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Bandekar, Neha. "The Study of Immediate Early Genes." Thesis, The University of Arizona, 2011. http://hdl.handle.net/10150/144229.
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Hazzalin, Catherine Ann. "Mitogen- and anisomycin-stimulated induction of immediate-early genes." Thesis, King's College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244746.
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Jenkins, Peter John. "Transcriptional regulation of the Epstein-Barr virus immediate early genes." Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367926.
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Jenkins, Robert. "The expression of immediate early genes in neuronal development and regeneration." Thesis, University of Cambridge, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260577.
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Edmunds, John W. "Histone methylation at immediate-early genes : distribution, dynamics and molecular mechanisms." Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.442789.
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Penner, Marsha Rae. "Subregion Specific Changes In Immediate-Early Genes in the Aged Hippocampus." Diss., The University of Arizona, 2008. http://hdl.handle.net/10150/194312.
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The normal aging process is accompanied by changes in cognitive function. One of the brain regions known to be an early target of the aging process is the hippocampus, a medial temporal lobe structure that is critically involved in spatial learning and memory function. The formation and maintenance of memory relies on rapid and sustainable synaptic modification, which requires new gene expression. Immediate-early genes are the first genes to be induced following relevant stimuli, and include genes that encode transcription factors, such as c-fos and zif268, and effector proteins that directly influence cellular function, such as Arc (activity-regulated cytoskeletal gene) and Homer1A. Blocking the expression of any one of these genes interferes with memory function, and thus, each of these genes is thought to have a memory enhancing effect. The hypothesis tested here was that aged animals would show a reduction in the expression of memory-promoting immediate-early genes within the hippocampus, and moreover, that these changes in expression would be subregion specific, based on the finding that the dentate gyrus is most vulnerable to the aging process.Potential age-related changes in immediate-early gene expression within the hippocampus was determined under basal conditions and after induction by a simple behavioral task. Of the genes under investigation, only c-fos did not show age-related changes under basal conditions, or following behavioral induction. The remaining genes, Arc, zif268 and Homer1A, each showed subregion specific patterns of change within the hippocampus under basal conditions or following induction (or both). The coordinate expression of immediate-early genes within the hippocampus was also investigated by assessing the extent to which Arc was expressed within the same neurons as c-fos, zif268 or H1a. The coordinate transcription of these genes was not significantly altered in the aged hippocampus, even though changes in the size of Arc and zif268 neural ensembles occurs within the aged denate gyrus.Taken together, these data indicate that age-related reductions in the basal and induced levels of immediate-early genes occur within the hippocampus, and that these changes are subregion specific.
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Nicholas, J. "Structural and functional characterisation of the immediate-early genes of Herpesvirus saimiri." Thesis, University College London (University of London), 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.379801.
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Beaulé, Christian. "Photic entrainment and instruction of immediate-early genes within the rat circadian system." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ39438.pdf.
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Chakrabarti, Arindam. "PKR DEPENDENT UPREGULATION OF IMMEDIATE EARLY GENES AND ANTI-INFLAMMATORY CYTOKINE IL-10." Kent State University / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=kent1176136341.
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Wagner, Jessica. "Effects of Transcranial Direct Current Stimulation on Expression of Immediate Early Genes (IEG’s)." Wright State University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=wright1407255006.
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Ohnmeiss, Amanda Sara. "ANALYSIS OF LIGHT-INDUCED IMMEDIATE-EARLY GENE EXPRESSION IN THE SUPRACHIASMATIC NUCLEUS." Kent State University / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=kent1247680456.
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Teoh, Peik Lin. "Mechanisms of MAP kinase signaling to transcriptional regulators." Thesis, University of Manchester, 2012. https://www.research.manchester.ac.uk/portal/en/theses/mechanisms-of-map-kinase-signaling-to-transcriptional-regulators(390ffd58-c599-4186-b9df-497850de0794).html.
