Teses em Neurociências e Biologia Celular (Doutorado) - PPGNBC/ICB

URI Permanente para esta coleçãohttps://repositorio.ufpa.br/handle/2011/2390

O Doutorado Acadêmico pertence ao Programa de Pós-Graduação em Neurociências e Biologia Celular (PPGNBC) do Instituto de Ciências Biológicas (ICB) da Universidade Federal do Pará (UFPA).

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Agora exibindo 1 - 11 de 11

Acesso aberto (Open Access)
Análise comparativa dos padrões neurodegenerativos da substância cinzenta em diferentes áreas corticais de ratos adultos submetidos à lesão isquêmica focal
(Universidade Federal do Pará, 2012-09-27) SANTOS, Enio Maurício Nery dos; LEAL, Walace Gomes; http://lattes.cnpq.br/2085871005197072
Stroke can occur in any region of the central nervous system (CNS). The cerebral cortex is one of the most often affected areaby this acute neural disorder, but there are no studies that have compared the damaging pattern in different cortical regions after acomparable focal ischemia. The aim of this investigation was to evaluate the degenerative pattern of different cortical areas after focal ischemic injury. Focal ischemia was induced by stereotaxic microinjections of endothelin-1 (ET-1) into the somatosensory, motor and association cortices of adult rats (N = 45). The control animals were injected with the same volume of sterile saline (N = 27). The animals were perfused 1, 3 and 7 days after the ischemic event. The brain was removed, postfixed, cryoprotected, and sectioned in a cryostat. The general histopathology was evaluated in 50μm sections stained with cresyl violet. 20μm sections were submitted to immunohistochemistry for astrocytes (anti-GFAP), activated microglia / macrophages (anti-ED1) and overall microglial population (anti-Iba1). The damaging patterns werequalitatively evaluated under optical microscopy and quantitatively by counting the number of cells in the ipsilateral and contralateral sides to injury.Descriptive statistics and comparisons within and between groups were performed using analysis of variance with Tukey post-hoc test. Conspicuous ischemic tissue loss, microglial activation and astrocytosis were observed mainly 3 and 7 days after ischemia, which was not observed in control animals. The tissue loss and activation of glial cells were more intense in the somatosensory cortex, followed by the motor cortex. The association cortex displayed less damage compared to other cortical areas, which was confirmed by quantitative analysis. The results suggest that an ischemic lesion of the same intensity induces a differential pattern of tissue loss and neuroinflammation, depending on the cortical area, and that the primary sensory and motor areas are more susceptible to ischemia than association areas.
Acesso aberto (Open Access)
Ativação microglial, lesão da substância branca e expressão de Nogo-A em ratos submetidos à isquemia estriatal
(Universidade Federal do Pará, 2012-05-10) LIMA, Rafael Rodrigues; LEAL, Walace Gomes; http://lattes.cnpq.br/2085871005197072
The objective of this investigation was to evaluate the degenerative pattern of several white matter tracts after striatal ischemic injury, correlating degenerative process standards with the microglial activation and expression of Nogo-A. For this purpose, focal ischemia was induced with stereotactic injection of endothelin in striatum of adult rats, and only in the control animals injected with sterile saline. The animals were perfused 3, 7, 14 and 30 days after ischemia. The brain removed, postfixed, cryoprotected, cut into cryostat sections obtained and submitted to immunohistochemical investigation with the following antibodies: anti-GFAP (1:2000, Dako), anti-Tau-1 (1:500, Chemicon), Anti-MBP (1:100, Chemicon International), Anti-Nogo-A (1:100, Invitrogen), Anti-Iba1 (1:1000, WAKO), ED1 (1:500, Serotec) and Anti-MHC II (Abcam 1:100), besides the viewing of the damage pattern with cresyl violet. Slides are marked by different methods were evaluated qualitatively and quantitatively also some (Anti-Nogo A, anti-ED-1, anti-MHC-II and anti-tau-1), counts were carried out in the striatum and in the corpus callosum. The data were tabulated, statistically analyzed by Tukey test (p <0.05) and micrographs taken of the findings more representative. The slides were stained with cresyl violet revealed an increase in cell density by the infiltration of inflammatory cells to the ischemic area, with a significant increase on day 7. The blades immunostained for GFAP was found progressive increase of the population of astrocytes and an increase in cell volume 7 and 14 days. Oligodendrocyte pathology marked with Tau-1 had peak marking the 3rd day in the striatum and the 7th day in the corpus callosum, and loss of myelin compaction identified by MBP was better at 14, in the different treatment. The microglial activation identified by different immunoblots showed a peak on day 7, both in striatum and in the corpus callosum, but in the corpus callosum with a much smaller number compared to the striatum. The morphology of microglial underwent changes, which found the branched phenotype in control animals, as well as in early and late times after ischemia and amoeboid default / phagocytic day 7, coinciding with the largest number of activated cells. The count of Nogo-A + cells peaked at 3 days observed in the striatum, and there were no differences in the corpus callosum expression Nogo-A 3 to 14 days, only a decrease compared to 30 days. Thus, microinjections of ET-1 induced conspicuous striatal tissue loss, concomitant with progressive microglial activation, astrocytosis, loss of immunoreactivity for myelin basic protein and oligodendrocytes damage in various survival times after focal ischemia. These events affect a few SB tracts, as the corpus callosum. The establishment of the temporal evolution of these events is the neuropathological basis for future studies, in which they should handle the inflammatory response in order to minimize these tissue changes.
