Navegando por Palavras-chave "cortex"

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    The brain decade in debate: I. Neurobiology of learning and memory
    (Associação Brasileira de Divulgação Científica, 2000-09-01) Baddeley, Alan; Bueno, Orlando Francisco Amodeo [UNIFESP]; Cahill, Larry; Fuster, Joaquin .m.; Izquierdo, Ivan Antônio; Mcgaugh, James.l; Morris, Richard.g.m.; Nadel, Lynn; Routtenberg, A.; Xavier, Gilberto Fernando; Da Cunha, Cláudio; University of Bristol Department of Psychology; Universidade Federal de São Paulo (UNIFESP); University of California Center for Neurobiology of Learning and Memory Department of Neurobiology and Behavior; University of California Neuropsychiatric Institute; Universidade Federal do Rio Grande do Sul Instituto de Biociências Departamento de Bioquímica; University of Edinburgh Department of Neuroscience; University of Arizona Department of Psychology; Northwestern University; Universidade de São Paulo (USP); Universidade Federal do Paraná Departamento de Farmacologia Laboratório de Fisiologia e Farmacologia do Sistema Nervoso Central
    This article is a transcription of an electronic symposium in which some active researchers were invited by the Brazilian Society for Neuroscience and Behavior (SBNeC) to discuss the last decade's advances in neurobiology of learning and memory. The way different parts of the brain are recruited during the storage of different kinds of memory (e.g., short-term vs long-term memory, declarative vs procedural memory) and even the property of these divisions were discussed. It was pointed out that the brain does not really store memories, but stores traces of information that are later used to create memories, not always expressing a completely veridical picture of the past experienced reality. To perform this process different parts of the brain act as important nodes of the neural network that encode, store and retrieve the information that will be used to create memories. Some of the brain regions are recognizably active during the activation of short-term working memory (e.g., prefrontal cortex), or the storage of information retrieved as long-term explicit memories (e.g., hippocampus and related cortical areas) or the modulation of the storage of memories related to emotional events (e.g., amygdala). This does not mean that there is a separate neural structure completely supporting the storage of each kind of memory but means that these memories critically depend on the functioning of these neural structures. The current view is that there is no sense in talking about hippocampus-based or amygdala-based memory since this implies that there is a one-to-one correspondence. The present question to be solved is how systems interact in memory. The pertinence of attributing a critical role to cellular processes like synaptic tagging and protein kinase A activation to explain the memory storage processes at the cellular level was also discussed.
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    GM1 ganglioside induces vasodilation and increases catalase content in the brain
    (Elsevier B.V., 2007-09-15) Furian, Ana Flavia; Oliveira, Mauro Schneider; Royes, Luiz Fernando Freire; Fiorenza, Natalia Gindri; Fighera, Michele Rechia; Myskiw, Jociane Carvalho; Weiblen, Rudi; Rubin, Maribel Antonello; Frussa-Filho, Roberto; Mello, Carlos Fernando; Universidade Federal de Sergipe (UFS); Univ Fed Rio Grande do Sul; Universidade Federal de São Paulo (UNIFESP)
    Monosialoganglioside (GM1) is a glycosphingolipid present in most cell membranes that displays antioxidant and neuroprotective properties. GM I increases catalase activity in cerebral cortices in vivo, but the mechanisms underlying this effect of GM I are not known. in the current study we investigated the effect of GM1 (50 mg/kg, ip) on the content of hemoglobin and catalase activity of hippocampus, cortex, and striatum of rats. GM I administration increased catalase activity and hemoglobin content in brain samples after 30 min, but had no effect on blood catalase activity. GM1-induced increase in catalase activity was abolished by brain perfusion with heparinized saline. Brain catalase activity in the absence of blood, estimated by regression analysis of data from perfused and nonperfused animals, was not altered by the systemic injection of GM1. Moreover, the addition of GM1 (30 or 100 mu M) did not increase catalase activity in slices of cerebral cortex in situ, further suggesting that blood circulation is required for this effect. the GM1-induced vasodilation was confirmed in vivo, because the systemic injection of GM1 (50 mg/kg, ip) increased (1.2-1.6 times) the width of pial vessels. (c) 2007 Elsevier Inc. All rights reserved.