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The MAPK pathway is important in various biological functions. It is also important in regulating processes associated with gene transcription via different mechanisms such as by phosphorylation of transcription factors, coactivators/corepressors and histone modifier complexes. H3K4 methylation is highly associated with active transcription. Deposition of this mark is catalysed by SET-domain methyltransferases which consists of a WAR complex (WDR5, ASH2L and RBBP5), a catalytic SET-domain protein and other subunits. However, potential links between ERK MAPK signaling and H3K4 methylation in gene expression are not well understood. Thus, the aim of this study was to probe the potential links between these two pathways towards gene-regulatory networks. This study attempted to elucidate their direct functional interaction by studying whether components of the SETD1A complex could be phosphorylated upon ERK activation. Our results showed that the core components of SETD1A complex were not phosphorylated in vivo and in vitro by ERK. Importantly, we reported that at least two splicing variants of RBBP5 exist. ERK-dependent stabilization of exogenous RBBP5 was observed but the mechanism underlying this is unknown. Surprisingly, we found that WAR complex depletion increased the pre-mRNA expression of immediate-early (IE) genes which did not necessarily reflect changes in their mRNA levels. In addition, this occurred in an H3K4me3-independent manner. This regulation is likely to be posttranscriptional that involves pre-mRNA processing events. First, we noticed a decrease of transcription initiation in WAR complex-depleted cells upon ERK activation. Second, depletion of the WAR complex affects the splicing efficiency of FOS and EGR1. Third, RBBP5 occupancy was observed and was significantly reduced upon siRNA-mediated RBBP5 depletion at the coding region and the 3' end of FOS gene. Therefore, we propose that the WAR complex regulates the pre-mRNA processing of IE genes through an interaction between RBBP5 and a splicing factor that has yet to be identified.
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Pfaffenseller, Bianca, Flavio Kapczinski, Amelia L. Gallitano, and Fábio Klamt. "EGR3 Immediate Early Gene and the Brain-Derived Neurotrophic Factor in Bipolar Disorder." FRONTIERS MEDIA SA, 2018. http://hdl.handle.net/10150/627052.
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Bipolar disorder (BD) is a severe psychiatric illness with a consistent genetic influence, involving complex interactions between numerous genes and environmental factors. Immediate early genes (IEGs) are activated in the brain in response to environmental stimuli, such as stress. The potential to translate environmental stimuli into long-term changes in brain has led to increased interest in a potential role for these genes influencing risk for psychiatric disorders. Our recent finding using network-based approach has shown that the regulatory unit of early growth response gene 3 (EGR3) of IEGs family was robustly repressed in postmortem prefrontal cortex of BD patients. As a central transcription factor, EGR3 regulates an array of target genes that mediate critical neurobiological processes such as synaptic plasticity, memory and cognition. Considering that EGR3 expression is induced by brain-derived neurotrophic factor (BDNF) that has been consistently related to BD pathophysiology, we suggest a link between BDNF and EGR3 and their potential role in BD. A growing body of data from our group and others has shown that peripheral BDNF levels are reduced during mood episodes and also with illness progression. In this same vein, BDNF has been proposed as an important growth factor in the impaired cellular resilience related to BD. Taken together with the fact that EGR3 regulates the expression of the neurotrophin receptor p75NTR and may also indirectly induce BDNF expression, here we propose a feed-forward gene regulatory network involving EGR3 and BDNF and its potential role in BD.
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Lewis, Sian. "Investigation into the involvement of immediate early genes in rodent models of seizure activity." Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.361710.
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Panegyres, Peter K. "A study of the relationship between brain seizure activity, immediate early genes, and the amyloid precursor protein gene." Thesis, University of Cambridge, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.311336.
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Dickey, Chad Anthony. "The influence of amyloid-beta, a major pathological marker in Alzheimer's disease, on molecular cognitive processes of APP+PS1 transgenic mice." [Tampa, Fla.] : University of South Florida, 2004. http://purl.fcla.edu/fcla/etd/SFE0000360.
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Marballi, Ketan K., and Amelia L. Gallitano. "Immediate Early Genes Anchor a Biological Pathway of Proteins Required for Memory Formation, Long-Term Depression and Risk for Schizophrenia." FRONTIERS MEDIA SA, 2018. http://hdl.handle.net/10150/627116.
