Adenosine A1 Receptor Agonist (R-PIA) before Pilocarpine Modulates Pro- and Anti-Apoptotic Factors in an Animal Model of Epilepsy.

We aimed to characterize the mechanisms involved in neuroprotection by R-PIA administered before pilocarpine-induced seizures. Caspase-1 and caspase-3 activities were assayed using fluorimetry, and cathepsin D, HSP-70, and AKT expression levels were assayed using Western Blot of hippocampal samples. R-PIA was injected before pilocarpine (PILO), and four groups were studied at 1 h 30 min and 7 days following initiation of status epilepticus (SE): PILO, R-PIA+PILO, SALINE, and R-PIA+SALINE. At 1 h 30 min, significantly higher activities of caspase-1 and -3 were observed in the PILO group than in the SALINE group. Caspase-1 and -3 activities were higher in the R-PIA+PILO group than in the PILO group. At 7 days following SE, caspase-1 and -3 activities were higher than in the initial post-seizure phase compared to the SALINE group. The pretreatment of rats receiving PILO significantly reduced caspase activities compared to the PILO group. Expression of HSP-70, AKT, and cathepsin D was significantly higher in the PILO group than in the SALINE. In the R-PIA+PILO group, the expression of AKT and HSP-70 was greater than in rats receiving only PILO, while cathepsin D presented decreased expression. Pretreatment with R-PIA in PILO-injected rats strongly inhibited caspase-1 and caspase-3 activities and cathepsin D expression. It also increased expression levels of the neuroprotective proteins HSP-70 and AKT, suggesting an important role in modulating the cellular survival cascade.

Relações e condições de trabalho dos professores paulistas (1995-2018) / Relaciones y condiciones de trabajo de los profesores paulistas (1995-2018) / Relations et conditions de travail des enseignants de são paulo (1995-2018) / Working relations and conditions of paulista teachers (1995-2018)

Resumo Neste artigo são analisadas as relações e condições de trabalho do professor da rede estadual paulista, destacando-se as formas de admissão, a progressão na carreira, o vencimento básico e a jornada de trabalho durante o período de 1995 a 2018. O artigo apresenta uma síntese dos dados obtidos por meio de pesquisa bibliográfica, estudo documental com base na legislação nacional e estadual e análise de dados estatísticos. Conclui-se que o período analisado foi caracterizado por uma política de desvalorização do trabalho docente expresso no grande número de professores contratados em caráter temporário, nos frágeis critérios de movimentação na carreira, no vencimento base abaixo do piso salarial e no descumprimento stricto sensu da composição da jornada expressa na Lei do Piso.

Resumen En este artículo son analizadas las relaciones y condiciones de trabajo del profesor de la red estadual paulista, destacándose las formas de admisión, la progresión en la carrera, el vencimiento básico y la jornada de trabajo durante el periodo de 1995 a 2018. El artículo presenta una síntesis de los datos obtenidos por medio de una investigación bibliográfica, estudio documental con base en la legislación nacional, estadual y análisis de datos estadísticos. Se concluye que el periodo analizado fue caracterizado por una política de desvalorización del trabajo docente expreso en el gran número de profesores contratados en carácter temporal, en los frágiles criterios de movilidad en la carrera, en el vencimiento base debajo del piso salarial y en el incumplimiento stricto sensu de la composición de la jornada expresa en la Ley del Piso.

Résumé Cet article analyse les relations et les conditions de travail des enseignants dans le réseau publique de l'État de São Paulo, en particulier les modalités d'admission et de progression dans la carrière, le salaire de base et la durée de la journée de travail, pour la période 1995 à 2018. L'article présente une synthèse des données obtenues à partir de recherches bibliographiques, d'études documentaires basées sur la législation nationale et de l'état de São Paulo et d'une analyse des données statistiques. En conclusion, la période se caractérise par une politique de dévalorisation du travail enseignant, manifeste par le grand nombred'embauches temporaires, par la fragilité des critères d'avancement professionnel, par le salaire de base qui reste inférieur au minimum et par le non-respect stricto sensu de la réglementation de la journée de travail établie par la Lei do Piso, censée garantir les conditions de travail et l'application du salaire minimum national pour les enseignants.

