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1.
Stem Cell Reports ; 19(2): 254-269, 2024 Feb 13.
Artigo em Inglês | MEDLINE | ID: mdl-38181785

RESUMO

Pluripotent stem cell-based therapy for retinal degenerative diseases is a promising approach to restoring visual function. A clinical study using retinal organoid (RO) sheets was recently conducted in patients with retinitis pigmentosa. However, the graft preparation currently requires advanced skills to identify and excise suitable segments from the transplantable area of the limited number of suitable ROs. This remains a challenge for consistent clinical implementations. Herein, we enabled the enrichment of wild-type (non-reporter) retinal progenitor cells (RPCs) from dissociated ROs using a label-free ghost cytometry (LF-GC)-based sorting system, where a machine-based classifier was trained in advance with another RPC reporter line. The sorted cells reproducibly formed retinal spheroids large enough for transplantation and developed mature photoreceptors in the retinal degeneration rats. This method of enriching early RPCs with no specific surface antigens and without any reporters or chemical labeling is promising for robust preparation of graft tissues during cell-based therapy.


Assuntos
Células-Tronco Pluripotentes , Degeneração Retiniana , Retinose Pigmentar , Humanos , Animais , Ratos , Espécies Reativas de Oxigênio , Retina , Células-Tronco Pluripotentes/transplante , Degeneração Retiniana/terapia , Retinose Pigmentar/terapia , Transplante de Células-Tronco/métodos
2.
Epigenetics Chromatin ; 16(1): 14, 2023 04 28.
Artigo em Inglês | MEDLINE | ID: mdl-37118773

RESUMO

BACKGROUND: Single-cell technologies to analyze transcription and chromatin structure have been widely used in many research areas to reveal the functions and molecular properties of cells at single-cell resolution. Sample multiplexing techniques are valuable when performing single-cell analysis, reducing technical variation and permitting cost efficiencies. Several commercially available methods have been used in many scRNA-seq studies. On the other hand, while several methods have been published, multiplexing techniques for single nuclear assay for transposase-accessible chromatin (snATAC)-seq assays remain under development. We developed a simple nucleus hashing method using oligonucleotide-conjugated antibodies recognizing nuclear pore complex proteins, NuHash, to perform snATAC-seq library preparations by multiplexing. RESULTS: We performed multiplexing snATAC-seq analyses on a mixture of human and mouse cell samples (two samples, 2-plex, and four samples, 4-plex) using NuHash. The analyses on nuclei with at least 10,000 read counts showed that the demultiplexing accuracy of NuHash was high, and only ten out of 9144 nuclei (2-plex) and 150 of 12,208 nuclei (4-plex) had discordant classifications between NuHash demultiplexing and discrimination using reference genome alignments. The differential open chromatin region (OCR) analysis between female and male samples revealed that male-specific OCRs were enriched in chromosome Y (four out of nine). We also found that five female-specific OCRs (20 OCRs) were on chromosome X. A comparative analysis between snATAC-seq and deeply sequenced bulk ATAC-seq on the same samples revealed that the bulk ATAC-seq signal intensity was positively correlated with the number of cell clusters detected in snATAC-seq. Moreover, when we categorized snATAC-seq peaks based on the number of cell clusters in which the peak was present, we observed different distributions over different genomic features between the groups. This result suggests that the peak intensities of bulk ATAC-seq can be used to identify different types of functional loci. CONCLUSIONS: Our multiplexing method using oligo-conjugated anti-nuclear pore complex proteins, NuHash, permits high-accuracy demultiplexing of samples. The NuHash protocol is straightforward, works on frozen samples, and requires no modifications for snATAC-seq library preparation.


Assuntos
Núcleo Celular , Sequenciamento de Cromatina por Imunoprecipitação , Masculino , Feminino , Humanos , Animais , Camundongos , Análise de Sequência de DNA/métodos , Núcleo Celular/genética , Núcleo Celular/metabolismo , Cromatina/genética , Cromatina/metabolismo , Oligonucleotídeos/metabolismo
3.
Elife ; 102021 12 21.
Artigo em Inglês | MEDLINE | ID: mdl-34930522