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While the causes of myriad medical and infectious illnesses have been identified, the etiologies of neuropsychiatric illnesses remain elusive. This is due to two major obstacles. First, the risk for neuropsychiatric disorders, such as schizophrenia, is determined by both genetic and environmental factors. Second, numerous genes influence susceptibility for these illnesses. Genome-wide association studies have identified at least 108 genomic loci for schizophrenia, and more are expected to be published shortly. In addition, numerous biological processes contribute to the neuropathology underlying schizophrenia. These include immune dysfunction, synaptic and myelination deficits, vascular abnormalities, growth factor disruption, and N-methyl-D-aspartate receptor (NMDAR) hypofunction. However, the field of psychiatric genetics lacks a unifying model to explain how environment may interact with numerous genes to influence these various biological processes and cause schizophrenia. Here we describe a biological cascade of proteins that are activated in response to environmental stimuli such as stress, a schizophrenia risk factor. The central proteins in this pathway are critical mediators of memory formation and a particular form of hippocampal synaptic plasticity, long-term depression (LTD). Each of these proteins is also implicated in schizophrenia risk. In fact, the pathway includes four genes that map to the 108 loci associated with schizophrenia: GRIN2A, nuclear factor of activated T-cells (NFATc3), early growth response 1 (EGR1) and NGFI-A Binding Protein 2 (NAB2); each of which contains the "Index single nucleotide polymorphism (SNP)" (most SNP) at its respective locus. Environmental stimuli activate this biological pathway in neurons, resulting in induction of EGR immediate early genes: EGR1, EGR3 and NAB2. We hypothesize that dysfunction in any of the genes in this pathway disrupts the normal activation of Egrs in response to stress. This may result in insufficient electrophysiologic, immunologic, and neuroprotective, processes that these genes normally mediate. Continued adverse environmental experiences, over time, may thereby result in neuropathology that gives rise to the symptoms of schizophrenia. By combining multiple genes associated with schizophrenia susceptibility, in a functional cascade triggered by neuronal activity, the proposed biological pathway provides an explanation for both the polygenic and environmental influences that determine the complex etiology of this mental illness.
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Hirata, Hugo Henrique. "Efeito da estimulação magnética na imunorreatividade da proteína zenk em diferentes regiões do encéfalo de pombos (Columba livia)." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/42/42137/tde-15092008-122501/.
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Um acúmulo de evidências sugere que animais vertebrados são capazes de detectar informações geomagnéticas, dentre eles, podemos citar os mais estudados, o caso clássico do pombo-correio (Columba livia). A descoberta de material biomagnético no epitélio do bico superior de pombos sugere a possibilidade de um mecanismo transdutor de campo magnético situado nessa região. Pelos resultados obtidos em outros contextos, a utilização de genes de resposta imediata (IEGs) combinada com tratamentos disruptivos e tarefas clássicas de orientação é tida como metodologia promissora para se conseguir uma descrição mais compreensiva dos canais sensoriais e dos mecanismos de processamento nervoso envolvidos no comportamento de orientação, entre os quais a putativa magnetocepção. Pela atividade de IEGs, especificamente a expressão da proteína ZENK, avaliamos diferencialmente áreas cerebrais ativadas em pombos expostos ou não a uma estimulação magnética, 1h e 3h após a estimulação. A análise quantitativa (teste T) mostrou um aumento no número de neurônios ZENK positivos na região do córtex pré-piriforme de pombos estimulados (p=0,051) em relação aos controles, não havendo diferença entre os grupos de 1h e 3h (ANOVA, uma via). Esses neurônios estão relacionados ao sistema olfativo, o que reforça a idéia de que esse sistema seja importante no comportamento de orientação mas ao mesmo tempo apresenta a primeira evidência experimental de um possível envolvimento da via olfatória na magnetocepção. Esse resultado indica que é necessário tomar o maior cuidado na interpretação de experimentos comportamentais inibindo a via olfativa, pois, além de causar anosmia, essas manipulações poderiam também lesar mecanismos magnetoceptivos.Much evidence suggests that vertebrate animals are capable of detecting geomagnetic