Abstract In this article, working relations and conditions of the teacher from the São Paulo state school system are analyzed, highlighting the forms of admission, career progression, base salary and working hours during the period from 1995 to 2018. The article presents a synthesis of data obtained through bibliographic research, documentary study based on national and state legislation and analysis of statistical data. It is concluded that the analyzed period was characterized by a policy of devaluation of the teaching work expressed in the large number of teachers hired on a temporary basis, in the fragile criteria of movement in the career, in the base salary below the base level of pay and in the strict noncompliance with the working hours composition expressed in the law (Lei do Piso).

Enriched environment and exercise effects on parvalbumin expression and distribution in the hippocampal formation of developing rats.

Several models of environmental enrichment and physical exercise have been used to explore the experience effects on brain functions and plasticity, mainly in adult animals. In order to examine the early influence of these stimuli on developing brain, the present study used calcium-binding protein parvalbumin as neuroplastic marker in the hippocampal formation of male Wistar rats subjected to environmental enrichment or physical exercise from postnatal days 21 to 60 (P21-P60). In our study, no significant difference in hippocampal expression and distribution of parvalbumin was found between enriched and control rats. However, a significant increase in parvalbumin protein expression as well as in the number of neurons stained with parvalbumin was observed in the hippocampal formation of rats submitted to daily treadmill exercise when compared to the control rats. The hippocampal region with the highest number of parvalbumin neurons in exercised rats was Cornus of Amon 2 e 3 (CA2/CA3). These findings indicate that developing brain may be differentially sensitive to environmental stimulation models. Specifically, our results show that hippocampal expression and distribution of parvalbumin in developing rats may be more influenced by exercise than by enriched environment. The mechanisms are not yet known.

Altered Proteins in the Hippocampus of Patients with Mesial Temporal Lobe Epilepsy.

Mesial temporal lobe epilepsy (MTLE) is usually associated with drug-resistant seizures and cognitive deficits. Efforts have been made to improve the understanding of the pathophysiology of MTLE for new therapies. In this study, we used proteomics to determine the differential expression of proteins in the hippocampus of patients with MTLE compared to control samples. By using the two-dimensional electrophoresis method (2-DE), the proteins were separated into spots and analyzed by LC-MS/MS. Spots that had different densitometric values for patients and controls were selected for the study. The following proteins were found to be up-regulated in patients: isoform 1 of serum albumin (ALB), proton ATPase catalytic subunit A (ATP6V1A), heat shock protein 70 (HSP70), dihydropyrimidinase-related protein 2 (DPYSL2), isoform 1 of myelin basic protein (MBP), and dihydrolipoamide S-acethyltransferase (DLAT). The protein isoform 3 of the spectrin alpha chain (SPTAN1) was down-regulated while glutathione S-transferase P (GSTP1) and protein DJ-1 (PARK7) were found only in the hippocampus of patients with MTLE. Interactome analysis of the nine proteins of interest revealed interactions with 20 other proteins, most of them involved with metabolic processes (37%), presenting catalytic activity (37%) and working as hydrolyses (25%), among others. Our results provide evidence supporting a direct link between synaptic plasticity, metabolic disturbance, oxidative stress with mitochondrial damage, the disruption of the blood⁻brain barrier and changes in CNS structural proteins with cell death and epileptogenesis in MTLE. Besides this, the presence of markers of cell survival indicated a compensatory mechanism. The over-expression of GSTP1 in MTLE could be related to drug-resistance.

Neurochemical Changes and c-Fos Mapping in the Brain after Carisbamate Treatment of Rats Subjected to Lithium-Pilocarpine-Induced Status Epilepticus.

The administration of lithium-pilocarpine (LiPilo) in adult rats is a validated model reproducing the main clinical and neuropathological features of temporal lobe epilepsy (TLE). Previous studies have shown that carisbamate (CRS) has the property of modifying epileptogenesis in this model. When treated with CRS, about 50% of rats undergoing LiPilo status epilepticus (SE) develop non-convulsive seizures (NCS) instead of convulsive ones (commonly observed in TLE). The goal of this work was to determine some of the early changes that occur after CRS administration, as they could be involved in the insult- and epileptogenesis-modifying effects of CRS. Thus, we performed high-performance liquid chromatography (HPLC) to quantify levels of amino acids and monoamines, and c-Fos immunohistochemical labeling to map cerebral activation during seizures. Comparing rats treated one hour after SE onset with saline (CT), CRS, or diazepam (DZP), HPLC showed that 4 h after SE onset, dopamine (DA), norepinephrine (NE), and GABA levels were normal, whereas serotonin levels were increased. Using c-Fos labeling, we demonstrated increased activity in thalamic mediodorsal (MD) and laterodorsal (LD) nuclei in rats treated with CRS. In summary, at early times, CRS seems to modulate excitability by acting on some monoamine levels and increasing activity of MD and LD thalamic nuclei, suggesting a possible involvement of these nuclei in insult- and/or epileptogenesis-modifying effects of CRS.