RESUMO

Characterization and isolation of a large population of cells are indispensable procedures in biological sciences. Flow cytometry is one of the standards that offers a method to characterize and isolate cells at high throughput. When performing flow cytometry, cells are molecularly stained with fluorescent labels to adopt biomolecular specificity which is essential for characterizing cells. However, molecular staining is costly and its chemical toxicity can cause side effects to the cells which becomes a critical issue when the cells are used downstream as medical products or for further analysis. Here, we introduce a high-throughput stain-free flow cytometry called in silico-labeled ghost cytometry which characterizes and sorts cells using machine-predicted labels. Instead of detecting molecular stains, we use machine learning to derive the molecular labels from compressive data obtained with diffractive and scattering imaging methods. By directly using the compressive 'imaging' data, our system can accurately assign the designated label to each cell in real time and perform sorting based on this judgment. With this method, we were able to distinguish different cell states, cell types derived from human induced pluripotent stem (iPS) cells, and subtypes of peripheral white blood cells using only stain-free modalities. Our method will find applications in cell manufacturing for regenerative medicine as well as in cell-based medical diagnostic assays in which fluorescence labeling of the cells is undesirable.


Assuntos
Citometria de Fluxo/instrumentação , Células-Tronco Pluripotentes Induzidas/citologia , Leucócitos/citologia , Coloração e Rotulagem/instrumentação , Corantes/análise , Simulação por Computador , Humanos , Aprendizado de Máquina
4.
Nat Commun ; 12(1): 6645, 2021 11 17.
Artigo em Inglês | MEDLINE | ID: mdl-34789765

RESUMO

The poles of the heart and branchiomeric muscles of the face and neck are formed from the cardiopharyngeal mesoderm within the pharyngeal apparatus. They are disrupted in patients with 22q11.2 deletion syndrome, due to haploinsufficiency of TBX1, encoding a T-box transcription factor. Here, using single cell RNA-sequencing, we now identify a multilineage primed population within the cardiopharyngeal mesoderm, marked by Tbx1, which has bipotent properties to form cardiac and branchiomeric muscle cells. The multilineage primed cells are localized within the nascent mesoderm of the caudal lateral pharyngeal apparatus and provide a continuous source of cardiopharyngeal mesoderm progenitors. Tbx1 regulates the maturation of multilineage primed progenitor cells to cardiopharyngeal mesoderm derivatives while restricting ectopic non-mesodermal gene expression. We further show that TBX1 confers this balance of gene expression by direct and indirect regulation of enriched genes in multilineage primed progenitors and downstream pathways, partly through altering chromatin accessibility, the perturbation of which can lead to congenital defects in individuals with 22q11.2 deletion syndrome.


Assuntos
Região Branquial/citologia , Mesoderma/citologia , Miocárdio/citologia , Proteínas com Domínio T/metabolismo , Animais , Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética , Fatores de Transcrição Hélice-Alça-Hélice Básicos/metabolismo , Região Branquial/embriologia , Região Branquial/metabolismo , Diferenciação Celular , Linhagem da Célula , Perfilação da Expressão Gênica , Regulação da Expressão Gênica no Desenvolvimento , Redes Reguladoras de Genes , Coração/embriologia , Mesoderma/embriologia , Mesoderma/metabolismo , Camundongos , Camundongos Transgênicos , Músculo Esquelético/citologia , Músculo Esquelético/metabolismo , Miocárdio/metabolismo , Análise de Célula Única , Células-Tronco/citologia , Células-Tronco/metabolismo , Proteínas com Domínio T/genética
5.
Hum Mol Genet ; 27(7): 1150-1163, 2018 04 01.
Artigo em Inglês | MEDLINE | ID: mdl-29361080