information, among them, we can cite the best studied classic example of homing pigeon (Columba livia). The discovery of biomagnetic material in the pigeon upper beak suggest the possibility of a magnetoceptor transduction mechanism situated in this area. Because of the results obtained in other contexts, the use of immediate early genes (IEGs), combined with disruptive treatments and classic orientation tasks is a promising tool towards a more accurate description of sensory channels and of neural processing mechanisms involved in orientation behaviour, particularly the putative magnetoception mechanism. Using IEG activity, specifically, the ZENK-immunoreactivity protein, we studied different pigeon brain areas activated after magnetic stimulation, compared to no stimulation, at two periods of latency after the end of the experimental session (1h and 3h). Quantitative analysis (T test) showed an increase in labeling in the prepiriform cortex (CPP) of stimulated pigeons in relatioin to controls (p=0,051), but no difference between 1h and 3h groups (one-way ANOVA). These neurons are related to the olfactory system, reforcing the idea that this system is important for orientation, but at the same time presents the first experimental evidence of a possible participation of olfactory pathways in magnetoception. This result indicates that it is important to take utmost care in interpreting results of behavioural experiments in which olfaction is inhibited, since such manipulations may not only cause anosmia, but also loss of magnetic sensitivity.
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Wainford, Richard D. "Cisplatin nephrotoxicity in vivo and in vitro and the use of the immediate early genes c-Fos and c-Jun as early markers of toxicity." Thesis, University of Aberdeen, 2004. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU179580.
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The aim of this thesis is to investigate the mechanism of cisplatin nephrotoxicity and to examine the responses of rat and human proximal tubular cell cultures to platinum analogues for potential early markers of toxicity. Nephrotoxicity was induced in male Sprague Dawley rats (N = 4 +/- standard deviation) and male C57BL/6 mice (N = 6 +/- standard deviation) with doses of 6 milligrams per kilogram and 10 milligrams per kilogram cisplatin administered by intraperitoneal injection respectively. These doses increased blood urea nitrogen and serum creatinine significantly. Male Spraque Dawley rats and C57BL/6 mice had control blood urea nitrogen day 5 and day 4 values of 8 +/- 1 micromoles per millilitre and 7 +/- 0.7 micromoles per millilitre respectively compared with values post cisplatin treatment of 36 +/- 4 micromoles per millilitre and 31 +/- 11.6 micromoles per millilitre. Histological analysis revealed significant damage to the proximal tubules, including loss of brush border membrane, cellular vacuolation and loss of cell-cell adhesion. The inhibition of aminopeptidase N and renal dipeptidase in vivo in male Sprague Dawley rats (N = 4 +/- standard deviation) or in rat and human proximal tubule cell cultures did not alter the toxicity of cisplatin (N = 5 +/- standard deviation). These data show that the dipeptidase enzymes are not implicated in the nephrotoxicity of cisplatin and contradict the publications of Hanigan and Townsend (2002) and Townsend et al (2003b), which hypothesise that dipeptidase activity is an integral part of a cisplatin biotransformation, pathway that is responsible for cisplatin nephrotoxicity. The inhibition of cysteine S-conjugate b-lyase activity in male Sprague Dawley rats (N = 4 +/- standard deviation) and C57BL/6 mice (N = 6 +/- standard deviation) did not affect the level of cisplatin toxicity. The inhibition of cysteine S-conjugate b-lyase in vitro significantly increased cisplatin toxicity in rat and human proximal tubule cell cultures at 24 hours (N = 5 +/- standard deviation). These data contradict the published data of Hanigan and Townsend (2002) and Townsend et al (2003b) in which cysteine S-conjugate b-lyase inhibition prevented cisplatin nepthrotoxicity in C57BL/6 mice and reduced toxicity in LLC-PK1 cell cultures.
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Martin, Michelle Elizabeth Denny. "Physical and genetic characterization of the genome of human herpesvirus 6 strain U1102 : identification of immediate-early and regulatory genes." Thesis, Open University, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.314868.
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Khan, Dilshad Hussain. "Role of histone deacetylases in gene expression and RNA splicing." Informa UK Limited, 2012. http://hdl.handle.net/1993/22163.