Hippocampal Proteome of Rats Subjected to the Li-Pilocarpine Epilepsy Model and the Effect of Carisbamate Treatment.

In adult rats, the administration of lithium-pilocarpine (LiPilo) reproduces most clinical and neuropathological features of human temporal lobe epilepsy (TLE). Carisbamate (CRS) possesses the property of modifying epileptogenesis in this model. Indeed, about 50% of rats subjected to LiPilo status epilepticus (SE) develop non-convulsive seizures (NCS) instead of motor seizures when treated with CRS. However, the mechanisms underlying these effects remain unknown. The aim of this study was to perform a proteomic analysis in the hippocampus of rats receiving LiPilo and developing motor seizures or NCS following CRS treatment. Fifteen adult male Sprague-Dawley rats were used. SE was induced by LiPilo injection. CRS treatment was initiated at 1 h and 9 h after SE onset and maintained for 7 days, twice daily. Four groups were studied after video-EEG control of the occurrence of motor seizures: a control group receiving saline (CT n = 3) and three groups that underwent SE: rats treated with diazepam (DZP n = 4), rats treated with CRS displaying NCS (CRS-NCS n = 4) or motor seizures (CRS-TLE n = 4). Proteomic analysis was conducted by 2D-SDS-PAGE. Twenty-four proteins were found altered. In the CRS-NCS group, proteins related to glycolysis and ATP synthesis were down-regulated while proteins associated with pyruvate catabolism were up-regulated. Moreover, among the other proteins differentially expressed, we found proteins related to inflammatory processes, protein folding, tissue regeneration, response to oxidative stress, gene expression, biogenesis of synaptic vesicles, signal transduction, axonal transport, microtubule formation, cell survival, and neuronal plasticity. Our results suggest a global reduction of glycolysis and cellular energy production that might affect brain excitability. In addition, CRS seems to modulate proteins related to many other pathways that could significantly participate in the epileptogenesis-modifying effect observed.

Neuroprotective agents and modulation of temporal lobe epilepsy.

Temporal Lobe Epilepsy (TLE) is a chronic condition characterized by epileptic seizures originating mainly in temporal lobe areas. Epileptogenesis is a process in which a central nervous system injury can lead surviving neuronal populations to generate abnormal, synchronous and recurrent epileptiform discharges producing focal or generalized seizures. Hipocampal sclerosis, a massive cell death in the hippocampal formation and in the other regions of temporal lobe, is considered as hallmark of TLE. Despite the numerous antiepileptic drugs (AEDs) commercially available, about 30-40% of patients remain with seizures refractory to pharmacological treatment. In addition, there is no drug with significant efficacy to modify the epileptogenesis process. In this review we present some data regarding the neuroprotective effect of some adenosinergic agents, erythropoietin and carisbamate regarding the disease- and epileptogenesis-modifying effect.

Epilepsia do lobo temporal: mecanismos e perspectivas / Temporal lobe epilepsy: mechanisms and perspectives

O artigo apresenta uma breve revisão sobre os achados históricos, epidemiológicos, tratamento e perspectivas terapêuticas para as epilepsias, com enfoque na epilepsia do lobo temporal. Apresenta dados obtidos com estudos de proteômica empregando tecido epiléptico e destaca a importância da aplicação desse método na busca de novos alvos terapêuticos.

Consequences of pilocarpine-induced status epilepticus in immunodeficient mice.