RESUMO

Recurrent, de novo, meiotic non-allelic homologous recombination events between low copy repeats, termed LCR22s, leads to the 22q11.2 deletion syndrome (22q11.2DS; velo-cardio-facial syndrome/DiGeorge syndrome). Although most 22q11.2DS patients have a similar sized 3 million base pair (Mb), LCR22A-D deletion, some have nested LCR22A-B or LCR22A-C deletions. Our goal is to identify additional recurrent 22q11.2 deletions associated with 22q11.2DS, serving as recombination hotspots for meiotic chromosomal rearrangements. Here, using data from Affymetrix 6.0 microarrays on 1680 22q11.2DS subjects, we identified what appeared to be a nested proximal 22q11.2 deletion in 38 (2.3%) of them. Using molecular and haplotype analyses from 14 subjects and their parent(s) with available DNA, we found essentially three types of scenarios to explain this observation. In eight subjects, the proximal breakpoints occurred in a small sized 12 kb LCR distal to LCR22A, referred to LCR22A+, resulting in LCR22A+-B or LCR22A+-D deletions. Six of these eight subjects had a nested 22q11.2 deletion that occurred during meiosis in a parent carrying a benign 0.2 Mb duplication of the LCR22A-LCR22A+ region with a breakpoint in LCR22A+. Another six had a typical de novo LCR22A-D deletion on one allele and inherited the LCR22A-A+ duplication from the other parent thus appearing on microarrays to have a nested deletion. LCR22A+ maps to an evolutionary breakpoint between mice and humans and appears to serve as a local hotspot for chromosome rearrangements on 22q11.2.


Assuntos
Alelos , Mapeamento Cromossômico , Síndrome de DiGeorge/genética , Meiose , Deleção Cromossômica , Cromossomos Humanos Par 22/genética , Feminino , Humanos , Masculino
6.
Circ Cardiovasc Genet ; 10(5)2017 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-29025761

RESUMO

BACKGROUND: The 22q11.2 deletion syndrome (22q11.2DS; DiGeorge syndrome/velocardiofacial syndrome) occurs in 1 of 4000 live births, and 60% to 70% of affected individuals have congenital heart disease, ranging from mild to severe. In our cohort of 1472 subjects with 22q11.2DS, a total of 62% (n=906) have congenital heart disease and 36% (n=326) of these have tetralogy of Fallot (TOF), comprising the largest subset of severe congenital heart disease in the cohort. METHODS AND RESULTS: To identify common genetic variants associated with TOF in individuals with 22q11.2DS, we performed a genome-wide association study using Affymetrix 6.0 array and imputed genotype data. In our cohort, TOF was significantly associated with a genotyped single-nucleotide polymorphism (rs12519770, P=2.98×10-8) in an intron of the adhesion GPR98 (G-protein-coupled receptor V1) gene on chromosome 5q14.3. There was also suggestive evidence of association between TOF and several additional single-nucleotide polymorphisms in this region. Some genome-wide significant loci in introns or noncoding regions could affect regulation of genes nearby or at a distance. On the basis of this possibility, we examined existing Hi-C chromatin conformation data to identify genes that might be under shared transcriptional regulation within the region on 5q14.3. There are 6 genes in a topologically associated domain of chromatin with GPR98, including MEF2C (Myocyte-specific enhancer factor 2C). MEF2C is the only gene that is known to affect heart development in mammals and might be of interest with respect to 22q11.2DS. CONCLUSIONS: In conclusion, common variants may contribute to TOF in 22q11.2DS and may function in cardiac outflow tract development.


Assuntos
Síndrome de DiGeorge/genética , Estudo de Associação Genômica Ampla , Receptores Acoplados a Proteínas G/genética , Tetralogia de Fallot/genética , Cromatina/metabolismo , Cromossomos Humanos Par 5 , Síndrome de DiGeorge/complicações , Loci Gênicos , Genótipo , Sequenciamento de Nucleotídeos em Larga Escala , Humanos , Desequilíbrio de Ligação , Fatores de Transcrição MEF2/genética , Análise de Sequência com Séries de Oligonucleotídeos , Fenótipo , Polimorfismo de Nucleotídeo Único , Receptores Acoplados a Proteínas G/metabolismo , Análise de Sequência de DNA , Tetralogia de Fallot/complicações
7.
Biol Psychiatry ; 79(5): 415-420, 2016 Mar 01.
Artigo em Inglês | MEDLINE | ID: mdl-26520239

RESUMO

Matrix-assisted laser desorption ionization (MALDI) imaging mass spectrometry (IMS) (MALDI-IMS) provides a technical means for simultaneous analysis of precise anatomic localization and regulation of peptides. We explored the technical capability of matrix-assisted laser desorption ionization mass spectrometry for characterization of peptidomic regulation by an addictive substance along two distinct projection systems in the mouse striatum. The spatial expression patterns of substance P and proenkephalin, marker neuropeptides of two distinct striatal projection neurons, were negatively correlated at baseline. We detected 768 mass/charge (m/z) peaks whose expression levels were mostly negatively and positively correlated with expression levels of substance P and proenkephalin A (amino acids 218-228), respectively, within the dorsal striatum. After nicotine administration, there was a positive shift in correlation of mass/charge peak expression levels with substance P and proenkephalin A (218-228). Our exploratory analyses demonstrate the technical capacity of MALDI-IMS for comprehensive identification of peptidomic regulation patterns along histochemically distinguishable striatal projection pathways.