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Histone deacetylases (HDAC) 1 and 2 play crucial role in chromatin remodeling and gene expression regimes, as part of multiprotein corepressor complexes. Protein kinase CK2-driven phosphorylation of HDAC1 and 2 regulates their catalytic activities and is required to form the corepressor complexes. Phosphorylation-mediated differential distributions of HDAC1 and 2 complexes in regulatory and coding regions of transcribed genes catalyze the dynamic protein acetylation of histones and other proteins, thereby influence gene expression.
During mitosis, highly phosphorylated HDAC1 and 2 heterodimers dissociate and displace from mitotic chromosomes. Our goal was to identify the kinase involved in mitotic phosphorylation of HDAC1 and 2. We postulated that CK2-mediated increased phosphorylation of HDAC1 and 2 leads to dissociation of the heterodimers, and, the mitotic chromosomal exclusions of HDAC1 and 2 are largely due to the displacement of HDAC-associated proteins and transcription factors, which recruit HDACs, from chromosomes during mitosis. We further explored the role of un- or monomodified HDAC1 and 2 complexes in immediate-early genes (IEGs), FOSL1 (FOS-like antigen-1) and MCL1 (Myeloid cell leukemia-1), regulation. Dynamic histone acetylation is an important regulator of these genes that are overexpressed in a number of diseases and cancers. We hypothesized that transcription dependent recruitment of HDAC1 and 2 complexes over the gene body regions plays a regulatory role in transcription and splicing regulation of these genes.
We present evidence that CK2-catalyzed increased phosphorylation of HDAC1 and 2 regulates the formation of distinct corepressor complexes containing either HDAC1 or HDAC2 homodimers during mitosis, which might target cellular factors. Furthermore, the exclusion of HDAC-recruiting proteins is the major factor for their displacement from mitotic chromosomes. We further demonstrated that un- or monophosphorylated HDAC1 and 2 are associated with gene body of FOSL1 in a transcription dependent manner. However, HDAC inhibitors prevented FOSL1 activation independently of the nucleosome response pathway, which is required for IEG induction. Interestingly, our mass spectrometry results revealed that HDAC1 and 2 interact with a number of splicing proteins, in particular, with serine/arginine-rich splicing factor 1 (SRSF1). HDAC1 and 2 are co-occupied with SRSF1 over gene body regions of FOSL1 and MCL1, regardless of underlying splicing mechanisms. Using siRNA-mediated knockdown approaches and HDAC inhibitors, we demonstrated that alternative splicing of MCL1 is regulated by RNA-directed localized changes in the histone acetylation levels at the alternative exon. The change in histone acetylation levels correlates with the increased transcription elongation and results in change in MCL1 splicing by exon skipping mechanism.
Taken together, our results contribute to further understanding of how the multi-faceted HDAC1 and 2 complexes can be regulated and function in various processes, including, but not limited to, transcription regulation and alternative splicing. This can be an exciting area of future research for therapeutic interventions.
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Meddle, Simone Louise. "Photoneuroendocrine control of reproduction in Japanese quail : the use of immediate early genes (C-FOC) as a marker of cell activation." Thesis, University of Bristol, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.261255.
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Ortega, Sánchez Juan Antonio. "Interacción entre estímulos estresantes emocionales y psicoestimulantes: Activación de poblaciones neuronales específicas en áreas clave del sistema nervioso central." Doctoral thesis, Universitat Autònoma de Barcelona, 2018. http://hdl.handle.net/10803/665546.