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    Intrastriatal methylmalonic acid administration induces convulsions and TBARS production, and alters Na+,K+-ATPase activity in the rat striatum and cerebral cortex
    (Blackwell Publishing Inc, 2003-06-01) Malfatti, CRM; Royes, LFF; Francescato, L.; Sanabria, Emilio Rafael Garrido [UNIFESP]; Rubin, M. A.; Cavalheiro, Esper Abrão [UNIFESP]; Mello, C. F.; Universidade Federal de Sergipe (UFS); Univ Santa Cruz Do Sul; Universidade Federal de São Paulo (UNIFESP)
    Purpose: Methylmalonic acid (MMA) inhibits succinate dehydrogenase (SDH) and beta-hydroxybutyrate dehydrogenase activity in vitro. Acute intrastriatal administration of MMA induces convulsions through glutamatergic mechanisms probably involving primary adenosine triphosphate (ATP) depletion and free radical generation. in this study we investigated whether the intrastriatal administration of MMA causes lipoperoxidation and alteration in Na+, K+-ATPase activity ex vivo and characterized the electrographic changes elicited by the intrastriatal administration of this organic acid.Methods: MMA-induced lipoperoxidation, alterations in Na+, K+-ATPase activity and electrographic changes were measured by measuring total thiobarbituric acid-reacting substances and inorganic phosphate release by spectrophotometry, and by depth electrode recording, respectively.Results: We demonstrated that intrastriatal NIMA (6 mmol) injection causes convulsive behavior and electrographically recorded convulsions that last similar to2 h. Concomitant with the increase of thiobarbituric acid-reacting substances (TBARS) content, we observed a significant inhibition of Na+,K+-ATPase activity in the striatum, and activation of Na+K+-ATPase activity in the ipsilateral cerebral cortex. Intrastriatal MMA injection increased the content of TBARS in the striatum measured 30 min (32.4 +/- 12.0%, compared with the noninjected contralateral striatum) and 3 h (39.7 +/- 5.1%, compared with the noninjected contralateral striatum) after MMA injection. TBARS content of the ipsilateral cerebral cortex increased after MMA injection at 30 min (42.1 +/- 6.0%) and 3 h (40.4 +/- 20.2%), and Na+K+-TPase activity in the ipsilateral cerebral cortex increased during ictal activity (113.8 +/- 18%) and returned to basal levels as electrographic convulsions vanished in the cortex. Interestingly, intrastriatal MMA administration induced a persistent decrease in Na+K+-ATPase activity only in the injected striatum (44.9 +/- 8.1 % at 30 min and 68.7 +/- 9.4 at 3 h).Conclusions: These data suggest that MMA induces lipoperoxidation associated with Na+,K+-ATPase inhibition or activation, depending on the cerebral structure analyzed. It is suggested that Na+,K+-ATPase inhibition may play a primary role in generating MMA-induced convulsions.
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    Monoamines and their metabolites in cerebrospinal fluid and temporal cortex of epileptic patients
    (Elsevier B.V., 1996-10-01) NaffahMazzacoratti, M. G.; Amado, D.; Cukiert, A.; Gronich, G.; Marino, R.; Calderazzo, L.; Cavalheiro, E. A.; Universidade Federal de São Paulo (UNIFESP)
    The involvement of monoamines in the initiation or maintenance of epileptic phenomena has been extensively studied in cerebral tissues and in cerebrospinal fluid. the present work was undertaken to study monoamines and their metabolites in human spiking and non-spiking temporal cortex excised from patients with complex partial seizures unresponsive to available anticonvulsants. the same substances were also analyzed by HPLC-ED in cerebrospinal fluid obtained 24 h before the surgical procedure and compared with those from patients with chronic headache and normal neurological evaluation. the results show increased 5-HT, 5-HIAA and HVA levels in spiking compared with non-spiking cortex. Cerebrospinal fluid levels of 5-HIAA and HVA are concomitantly increased in epileptic compared with headache patients.
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    The renin-angiotensin system is upregulated in the cortex and hippocampus of patients with temporal lobe epilepsy related to mesial temporal sclerosis
    (Blackwell Publishing, 2008-08-01) Arganaraz, Gustavo Adolfo [UNIFESP]; Konno, Ana Carla [UNIFESP]; Perosa, Sandra Regina [UNIFESP]; Santiago, Joselita Ferreira Carvalho [UNIFESP]; Boim, Mirian A. [UNIFESP]; Vidotti, Daniela Berguio [UNIFESP]; Varella, Pedro Paulo Vasconcellos [UNIFESP]; Costa, Luciana Gilbert [UNIFESP]; Canzian, Mauro; Porcionatto, Marimelia Aparecida [UNIFESP]; Yacubian, Elza Márcia Targas [UNIFESP]; Sakamoto, Americo Ceiki [UNIFESP]; Carrete, Henrique [UNIFESP]; Centeno, Ricardo Silva [UNIFESP]; Amado, Debora [UNIFESP]; Cavalheiro, Esper Abrao [UNIFESP]; Silva, Jose Antonio; Naffah-Mazzacoratti, Maria da Graca [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Universidade de São Paulo (USP); Nove Julho Univ
    Purpose: As reported by several authors, angiotensin II (AngII) is a proinflammatory molecule that stimulates the release of inflammatory cytokines and activates nuclear factor kappa B (NF kappa B), being also associated with the increase of cellular oxidative stress. Its production depends on the activity of the angiotensin converting enzyme (ACE) that hydrolyzes the inactive precursor angiotensin I (AngI) into AngII. It has been suggested that AngII underlies the physiopathological mechanisms of several brain disorders such as stroke, bipolar disorder, schizophrenia, and disease. the aim of the present work was to localize and quantify AngII AT1 and AT2 receptors in the cortex and hippocampus of patients with temporal lobe epilepsy related to mesial temporal sclerosis (MTS) submitted to corticoamygdalohippocampectomy for seizure control.Method: Immunohistochemistry, Western blot, and real-time PCR techniques were employed to analyze the expression of these receptors.Results: the results showed an upregulation of AngII AT1 receptor as well as its messenger ribonucleic acid (mRNA) expression in the cortex and hippocampus of patients with MTS. in addition, an increased immunoexpression of AngII AT2 receptors was found only in the hippocampus of these patients with no changes in its mRNA levels.Discussion: These data show, for the first time, changes in components of renin-angiotensin system (RAS) that could be implicated in the physiopathology of MTS.