Acesso aberto (Open Access)
Efeitos anti-inflamatórios e neuroprotetores do extrato de gergelim (Sesamum indicum L.) em um modelo experimental de lesão aguda da medula espinhal de ratos
(Universidade Federal do Pará, 2016-06-10) PENHA, Nelson Elias Abrahão da; LIMA, Rafael Rodrigues; http://lattes.cnpq.br/3512648574555468; LEAL, Walace Gomes; http://lattes.cnpq.br/2085871005197072
The spinal cord is a component of central nervous system (CNS) with crucial functions for locomotion, motor skills, somatosensory and authonomic control. Spinal injuries are among the more serious and debilitating pathological conditions to human health with large worldwide. The use of experimental models of spinal cord injury (SCI) is pivotal to understandthe SCI pathophysiology as well as search for treatments to minimize the neurological deficits and improve functional recovery. In this work, we aimed to investigate the neuroprotective and anti-inflammatory effects of supercritical gergelim (Sesamum indicum L.) extract in the acute phase of SCI in adult rats. Male Adult rats were submitted to spinal cord (SC) hemissection at T8. The sham (non lesioned) and control animals were treated with 5% tween(veicle), while treated animals received intraperitoneal (i.p) injections of Gergelim extract (150 mg/kg divided in two doses per day). Animals were allowed to recovery and were perfused at 1, 3 and 7 days post-lesion. 20 μm sections were obtained using a cryostat and stained with methylen blue, hematoxylin-eosin (HE), trichromic of Gomori and cresyl violet for gross histopathology. In addition, sections were immunolabeled with specific antibodies against neutrophils (anti-MBS-1) and activated microglia/macrophages (anti-ED1). The muscle force was assessed through electromiographic records performed in both control and treated animals at 1 and 7 days postlesion. The control animals presented progressive SC cavitation concomitant with neutrophil recruitment and microglia/macrophage activation. The treatment with gergelim extract induced tissue preservation and considerable decrease of neutrophil recruitment at 1 and 3 days, which was confirmed by quantitative analysis (ANOVA-Tukey, p<0.05). The gergelim treatment also decreased the microglia/macrophage activation at 7 days (ANOVA-Tukey, p<0.05). The electromiographic records revealed that the gergelim treatment improved the muscular force in about 50% compared to control animals. The results suggest that black gergelim seed extract is anti-inflammatory, neuroprotective and induces muscle force recovery in adults rats submitted to acute SCI. Future studies should confirm that a phytotherapic obtained from black sesame extract can be used as possible neuroprotective agent for human SCI.