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Aunque la mayoría de los estudios sobre estrés agudo se centran en la respuesta a cada estímulo por separado, la posible interacción entre estímulos estresantes, de diferente o similar naturaleza, tiene una gran relevancia teórica ya que en la naturaleza los organismos pueden enfrentarse a más de un estímulo de manera simultánea (o casi simultánea). Independientemente de su naturaleza, los estímulos estresantes tienen en común la activación del eje hipotálamo-hipofisario-adrenal (HPA), que puede ser activado por estímulos de naturaleza física o emocional. Dependiendo de sus características, los estímulos estresantes son procesados de manera en gran parte diferenciada por el SNC, aunque las señales finalmente convergen en el núcleo paraventricular del hipotálamo (PVN), estructura clave en la regulación del eje HPA. Muchas drogas como la cocaína y la anfetamina son capaces de activar amplias zonas del SNC y el propio eje HPA, siendo consideradas como estímulos estresantes farmacológicos. Estudios previos de nuestro laboratorio han puesto de manifiesto, en ratas, interacciones entre psicoestimulantes (anfetamina) y estímulos estresantes emocionales (v.g. natación forzada) cuando ambos se administran de manera simultánea, reduciéndose la activación del eje HPA y la hiperglucemia asociada al estrés emocional. Esta sinergia negativa también se observa con la exposición a la natación forzada y la administración de otro psicoestimulante como el metilfenidato, a dosis terapéuticamente relevantes en el tratamiento del trastorno por déficit de atención e hiperactividad (ADHD).
El primer objetivo de la presente tesis ha sido el estudio de cómo la exposición simultánea a psicoestimulantes (anfetamina o metilfenidato) y estímulos estresantes emocionales (natación forzada) afecta a la activación de poblaciones neuronales específicas en áreas del SNC relacionadas con el procesamiento de ambos tipos de estímulos. Al objeto de extender la posibilidad de interacción a la exposición conjunta a estímulos estresantes de tipo emocional, hemos también estudiado de forma preliminar las consecuencias de la exposición simultánea al olor a depredador y a la inmovilización en plancha. La caracterización de las poblaciones neuronales activadas se ha llevado a cabo fundamentalmente mediante doble hibridación in situ fluorescente (FISH) del gen de expresión temprana c-fos en combinación con marcadores específicos de fenotipos neuronales. Nuestro interés se ha centrado en las neuronas glutamatérgicas o GABAérgicas de la corteza prefrontal medial, las neuronas D1R+ o D2R+ del estriado, las neuronas CRH+ del PVN y las neuronas tirosina hidroxilasa (TH)+ del área tegmental ventral y el locus coeruleus.
Los resultados indican que la exposición simultánea a dos estímulos da lugar a diversos tipos de interacción respecto a las poblaciones neuronales activadas. Los efectos son más evidentes con la anfetamina, que por sí misma causa activación de un gran número de áreas del SNC, que con el metilfenidato, que por sí mismo apenas tuvo efecto. Pudieron observarse los siguientes patrones de respuesta: i) una falta de efecto aditivo, cuando la activación de un estímulo predomina sobre el otro; ii) un efecto aditivo, que parece reflejar una contribución independiente de cada estímulo; iii) una sinergia negativa, de tal manera que un estímulo reduce la activación causada por el otro; y iv) una sinergia positiva, en la que la exposición simultánea causa mayor activación que la suma de cada uno de los estímulos. También se han observado sinergias negativas tras la exposición simultánea al olor a gato y a la inmovilización. En conjunto, los datos presentados aportan una mejor comprensión de la interacción entre estímulos estresantes emocionales y psicoestimulantes respecto a la adicción y el tratamiento del ADHD. Además, aportan evidencias de una interacción entre estímulos emocionales procesados al mismo tiempo, lo que puede ser de interés en patologías como el trastorno de estrés postraumático.Although most acute stress studies focus on the response to each stimulus given separately, the possible interaction between stressors of different or similar nature has a critical theoretical relevance as in nature organisms can face more than one stimulus simultaneously (or almost simultaneously). Regardless of its nature (physical or emotional), stressors have in common the capability to activate the hypothalamus-pituitary-adrenal axis (HPA). Although depending on their characteristics stressors are differentially processed by the SNC, signals eventually converge at the paraventricular nucleus of the hypothalamus (PVN), the key area in the regulation of the HPA axis. Many drugs of abuse such as cocaine and amphetamine are able to activate a wide range of brain areas and also the HPA axis and, as such, are considered as pharmacological stressors. Previous research from our laboratory has demonstrated in rats some interactions between