Systemic injection of pilocarpine in rodents induces status epilepticus (SE) and reproduces the main characteristics of temporal lobe epilepsy (TLE). Different mechanisms are activated by SE contributing to cell death and immune system activation. We used BALB/c nude mice, a mutant that is severely immunocompromised, to characterize seizure pattern, neurochemical changes, cell death and c-Fos activation secondarily to pilocarpine-induced SE. The behavioral seizures were less severe in BALB/c nude than in BALB/c wild type mice. However, nude mice presented more tonic-clonic episodes and higher mortality rate during SE. The c-Fos expression was most prominent in the caudate-putamen, CA3 (p<0.05), dentate gyrus, entorhinal cortex (p<0.001), basolateral nucleus of amygdala (p<0.01) and piriform cortex (p<0.05) of BALB/c nude mice than of BALB/c. Besides, nude mice subjected to SE presented high number of Fluorojade-B (FJB) stained cells in the piriform cortex, amygdala (p<0.05) and hilus (p<0.001) in comparison with BALB/c mice. A significant increase in the level of glutamate and GABA was found in the hippocampus and cortex of BALB/c mice presenting SE in comparison to controls. However, the level of glutamate was higher in the brains of BALB nude mice than in the brains of BALB/c wild type mice, while the levels of GABA were unchanged. These results indicate that the brains of immunodeficient nude mice are more vulnerable to the deleterious effects of pilocarpine-induced SE as they present intense activation, increased glutamate levels and more cell death.

Differential neuroprotection by A(1) receptor activation and A(2A) receptor inhibition following pilocarpine-induced status epilepticus.

Aiming at a better understanding of the role of A(2A) in temporal lobe epilepsy (TLE), we characterized the effects of the A(2A) antagonist SCH58261 (7-(2-phenylethyl)-5-amino-2(2-furyl)-pyrazolo-[4,3-e]-1,2,4-triazolo[1,5-c]pyrimidine) on seizures and neuroprotection in the pilocarpine model. The effects of SCH58261 were further analyzed in combination with the A(1) agonist R-Pia (R(-)-N(6)-(2)-phenylisopropyl adenosine). Eight groups were studied: pilocarpine (Pilo), SCH+Pilo, R-Pia+Pilo, R-Pia+SCH+Pilo, Saline, SCH+Saline, R-Pia+Saline, and R-Pia+SCH+Saline. The administration of SCH58261, R-Pia, and R-Pia+SCH58261 prior to pilocarpine increased the latency to SE, and decreased either the incidence of or rate of mortality from SE compared with controls. Administration of R-Pia and R-Pia+SCH58261 prior to pilocarpine reduced the number of Fluoro-Jade B-stained cells in the hippocampus and piriform cortex when compared with control. This study showed that pretreatment with R-Pia and SCH58261 reduces seizure occurrence, although only R-Pia has neuroprotective properties. Further studies are needed to clarify the neuroprotective role of A(2A) in TLE.

The A1 receptor agonist R-Pia reduces the imbalance between cerebral glucose metabolism and blood flow during status epilepticus: could this mechanism be involved with neuroprotection?

It is well known that the uncoupling between local cerebral glucose utilization (LCGU) and local cerebral blood flow (LCBF), i.e. decrease in LCBF rates with high LCGU, is frequently associated with seizure-induced neuronal damage. This study was performed to assess if the neuroprotective effect of the adenosinergic A(1) receptor agonist R-N-phenylisopropyladenosine (R-Pia) injected prior to pilocarpine is able to reduce the uncoupling between LCGU and LCBF during status epilepticus (SE). Four groups of rats were studied: Saline, Pilo, R-Pia+Saline and R-Pia+Pilo. For LCGU and LCBF studies, rats were subjected to autoradiography using [(14)C]-2-deoxyglucose and [(14)C]-iodoantypirine, respectively. Radioligands were injected 4 h after SE onset. Neuronal loss was evaluated by Fluorojade-B (FJB) at two time points after SE onset (24 h and 7 days). The results showed a significant increase in LCGU in almost all brain regions studied in the Pilo and R-Pia+Pilo groups compared to controls. However, in R-Pia pretreated rats, the uncoupling between LCGU and LCBF was moderated in a limited number of structures as substantia nigra pars reticulata and hippocampal formation rather in favor of hyperperfusion. Significant increases in LCBF were observed in the entorhinal cortex, thalamic nuclei, mammillary body, red nucleus, zona incerta, pontine nucleus and visual cortex. The neuroprotective effect of R-Pia assessed by FJB showed a lower density of degenerating cells in the hippocampal formation, piriform cortex and basolateral amygdala. In conclusion our data shows that the neuroprotective effect of R-Pia was accompanied by a compensatory metabolic input in brain areas involved with seizures generation.