Acesso aberto (Open Access)
Efeitos anti-inflamatórios e neuroprotetores do extrato de gergelim preto (Sesamum indicum L.) em um modelo experimental de isquemia estrial
(Universidade Federal do Pará, 2024-03) SANTOS, Ijair Rogério Costa dos; LEAL, Walace Gomes; http://lattes.cnpq.br/2085871005197072
Acidente Vascular Encefálico (AVE) é uma neuropatologia caracterizada como o surgimento súbito global ou focal de déficits da função neurológica de duração superior a 24 horas ou que leve a morte, cuja única causa reside na origem vascular. Estudos sobre a incidência, comprometimento físico e mortalidade enquadram o AVE como a segunda causa de morte no mundo e a principal complicação orgânica que leva às disfunções físico-neurológicas, frequentemente, graves e permanentes. A indução do AVE em animais de experimentação e o entendimento de sua fisiopatologia, bem como a busca de tratamentos que minimizem os danos neurológicos e estimulem a recuperação morfofuncional do indivíduo afetado são temas de grande relevância científica e clínica. Neste estudo, investigamos os possíveis efeitos neuroprotetores e/ou anti-inflamatórios do extrato supercrítico de gergelim preto (Sesamun indicum L.) após lesão isquêmica focal por microinjeções de 80 pmol de endotelina-1 no estriado de ratos adultos, usando as coordenadasestereotáxicas: 1,2 mm, anterior-posterior; 2,5 mm, médio-lateral; 4,0 mm, dorsoventral. Após a indução do AVE, os grupos controles foram tratados com tween a 5% e os tratados receberam 150 mg/kg de gergelim, ambos, por via intraperitoneal, em duas doses diárias de 75 mg/kg. A neuropatologia foi obtida em secções encefálicas com 50 e 20 μm de espessuras e coradas com violeta de cresila, para identificar a área de lesão, e/ou imunomarcadas por anticorpos específicos à identificação de neurônios (anti-NeuN), astrócitos (anti-GFAP) e micróglia (anti-ED1). Secções de 5 μm de espessura de rim e fígado corados por métodos histológicos e histoquímicos não mostraram alterações morfológicas nas células que compõem esses órgãos essenciais, sugerindo baixa toxicidade do extrato. Todas as secções coradas e/ou imunomarcadas foram visualizadas em microscópio óptico e seuscampos mais ilustrativos, em todos os tempos de sobrevida e grupos experimentais,foram capturados digitalmente e editados em computador. A quantificação das célulasNeuN+(neurônios), micróglia/macrófagos (ED1+) e astrócitos (GFAP+) na área de lesão, três secções por lâmina, todo campo ao redor de lesão por secção, com auxílio de uma gradícula de área 0,0625 mm2 na ocular possibilitou o teste t-Student à análise estatística entre os grupos e o uso do programa Microsoft Excel à plotagem dos gráficos. Por fim, uma caracterização da citotoxicidade in vitro, bem como a verificação do índice de acidez do extrato revelou baixa acidez e mínima agressividade em células sanguíneas, que ratifica o uso do extrato supercrítico em estudos que visem otratamento de doenças agudas e crônicas no SNC.
Acesso aberto (Open Access)
Efeitos do transplante autólogo de células monocelulares da medula óssea após lesão incompleta da medula espinhal de ratos adultos
(Universidade Federal do Pará, 2017-03-30) SOUZA, Celice Cordeiro de; HAMOY, Moisés; http://lattes.cnpq.br/4523340329253911; LEAL, Walace Gomes; http://lattes.cnpq.br/2085871005197072
Spinal cord injury (SCI) causes permanent loss of neurological function below the level of injury, generating social and psychological physical consequences in patients. The pathophysiology of SCI involves complex processes, such as hemorrhage, excitotoxicity and inflammation, mainly generated by microglial cells. Despite advanced knowledge of pathological mechanisms, effective and approved therapeutic strategies for the treatment of lesions and their consequences are still lacking without serious adverse effects. Cell therapy may represent a good therapeutic strategy because it demonstrates good results in the modulation of the inflammatory environment of the lesion and by probable mechanisms of differentiation. In the present study, we investigated the action of bone marrow mononuclear cells (BMMC) in incomplete lesions (hemisection to the right of the spinal cord, T8-T9 segment) after 42 days of injury (chronic lesion). The cells were from the injured animal itself (autologous transplantation) and the transplantation was intramedullary, i.e. the cells were inserted near the site of the lesion. In the present study, the functional effects of transplantation were investigated through the BBB scale (Basso, Beatie and Bresnahan), which allows the motor function of the hind legs of the animals to be graded. The anti-inflammatory effects of BMMC were also investigated. Histological and immunohistochemical techniques using Cresila Violet staining and anti-ED-1 (microglial marker / activated macrophages) and anti-GFAP (fibrillar astrocyte marker) antibodies were used. Qualitative and quantitative analyzes were performed. For quantitative analysis, the number of field activated astrocytes and macrophages / microglia were counted using binocular microscope with counting gradient (0.0625mm2) in a 40x objective. The counting averages and the standard deviations obtained were plotted in Cartesian coordinates. The counting was as follows: on the right side of the spinal cord (lesion side) and three fields per medullary region (ventral funiculus - FV, dorsal funiculus - FD, lateral funiculus - FL, dorsal horn - CD, ventral horn - CV and intermediate gray matter-SCI), totaling 18 counting fields per section. Treatment with BMMC was not effective in improving the motor function of the injured animals when we compared the treated and untreated animals (means and standard deviations of the groups: false operated, n = 4, 21 ± 0, control, n = 4, 13,57 ± 3.88, treated, n = 5, 15.07 ± 3.46). In the qualitative analysis by means of the staining of Cresila Violet, treated animals presented better tissue preservation when compared to the untreated animals. In the quantitative analysis of microglial activation, we observed that treatment with BMMC reduced the activation of these inflammatory cells (control: 19.52 ± 7.79, treated: 10.04 ± 2.37), but did not significantly reduce the activation of the astrocytes (Mean of the groups: control 17.74 ± 2.757, treated 14.46 ± 5.283). The results suggest that further studies are needed to come up with an effective strategy for patients with SCI. A possible combined treatment with other strategies may turn out to be promising for patients' functionality.