Assuntos
Encefalinas/metabolismo , Neostriado/metabolismo , Neuropeptídeos/metabolismo , Precursores de Proteínas/metabolismo , Espectrometria de Massas por Ionização e Dessorção a Laser Assistida por Matriz , Animais , Masculino , Camundongos , Camundongos Endogâmicos C57BL
8.
Glia ; 62(8): 1284-98, 2014 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-24771617

RESUMO

The Fosb gene encodes subunits of the activator protein-1 transcription factor complex. Two mature mRNAs, Fosb and ΔFosb, encoding full-length FOSB and ΔFOSB proteins respectively, are formed by alternative splicing of Fosb mRNA. Fosb products are expressed in several brain regions. Moreover, Fosb-null mice exhibit depressive-like behaviors and adult-onset spontaneous epilepsy, demonstrating important roles in neurological and psychiatric disorders. Study of Fosb products has focused almost exclusively on neurons; their function in glial cells remains to be explored. In this study, we found that microglia express equivalent levels of Fosb and ΔFosb mRNAs to hippocampal neurons and, using microarray analysis, we identified six microglial genes whose expression is dependent on Fosb products. Of these genes, we focused on C5ar1 and C5ar2, which encode receptors for complement C5a. In isolated Fosb-null microglia, chemotactic responsiveness toward the truncated form of C5a was significantly lower than that in wild-type cells. Fosb-null mice were significantly resistant to kainate-induced seizures compared with wild-type mice. C5ar1 mRNA levels and C5aR1 immunoreactivity were increased in wild-type hippocampus 24 hours after kainate administration; however, such induction was significantly reduced in Fosb-null hippocampus. Furthermore, microglial activation after kainate administration was significantly diminished in Fosb-null hippocampus, as shown by significant reductions in CD68 immunoreactivity, morphological change and reduced levels of Il6 and Tnf mRNAs, although no change in the number of Iba-1-positive cells was observed. These findings demonstrate that, under excitotoxicity, Fosb products contribute to a neuroinflammatory response in the hippocampus through regulation of microglial C5ar1 and C5ar2 expression.


Assuntos
Hipocampo/fisiopatologia , Microglia/fisiologia , Proteínas Proto-Oncogênicas c-fos/metabolismo , Receptor da Anafilatoxina C5a/metabolismo , Processamento Alternativo , Animais , Antígenos CD/metabolismo , Antígenos de Diferenciação Mielomonocítica/metabolismo , Astrócitos/fisiologia , Proteínas de Ligação ao Cálcio/metabolismo , Células Cultivadas , Quimiotaxia/fisiologia , Agonistas de Aminoácidos Excitatórios/toxicidade , Hipocampo/efeitos dos fármacos , Hipocampo/patologia , Interleucina-6/metabolismo , Ácido Caínico/toxicidade , Masculino , Camundongos Endogâmicos C57BL , Camundongos Knockout , Proteínas dos Microfilamentos/metabolismo , Microglia/efeitos dos fármacos , Microglia/patologia , Neurônios/fisiologia , Proteínas Proto-Oncogênicas c-fos/genética , RNA Mensageiro/metabolismo , Convulsões/patologia , Convulsões/fisiopatologia , Fator de Necrose Tumoral alfa/metabolismo
9.
Neuroreport ; 25(3): 171-6, 2014 Feb 12.
Artigo em Inglês | MEDLINE | ID: mdl-24323124

RESUMO

Galectin-1 (gal-1) is one of several well-studied proteins from the galectin families. It is a 14.5 kDa glycoprotein with a single carbohydrate-binding domain. To examine the distribution and properties of gal-1 in the mouse hippocampus, we performed immunohistochemistry using an anti-gal-1 antibody. We found that most gal-1-positive cells showed both NeuN and ß-tubulin III (Tuj-1) immunoreactivity (NeuN: 93%, ß-tubulin III: 88%). Furthermore, we clarified that 77% of gal-1-positive cells expressed somatostatin, 79% of gal-1-positive cells expressed GAD67, 34% of gal-1-positive cells expressed parvalbumin, 5% of gal-1-positive cells expressed calretinin, 2% of gal-1-positive cells expressed calbindin, and 31% of gal-1-positive cells expressed neuropeptide Y in the mouse hippocampus. These results indicate that gal-1 is expressed in interneurons that also express ß-tubulin III and gal-1 may be a novel marker for interneuron subpopulations in the hippocampus.