As recentes reformas educacionais paulistas na visão dos professores / Recent educational reforms in the state of são paulo from the teacher's point of view

As reformas educacionais atuais introduziram conceitos econômicos na gestão das escolas e transferiram a responsabilidade pelas ações educativas a seus sujeitos, a quem cabe o sucesso ou o fracasso das mudanças. Nesse contexto, novas formas de controle do trabalho docente passaram a ser utilizadas pelo sistema escolar, tais como as avaliações externas, a imposição de projetos e o pagamento de bônus aos responsáveis pelo trabalho docente. Este artigo resulta de uma pesquisa empírica realizada entre 20062008 e visa a apresentar a análise da escola e do trabalho docente a partir do ponto de vista de trinta professores de três diferentes regiões do estado de São Paulo. Os resultados apontam o forte impacto das reformas educacionais e da introdução dos elementos gerencialistas e performáticos no trabalho dos professores, implicando profundas alterações no "ofício" docente, especialmente do professor secundário, o que evidencia um sofrimento ético perante a perda da especificidade histórica do seu trabalho.

The reforms, organized and supported by international agencies, reduced the role of the State, introduced economic concepts to school management and delegated the responsibility towards educational actions to the characters responsible for the success or failure of such changes. In this context, new ways of controlling teaching practices started to be used by the school system such as external assessments, imposition of formatted projects by superior bodies and payment of bonus to the education workers. This article results from an empirical research carried out between 2006 and 2008 and is aimed at presenting the analysis of the school and the teaching practices from the point of view of 30 teachers from three different regions of the state of São Paulo. The results show the strong impact of management elements on the teachers' daily practices contributing for their feeling of unease and blame due to the failure of reformed projects.

Adenosina e neuroproteção na epilepsia do lobo temporal: da ativação do receptor A1 ao bloqueio do receptor A2A / Adenosine and neuroprotection in the temporal lobe epilepsy: from A1 receptor activation to A2A receptor blockade

OBJETIVO: Caracterizar o efeito do bloqueio do receptor A2A pelo SCH58261 na modulação da crise e neuroproteção de áreas cerebrais vulneráveis à lesão por pilocarpina. O efeito do SCH58261 foi também analisado em combinação com a ativação dos receptores A1 por R-Pia. MÉTODOS: Oito grupos foram estudados: Pilo, SCH+Pilo, R-Pia+Pilo, R-Pia+SCH+Pilo, e seus respectivos controles. O número de animais em status epilepticus (SE), a latência para o início do SE e a taxa de mortalidade foram avaliados. O método de Fluoro Jade B (FJB) foi realizado 24 horas e sete dias após SE. RESULTADOS: O pré-tratamento com SCH58261, R-Pia e R-Pia+ SCH58261 reduziu o número de animais em SE, aumentou a latência para o SE e diminuiu a taxa de mortalidade, comparado ao tratamento com pilocarpina. Os grupos R-Pia e R-Pia+SCH58261 apresentaram uma redução no número de células marcadas com FJB em CA3 e hilo, 24 horas e sete dias após SE, e no córtex piriforme apenas 24 horas após SE, comparado ao grupo Pilo. CONCLUSÃO: O antagonista A2A demonstrou um potente efeito anticonvulsivante, enquanto o agonista A1 teve um papel crucial na modulação da crise e promoveu significante neuroproteção.

OBJECTIVE: To characterize the effect of the A2A receptor blockage by the SCH58261 in the seizure modulation and neuroprotection of the brain areas vulnerable to injury by pilocarpine. The effect of SCH58261 was also analyzed in combination with the activation of the A1 receptors by R-Pia. METHODS: Eight groups were studied: Pilo, SCH+Pilo, R-Pia+Pilo, R-Pia+SCH+Pilo, and respective controls. The number of animals in status epilepticus (SE), the latency to the SE onset and the mortality rate were evaluated. The Fluoro Jade B (FJB) method was performed 24 hours and seven days after SE. RESULTS: The pretreatment with SCH58261, R-Pia and R-Pia+SCH58261 reduced the number of animals in SE, increased the latency to the SE and decreased the mortality rate, compared to pilocarpine treatment. The R-Pia and R-Pia+SCH58261 groups exhibited a reduction in the number of FJB stained cells in CA3 and hilus, 24 hours and seven days after SE, and in the piriform cortex only 24 hours after SE, compared to Pilo group. CONCLUSION: The A2A antagonist demonstrated a potent anticonvulsant effect, while the A1 agonist had a crucial role in the seizure modulation and promoted significant neuroprotection.

