysteinyl‐Leukotriene Formation in Brain Tissue of Convulsion‐Prone Gerbils

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Neuroprotective Function of the PGE₂EP2 Receptor in Cerebral Ischemia