Assuntos
Galectina 1/metabolismo , Hipocampo/citologia , Hipocampo/metabolismo , Interneurônios/metabolismo , Animais , Calbindina 2/metabolismo , Proteínas de Ligação a DNA , Glutamato Descarboxilase/metabolismo , Imuno-Histoquímica , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Microscopia Confocal , Microscopia de Fluorescência , Proteínas do Tecido Nervoso/metabolismo , Neuropeptídeo Y/metabolismo , Proteínas Nucleares/metabolismo , Parvalbuminas/metabolismo , Somatostatina/metabolismo , Tubulina (Proteína)/metabolismo
10.
Neuropsychopharmacology ; 38(5): 895-906, 2013 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-23303048

RESUMO

Patients with epilepsy are at high risk for major depression relative to the general population, and both disorders are associated with changes in adult hippocampal neurogenesis, although the mechanisms underlying disease onset remain unknown. The expression of fosB, an immediate early gene encoding FosB and ΔFosB/Δ2ΔFosB by alternative splicing and translation initiation, is known to be induced in neural progenitor cells within the subventricular zone of the lateral ventricles and subgranular zone of the hippocampus, following transient forebrain ischemia in the rat brain. Moreover, adenovirus-mediated expression of fosB gene products can promote neural stem cell proliferation. We recently found that fosB-null mice show increased depressive behavior, suggesting impaired neurogenesis in fosB-null mice. In the current study, we analyzed neurogenesis in the hippocampal dentate gyrus of fosB-null and fosB(d/d) mice that express ΔFosB/Δ2ΔFosB but not FosB, in comparison with wild-type mice, alongside neuropathology, behaviors, and gene expression profiles. fosB-null but not fosB(d/d) mice displayed impaired neurogenesis in the adult hippocampus and spontaneous epilepsy. Microarray analysis revealed that genes related to neurogenesis, depression, and epilepsy were altered in the hippocampus of fosB-null mice. Thus, we conclude that the fosB-null mouse is the first animal model to provide a genetic and molecular basis for the comorbidity between depression and epilepsy with abnormal neurogenesis, all of which are caused by loss of a single gene, fosB.


Assuntos
Depressão/genética , Epilepsia/genética , Hipocampo/patologia , Mutação/genética , Neurogênese/genética , Proteínas Proto-Oncogênicas c-fos/deficiência , Animais , Bromodesoxiuridina/metabolismo , Proliferação de Células/efeitos dos fármacos , Depressão/complicações , Modelos Animais de Doenças , Proteínas do Domínio Duplacortina , Eletroencefalografia , Epilepsia/complicações , Agonistas de Aminoácidos Excitatórios/farmacologia , Regulação da Expressão Gênica/efeitos dos fármacos , Regulação da Expressão Gênica/genética , Ácido Caínico/farmacologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Transgênicos , Análise em Microsséries , Proteínas Associadas aos Microtúbulos/metabolismo , Neuropeptídeos/metabolismo , Fosfopiruvato Hidratase/metabolismo , Proteínas Proto-Oncogênicas c-fos/genética
11.
J Clin Invest ; 122(12): 4344-61, 2012 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-23143307