Epilepsia e neuroproteção: o papel do agonista adenosinérgico A1(RPia) na modulação da crise induzida por pilocarpina / Epilepsy and neuroprotection: employment of the RPia during status epilepticus induced by pilocarpine

OBJETIVO: O objetivo desse estudo foi caracterizar a neuroproteção do RPia em ratos submetidos ao status epilepticus (SE) induzido pela pilocarpina (Pilo). MÉTODOS: Avaliou-se o balanço entre utilização local da glicose cerebral (ULGC) e fluxo sanguíneo cerebral local (FSCL) após 4 horas de SE, e a marcação por Fluoro Jade-B (FJB), 24 horas e 90 dias após SE. Quatro grupos foram avaliados: Salina, Pilo, RPia+Salina e RPia+Pilo. RESULTADOS E CONCLUSÃO: Aumentos significantes na ULGC foram observados na maioria das regiões avaliadas nos grupos Pilo e RPia+Pilo quando comparados ao controle. Entretanto, redução significante na ULGC ocorreu na substância negra pars reticulata e giro denteado do grupo RPia+Pilo versus Pilo. Houve aumento significante do FSCL em todas as áreas estudadas, comparando-se os grupos Pilo e RPia+Pilo com o controle. Foi observado um aumento significante do FSCL durante SE em CA2, CA3, giro denteado, córtex entorrinal, corpo mamilar, núcleos talâmicos, núcleo rubro, zona incerta, núcleo oral da ponte e córtex visual, no grupo pré-tratado com RPia comparado ao tratado somente com Pilo. Grande número de células marcadas com FJB foi observado no grupo Pilo e o pré-tratamento com RPia reduziu essa marcação na formação hipocampal, córtex piriforme, amígdala basolateral e substância negra pars compacta.

OBJECTIVE: The aim of this study was to characterize the neuroprotection of the RPia in rats subjected to status epilepticus (SE) induced by pilocarpine (Pilo). METHODS: We evaluated the mismatch between local cerebral glucose utilisation (LCGU) and local cerebral blood flow (LCBF) 4 hours after SE induction. Neuronal loss was evaluated by Fluoro Jade-B (FJB) 24 hours and 90 days after SE. Four groups were studied: Saline, Pilo, RPia+Saline and RPia+Pilo. RESULTS AND CONCLUSIONS: Significant increases in the LCGU were observed in the almost all brain regions of Pilo and RPia+Pilo groups compared to control. However, significant reduction in the LCGU occurred in the substantia nigra pars reticulata and hippocampal formation of RPia+Pilo group versus Pilo. There was significant increase of the LCBF in all the studied areas, comparing the Pilo and RPia+Pilo groups with the control. The increases of LCBF was more intense in rats from RPia+Pilo compared to Pilo, and located mainly in CA2, CA3, dentate gyrus, entorhinal cortex, thalamic nuclei, mammillary body, red nucleus, zone incerta, pontine nucleus and visual cortex. A great number FJB stained cells was observed in the Pilo group and RPia pretreatment reduced the staining in the hippocampal formation, piriform cortex, basolateral amygdala and substantia nigra pars compacta.

Protective effect of the organotelluroxetane RF-07 in pilocarpine-induced status epilepticus.

Temporal lobe epilepsy is the most common form of epilepsy in humans. Caspase activation is a mechanism of cell death induced by seizures. Tellurium (IV) compounds present antitumoral, immunomodulatory and neuroprotective effects due to their ability to inhibit cysteine proteases. We studied the activity of caspase-1, -3 and -8 in the hippocampus of rats exhibiting status epilepticus induced by pilocarpine. All three caspases were activated. Tellurium (IV) compounds RF-07, RF-03 and AS-101 inhibited caspases in vitro, showing high second-order inhibition rate constants. The intraperitoneal injection of RF-07 prior to pilocarpine suppressed the behavioral and electroencephalographic seizure occurrence. According to our results, the caspases are activated as early as 90 min following SE. Tellurium (IV) compounds exerted anticonvulsant effects associated with the inhibition of caspases. These results suggest a promising therapeutic potential of organotellurium (IV) compounds as antiepileptogenic agents.

Bone marrow cells are able to increase vessels number during repair of sciatic nerve lesion.

