Navegando por Palavras-chave "cerebral cortex"

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    Amino acid and monoamine alterations in the cerebral cortex and hippocampus of mice submitted to ricinine-induced seizures
    (Elsevier B.V., 2002-07-01) Ferraz, A. C.; Anselmo-Franci, J. A.; Perosa, SR; Castro-Neto, E. F. de; Bellissimo, M. I.; Oliveira, B. H. de; Cavalheiro, E. A.; Naffah-Mazzacoratti, MDG; Da Cunha, C.; Univ Fed Parana; Fac Odontol; Universidade Federal de São Paulo (UNIFESP)
    The alkaloid ricinine isolated from the plant Ricinus communis, when administered to mice at high doses, induces clonic seizures accompanied by electroencephalographic alterations in the cerebral cortex and hippocampus. the lethal nature of ricinine-induced seizures is considered to be a good model for the study of the events that cause death during clonic seizures, particularly those related to respiratory spasms. the initial signs (pre-seizure period) were marked by exophthalmus and decreased locomotor behavior. Animals killed during the preseizure period presented an increased utilization rate (HVA/DA) of dopamine (DA), an increased concentration of noradrenaline (NA), and a decreased concentration of glutamate (Glu), glutamine (Gln), taurine (Tau), and serotonin (5-HT) in the cerebral cortex. the seizure period is characterized by the occurrence of hind limb myoclonus and respiratory spasms, which are followed by death. Alterations in the cerebral cortex concentration of these neurotransmitters persisted during the seizure period. These alterations are only partially observed in the hippocampus, mainly during the seizure period. the present results suggest that an increased release of Glu in the cerebral cortex can be implicated in the genesis of the ricinine-induced seizure and that it triggers many anticonvulsive mechanisms, like the release of Tau, DA, 5-HT, and NA. (C) 2002 Elsevier Science Inc. All rights reserved.
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    Rapid eye movement sleep deprivation induces changes in the high-affinity binding of [H-3]-ouabain to the rat cortical membranes
    (Elsevier B.V., 2006-03-27) Bignotto, Magda; Andrade, UJA de; Carvalho, JGB de; Venditti, Marco Antonio Campana [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Rapid eye movement sleep (REMS) suppresses seizures. On the other hand, REMS deprivation (REMSD) increases brain susceptibility to seizures. Sodium-postassium/ATPase is involved in the control of brain excitability. Ouabain, a cardiotonic glycoside, binds to a regulatory extracellular allosteric site in the sodium-potassium/ATPase inhibiting/stimulating its activity depending on its concentration. Endogenous ouabain-like substances exist in the brain; therefore, changes in the ouabain binding site may be involved in the increased brain excitability induced by REMSD. Adult, Wistar male rats were deprived of REMS for 96 hours by the flower-pot method (REMSD). A stress control group was kept in the same environment on a larger platform (LP). A third group of rats was kept in the same room in their home-cages (CONTROL). After REMSD all rats were sacrificed by decapitation and their cerebral cortex dissected. High-affinity [H-3]-ouabain binding was carried out in cortical crude membrane preparation using 8 concentrations of [H-3]-ouabain (1-24 nM). the results show a statistically significant increase of KID in the REMSD rats compared to both CONTROL and LP groups. There were no statistically significant differences in th B-max among the experimental groups. There was also no change either in cortical activity of K+ stimulated p-nitrophenylphosphatase, the dephosphorylation reaction of phosphorylated sodium-potassium/ATPase or in Mg2+-stimulated p-nitrophenylphosphatase. An increase in the KD of [H-3]-ouabain binding to the sodium-potassium/ATPase in REMSD rats indicates a lower affinity to the endogenous inhibitors/stimulators of the enzyme. Therefore, this decreased affinity of the endogenous ouabain-like substances may be involved in the increased excitability induced by REMSD. (c) 2005 Elsevier Ireland Ltd. All rights reserved.