RESUMO

8-Oxoguanine (8-oxoG), a common DNA lesion caused by reactive oxygen species, is associated with carcinogenesis and neurodegeneration. Although the mechanism by which 8-oxoG causes carcinogenesis is well understood, the mechanism by which it causes neurodegeneration is unknown. Here, we report that neurodegeneration is triggered by MUTYH-mediated excision repair of 8-oxoG-paired adenine. Mutant mice lacking 8-oxo-2'-deoxyguanosine triphosphate-depleting (8-oxo-dGTP-depleting) MTH1 and/or 8-oxoG-excising OGG1 exhibited severe striatal neurodegeneration, whereas mutant mice lacking MUTYH or OGG1/MUTYH were resistant to neurodegeneration under conditions of oxidative stress. These results indicate that OGG1 and MTH1 are protective, while MUTYH promotes neurodegeneration. We observed that 8-oxoG accumulated in the mitochondrial DNA of neurons and caused calpain-dependent neuronal loss, while delayed nuclear accumulation of 8-oxoG in microglia resulted in PARP-dependent activation of apoptosis-inducing factor and exacerbated microgliosis. These results revealed that neurodegeneration is a complex process caused by 8-oxoG accumulation in the genomes of neurons and microglia. Different signaling pathways were triggered by the accumulation of single-strand breaks in each type of DNA generated during base excision repair initiated by MUTYH, suggesting that suppression of MUTYH may protect the brain under conditions of oxidative stress.


Assuntos
DNA Glicosilases/fisiologia , Reparo do DNA , Guanina/análogos & derivados , Doenças Neurodegenerativas/metabolismo , Estresse Oxidativo , Animais , Fator de Indução de Apoptose/metabolismo , Benzamidas/farmacologia , Calpaína/antagonistas & inibidores , Calpaína/metabolismo , Núcleo Celular/metabolismo , Corpo Estriado/patologia , Quebras de DNA de Cadeia Simples , DNA Glicosilases/genética , DNA Glicosilases/metabolismo , DNA Mitocondrial/genética , Dipeptídeos/farmacologia , Guanina/metabolismo , Guanina/fisiologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Microglia/metabolismo , Mitocôndrias/metabolismo , Atividade Motora , Doenças Neurodegenerativas/etiologia , Doenças Neurodegenerativas/patologia , Nitrocompostos , Monoéster Fosfórico Hidrolases/genética , Poli(ADP-Ribose) Polimerase-1 , Inibidores de Poli(ADP-Ribose) Polimerases , Poli(ADP-Ribose) Polimerases/metabolismo , Propionatos
12.
Biol Psychiatry ; 70(5): 487-95, 2011 Sep 01.
Artigo em Inglês | MEDLINE | ID: mdl-21679928

RESUMO

BACKGROUND: Molecular mechanisms underlying stress tolerance and vulnerability are incompletely understood. The fosB gene is an attractive candidate for regulating stress responses, because ΔFosB, an alternative splice product of the fosB gene, accumulates after repeated stress or antidepressant treatments. On the other hand, FosB, the other alternative splice product of the fosB gene, expresses more transiently than ΔFosB but exerts higher transcriptional activity. However, the functional differences of these two fosB products remain unclear. METHODS: We established various mouse lines carrying three different types of fosB allele, wild-type (fosB(+)), fosB-null (fosB(G)), and fosB(d) allele, which encodes ΔFosB but not FosB, and analyzed them in stress-related behavioral tests. RESULTS: Because fosB(+/d) mice show enhanced ΔFosB levels in the presence of FosB and fosB(d/d) mice show more enhanced ΔFosB levels in the absence of FosB, the function of FosB can be inferred from differences observed between these lines. The fosB(+/d) and fosB(d/d) mice showed increased locomotor activity and elevated Akt phosphorylation, whereas only fosB(+/d) mice showed antidepressive-like behaviors and increased E-cadherin expression in striatum compared with wild-type mice. In contrast, fosB-null mice showed increased depression-like behavior and lower E-cadherin expression. CONCLUSIONS: These findings indicate that FosB is essential for stress tolerance mediated by ΔFosB. These data suggest that fosB gene products have a potential to regulate mood disorder-related behaviors.


Assuntos
Adaptação Psicológica/fisiologia , Comportamento Exploratório/fisiologia , Atividade Motora/fisiologia , Proteínas Proto-Oncogênicas c-fos/fisiologia , Estresse Psicológico/fisiopatologia , Animais , Caderinas/biossíntese , Corpo Estriado/metabolismo , Dopamina/fisiologia , Masculino , Aprendizagem em Labirinto/fisiologia , Camundongos , Camundongos Mutantes , Atividade Motora/genética , Proteínas Proto-Oncogênicas c-akt/metabolismo , Proteínas Proto-Oncogênicas c-fos/genética , Estresse Psicológico/genética , Estresse Psicológico/metabolismo
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