The aim of this study was to compare the outcomes of nerve autografts (GRF) and venous grafts containing mononuclear bone marrow cells (BMCs) in sciatic nerve-lesioned rats. Control animals underwent sham operations (SHAM), received empty venous grafts (EPV), or received venous grafts containing BMC vehicle (AGR). Outcome was evaluated through sciatic functional index (SFI), morphometric and morphologic analyses of the nerve distal to the lesion, and the number of spinal cord motor neurons positive for the retrograde tracer, Fluoro-Gold. All groups exhibited poor results in SFI when compared to SHAM animals throughout the postoperative period. All groups also had a significantly greater fiber density, decreased fiber diameter, and decreased motor neuron number than the SHAM group. No significant difference between the GRF and BMC groups was observed in any of these parameters. On the other hand, vessel density was significantly higher in BMC than all other groups. BMC-containing venous grafts are superior to nerve autografts in increasing vessel density during sciatic nerve regeneration.

Estudo comparativo entre enxerto autógeno e enxerto muscular coberto com tubo de veia autógeno em nervos tibiais de ratos wistar, utilizando o fluoro-gold® como marcador neuronal / Comparative study between autogenous graft and muscular graft covered with autogenous vein tube in wistar rats' tibial nerves using the fluoro-gold® as a neuronal marker

Este trabalho teve como objetivo o estudo da regeneração nervosa através da contagem de neurônios comparando duas técnicas cirúrgicas no tratamento da perda de substância nervosa nos membros inferiores em 15 ratos. Inicialmente obteve-se tubo de veia de 12mm de comprimento retirado da jugular externa esquerda. A seguir, opera-se os dois membros inferiores, expondo o nervo tibial de cada lado e ressecando um segmento de 8 mm do nervo, simulando, ao mesmo tempo, a perda de substância e a obtenção do enxerto nervoso autógeno. A reparação da perda de substância do lado esquerdo consistiu numa enxertia convencional simples para a reparação de lesão nervosa por meio de sutura microcirúrgica. A do membro inferior direito foi pela tubulização com 8 mm de enxerto de músculo quadríceps denaturado com nitrogênio líquido coberto com veia jugular. Após quatro meses, os animais foram submetidos à nova cirurgia para exposição dos nervos tibiais ao marcador neuronal Fluoro Gold®. Após 48 horas, foram perfundidos e o segmento medular entre L3 e S1 foi removido e posteriormente cortado em secções de 40 æm. Houve contagem neuronal de todos os cortes e não foram verificadas diferenças estatísticas entre as duas técnicas cirúrgicas.

The purpose of this work was to study nervous regeneration through neurons counts by comparing two surgical techniques for addressing nervous gaps on 15 rats' lower limbs. Initially, a 12-mm long vein tube from the left outer jugular was obtained, and then both lower limbs are operated, exposing the tibial nerve at each side and performing a resection of an 8-mm nerve segment, at the same time simulating a gap and an autogenous nerve graft. Left gap repair consisted of a usual conventional graft for nervous injury repair by means of microsurgical suture. The gap repair on right lower limbs was made through quadriceps muscle, treated with liquid nitrogen, covered with an 8-mm tube of jugular vein. After four months, the animals were submitted to a new surgery for exposing tibial nerves to the Fluoro-Gold® neuronal marker. After 48 hours, the rats were perfused and medullar segment between L3 and S1 was removed and subsequently cut into 40æm sections. Neurons on all sections were counted, and no statistical differences were found between both surgical techniques.

Physical training does not influence interictal LCMRglu in pilocarpine-treated rats with epilepsy.

This study evaluated, using local cerebral metabolic rates for glucose (LCMRglu) in 39 brain regions, whether physical training modifies the functional activity in rats with epilepsy. Most animals present seizures at rest rather than during exercise and LCMRglu was measured during the interictal phase of the chronic period of a pilocarpine model of epilepsy by the [14C]2-deoxyglucose (2DG) method. Wistar rats were allocated randomly into four groups: control rats (n=6), rats with epilepsy (n=6), trained control rats (n=6), and trained rats with epilepsy (n=6). Trained control rats did not show significant changes in LCMRglu when compared to control rats. LCMRglu was significantly higher in rats with epilepsy in the lateral posterior thalamic nucleus and in the visual cortex compared to control rats. Trained rats with epilepsy presented a higher LCMRglu than rats with epilepsy only in the inferior colliculus and auditory cortex. Increases in LCMRglu were also observed in the inferior colliculus of trained rats with epilepsy when compared to the trained control rats. Taken together, the results suggest that physical training does not influence interictal LCMRglu metabolism in most cerebral regions of rats with epilepsy.