Acesso aberto (Open Access)
Imunoreatividade para os receptores de neurotrofinas P75NTR e TrkA na zona subventricular de ratos adultos após isquemia estriatal
(Universidade Federal do Pará, 2015-08-21) TAVARES, Patrycy Assis Noronha; LIMA, Rafael Rodrigues; http://lattes.cnpq.br/3512648574555468; LEAL, Walace Gomes; http://lattes.cnpq.br/2085871005197072
Neurotrophins are growth factors expressed by cells of the nervous system both during development and in adulthood. The Nerve Growth Factor (NGF, the English- Nerve Growth Factor), brain-derived neurotrophic factor (English- BDNF- of Brain-Derived Neurotrophic Factor), Neurotrophin-3 (NT-3), Neurotrophin-4/5 ( NT-4/5), have many functions related to aging and response of nervous tissue to the pathology such as vascular accident (CVA). In this pathology, the increase of the neurotrophin expression can interfere with the degree of neurogenesis in the sub-ventricular zone (SVZ) and redirect the rostral migratory flow of Adult Neural Stem Cells (CTNAs) to the ischemic region. The presence of neurotrophin receptors TrkA and p75NTR in the CTNAs of SVZ indicates that they may participate in the regulation of neurogenesis in this region. Here we describe the influence of an experimental ischemia by microinjection of a vasconstritor Endothelin-1 peptide, which is restricted to the striatum adjacent SVZ; on the pattern of immunoreactivity for TrkA and p75NTR receptors in different survival times. The histopathological pattern of ischemic striatum and the cytoarchitecture of the SVZ, followed by immunohistochemical analysis to the receptors were analyzed. Numerous p75NTR + cells were found in the ipsilateral SVZ and against the injection site, with had a reduction in immunoreactivity at first and third day after ischemia. Few TrkA + cells were found in SVZ of both groups, however, many TrkA + axonal terminals were saw in the ischemic ipsilateral SVZ. Soon after the ischemic process, there was thickening of the SVZ, the concomitant reduction in immunoreactivity for p75NTR and TrkA + arisings of axonal terminals.
Acesso aberto (Open Access)
Intoxicação crônica experimental com alumínio: padrões degenerativos, comportamentais e terapia experimental com magnésio após lesão hipocampal
(Universidade Federal do Pará, 2013-01-17) SILVA JÚNIOR, Ademir Ferreira da; MAIA, Cristiane do Socorro Ferraz; http://lattes.cnpq.br/4835820645258101; LEAL, Walace Gomes; http://lattes.cnpq.br/2085871005197072
Experimental evidence suggests that aluminum is a neurotoxic agent with harmful effects on cognitive processes. In this study, we investigated the behavioral, biochemical and histopathological effects of chronic intoxication with aluminum citrate on the hippocampus of adult rats, in the same time investigated experimental therapy treatment with magnesium for reversing the neuropathological changes. We used 70 male Wistar rats of 200-250 g that were divided in groups as follows: control, sodium citrate (CNa), aluminum citrate (CAl), aluminum citrate + magnesium sulphate (CAl+Mg), sodium citrate + sulfate magnesium (Mg+CNa). The dose used of aluminum citrate was 100 mg/kg and 250 mg/kg of magnesium sulfate. The neurotoxic compound was taken orally for 30 days. The animals were subjected to behavioral tests of open field, Rota Rod, social recognition and the elevated T maze (LTE). Furthermore, aluminum levels in plasma and hippocampus of animals was found by atomic absorption spectrometer graphite furnace (GF AAS), biochemical analysis, histopathology and immunohistochemistry for GFAP. It was found that the CAl group showed increase locomotor activity in the open field test compared to the control group, and CAl+Mg group showed a decrease (P <0.001). In memory tests of LTE and social Recognition, the CAl group showed cognitive deficits in relation to other groups, and CAl+Mg group performed well in the test (P <0.001). Aluminum levels found in the hippocampus of CAl group were considerably higher but in the other groups the levels were below to the detection limit of the equipment. Histopathology and imunistochemistry analysis in CAl group showed decreased in cell density and astrocytic reactivity in layers CA1, CA3 and hilus of the hippocampus. These results suggest that the experimental poisoning with aluminum citrate induce deficits of learning and memory and that the administration of magnesium sulphate may have the ability to minimize the damage caused by metal in the hippocampus of intoxicated animals.
Acesso aberto (Open Access)
Investigação de tipos e origem celular neurogênicos em áreas diversas do sistema nervoso central da espécie Cebus apella
(Universidade Federal do Pará, 2015-07-27) SANTOS, Adriano Guimarães; HAMOY, Moisés; http://lattes.cnpq.br/4523340329253911; LEAL, Walace Gomes; http://lattes.cnpq.br/2085871005197072
Identifying populations of neuronal precursors and stem cells generated by own central nervous system has held discussions on its possible use in the repair of damage caused by acute disorders of the central nervous system. However, in the case of adult mammalian brain, such generation is considered evolutionarily restricted to two areas: subgranular zone of the dentate gyrus of the hippocampus, and the walls of the lateral ventricles where new neurons are continuously generated. We used 6 non-human primates, adults, males of the species Cebus (capuchin monkey, 10 years old), weighing between 2.1 and 2.8 kg (mean 2.5 kg) pretreated with BrdU that after sacrifice and because histological processing, their tissues were analyzed for immunohistochemical analysis using anti-BrdU anti-Nestin, and Sox2 anti-DCX in diverse areas of the Central Nervous System. The ventricular walls showed the presence of neuroblasts similar to that observed in previous studies, but unexpected results were also observed in areas such as the frontal cortex.
Acesso aberto (Open Access)
Modulação da neuroinflamação celular e neuroproteção induzidas por tratamento com betacariofileno em um modelo experimental de isquemia estriatal em ratos adultos
(Universidade Federal do Pará, 2016-10-11) LOPES, Rosana Telma Santos; SANTOS, Enio Maurício Nery dos; http://lattes.cnpq.br/7789458294239924; LEAL, Walace Gomes; http://lattes.cnpq.br/2085871005197072
Stroke results from the transitory or permanent reduction of cerebral blood flow. It can be classified as hemorrhagic or ischemic. Ischemic stroke is responsible for around 87% of all cases. This acute neural disorder is the second cause of mortality and disability around the world and the main cause of death in Brazil. Since ischemic stroke in patients usually results from a thrombotic or embolic occlusion of the middle cerebral artery (MCA), experimental models of ischemia have been developed to mimic human stroke. There are no neuroprotective drugs available for human stroke. It follows that research on development of alternative neuroprotective drugs are of important clinical relevance. In this study, we investigated the effects of betacaryophyllene, the main sesquiterpene present in about 40% of the copaiba oil-resin composition, on microglial activation, astrocytic reactivity and neuronal preservation following experimental MCAO in adult rats. Animals were submitted to experimental stroke by microinjections of endothelin-1 (ET-1) and treated (i.p) with betacaryophillene (N=4) or vehicle control (N=4) and perfused at 3 days or 7 days post-MCAO. Gross histopathology was performed using cresyl violet staining. Immunohistochemistry was used to assess neuronal loss (anti-NeuN), microglial activation (anti-ED1) and astrocytosis (anti-GFAP). Numbers of NeuN+ and GFAP+ cells were quantified in the ischemic striatum. Betacaryophyllene treatment reduced microglial activation, increased neuronal preservation and decreased astrocytic reactivity at 7 days post-MCAO. These results suggest that betacaryophylene modulates neuroinflammation and is neuroprotective following experimental striatal. Considering that betacaryophyllene is a natural dietetic extract already used in non-neural human diseases with antiinflammatory, anti-microbial and anti-carcinogenic properties, its use as a neuroprotective agent is a promising future therapy for human stroke.
Acesso aberto (Open Access)
Perda neuronal, ativação glial, neurogênese e alterações sensório-motoras após isquemia focal no córtex somestésico de ratos adultos
(Universidade Federal do Pará, 2012-09-26) CORRÊA, Vania Castro; LEAL, Walace Gomes; http://lattes.cnpq.br/2085871005197072
Stroke is considered one of the most important causes of death and functional deficits in the world. Few neurological conditions are so complex and devastating, resulting in severe neurological deficits and death in the survivors. The cortical regions are commonly affected by stroke, resulting in sensory and motor loss. The establishment of neuropathological patterns in cortical regions, including the somatosensory area, is critical for the investigation of possible therapeutic interventions. In the present study, we investigated the patterns of neuronal loss, microgliosis, astrocytosis, neurogenesis and functional deficits in the primary somatosensory cortex of adult rats submitted to focal ischemia induced by microinjections of 40 pmol of endothelin-1 (ET-1). A total of 30 young adult Wistar rats (Rattus norvegicus) of Wistar, weighing between 250-280g were used in the study. The animals were divided into ischemic (N = 21) and control (N = 9) groups. They were perfused at survival times of 1, 3 and 7 days. The 7 days animals were submitted to behavioral tests to evaluate sensorimotor impairment. Sections were stained with cresyl violet, cytochrome oxidase and immunostained to identify neurons (anti-NeuN), activated and non-activated microglia (Iba-1), activated macrophages/microglia (ED-1), astrocytes (GFAP) and neuroblasts (DCX ). Statistical comparisons between groups were made by one analysis of variance (ANOVA) with Tukey post-hoc test. The animals showed ischemic sensorimotor deficits revealed by Bederson Neurological Scale, Paw Placement and corner tests. Microinjections of ET-1 induced focal ischemic lesion in the primary somatosensory cortex with neuronal loss and progressive astrocytosis and microgliosis mainly in the late survival times. The cytochrome oxidase histochemistry revealed the barrel fields, but unexpectedly marked a population of inflammatory cells with macrophage characteristics in the ischemic region. Increased numbers of SVZ neuroblasts were observed mainly in late survival times of ipsilateral hemisphere in comparison to contralateral side and control animals. There was no significant migration of neuroblasts to the ischemic cortex. The results show that microinjections of ET-1 are an effective method for inducing tissue loss and sensorymotor deficits in the primary somatosensory cortex of adult rats. It was evident that the SVZ is influenced by distant ischemic events distant and that macrophage populations seem to increase the cytochrome oxidase expression. The implemented experimental model can be used in future studies, in which potential neuroprotective drugs can be tested to minimize the described neuropathological alterations.
Acesso aberto (Open Access)
Sobrevivência e dispersão de células da fração mononuclear da medula óssea transplantadas heterologamente no estriado após isquemia experimental
(Universidade Federal do Pará, 2015-02-27) CARDOSO, Marcelo Marques; SAUNIER, Ghislain; http://lattes.cnpq.br/6254015055212071; LEAL, Walace Gomes; http://lattes.cnpq.br/2085871005197072
The studies show the promising potential of bone marrow mononuclear cells (BMMC) for the treatment of stroke models. It is known that the BMMC are sensitive to environmental changes, like those induced by ischemia, such as events associated with inflammation. However, little is known about the biodistribution and survival of these cells in the post-injury nerve tissue. Aims to investigate whether the survival and spread of BMMC are influenced by the inflammatory response after striatum stroke. Heterologous transplantation (5x105 BMMC) in the striatum of rats clustered among untreated controls (CNT) and sham (SHM) and treated (STBC) perfused at 1, 3, 7 and 28 days. BMMC were impregnated with Qdot nanocrystals for identification by fluorescence microscopy in the host tissue. Staining for cresyl violet, and basic immunohistochemistry (IBA1 and ED1) were applied for histopathological analysis of tissue by light microscopy. Neurobehavioral tests (adhesive removal test and cylinder test) were performed to assess the response of groups for interventions. The results show the effectiveness of the experimental model of ischemic induction to reproduce the injury in the dorsolateral striatum. The cell infiltrate in the CNT group shows the inflammatory response, later confirmed by immunohistochemistry for ED1 and IBA1; the cellular infiltrate in STBM group, shows the BMMC of stay in all studied survival. The loss profile for death of BMMC transplanted into the injury site is similar between STBM and SHM groups, however, shows that inflammatory response of the receptor causes more decay of cell amount in STBM group. More refined or automated cell infusion procedures can improve the sensitivity of behavioral tests to discriminate the evolution between groups. To summarize the change of post-ischemic microenvironment creates conditions that determine the distribution and survival of BMMC. Other immunohistochemical procedures may point to the results presented as microglial profile and the degree of the immunomodulation study of the dynamics of inflammatory cytokines produced.

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