psychostimulants (amphetamine) and emotional stressors (forced swim) when both stimuli were administered simultaneously, resulting in reduced activation of the HPA axis and stress-induced hyperglycemia. The aforementioned interaction was also observed with the exposure to forced swim and the administration of another psychostimulant, methylphenidate, at doses that are used for the treatment of the attention deficit and hyperactivity disorder (ADHD). The first aim of the present work objective has been the study of how simultaneous exposure to psychostimulants (amphetamine or methylphenidate) and emotional stressors (forced swim) alter the activation of specific neuronal populations in brain areas related to the processing of both stimuli. In order to extend the possibility of interaction to simultaneous exposure to two emotional stressors, we have also preliminary studied the consequences of simultaneous exposure to predator odor and immobilization. The characterization of activated neuronal populations has been carried out mainly by double in situ hybridization (FISH) of the immediately early gene c-fos in combination with specific neuronal phenotype markers. Our interest has focused on glutamatergic and GABAergic neurons of the medial prefrontal cortex, D1R+ and D2R+ neurons of the striatum, CRH+ neurons of the PVN, and tyrosine hydroxylase (TH+) neurons of the ventral tegmental area and the locus coeruleus. Our results indicate that simultaneous exposure to two stimuli leads to different types of interactions with respect to activated neuronal populations. The effects are more evident with amphetamine, which by itself, causes wide-spread activation of the brain, than with methylphenidate, which by itself has null or modest effect. The following response patterns were observed: i) lack of additive effect, when activation of one stimulus dominate over the other; ii) additive effect, which seems to reflect an independent contribution of each stimulus; iii) negative synergy, when one stimulus reduces the activation caused by the other stimulus; and iv) positive synergy, when simultaneous exposure causes more activation than the sum of each stimulus. Negative synergies have also been observed after simultaneous exposure to predator odor and immobilization. Taken together, the present data contribute to a better understanding of the interaction between emotional stressors and two types of psychostimulants that are important for addiction and the treatment of ADHD. In addition, we add some evidence on the interaction between two emotional stressors when processed simultaneously, what may be of interest in pathologies such as the post-traumatic stress disorder.
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Gerhauser, Ingo [Verfasser]. "The role of "Immediate Early Genes" in the central nervous system of susceptible and resistant mouse strains during Theiler' s murine encephalomyelitis / Ingo Gerhauser." Hannover : Stiftung Tierärztliche Hochschule Hannover, 2007. http://d-nb.info/1179200330/34.
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Cardozo, Leonardo Minete 1988. "Identificação de receptores moleculares para ligantes detectados pelo Órgão Vomeronasal." [s.n.], 2012. http://repositorio.unicamp.br/jspui/handle/REPOSIP/316719.
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Orientador: Fabio PapesDissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia
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Resumo: Uma propriedade fundamental do sistema nervoso em todas as espécies animais e a transformação dos estímulos sensoriais em atividade neural, levando a mudanças comportamentais e endócrinas. Dentre os sistemas sensoriais, o Sistema Olfatório destaca-se por sua complexidade molecular, capacidade de detecção de odores e modulação de comportamentos inatos. Entretanto, ainda muito pouco e conhecido sobre como este Sistema detecta, processa e interpreta as informações químicas que recebe do meio externo... Observação: O resumo, na íntegra, poderá ser visualizado no texto completo da tese digital
Abstract: A fundamental property of the nervous system in all animal species is the transformation of sensory stimulation into neural activity, leading to endocrine and behavioral changes. Among the sensory systems, the olfactory system stands out due to its molecular complexity, detection capacity and the modulation of innate behaviors. However, little is known about how this system detects, processes and interprets chemosignals from the environment... Note: The complete abstract is available with the full electronic document
Mestrado
Genetica Animal e Evolução
Mestre em Genética e Biologia Molecular
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Sommerlandt, Frank M. J. [Verfasser], Johannes [Gutachter] Spaethe, Wolfgang [Gutachter] Rössler, and Adrian [Gutachter] Dyer. "Mechanisms of visual memory formation in bees: About immediate early genes and synaptic plasticity / Frank M. J. Sommerlandt ; Gutachter: Johannes Spaethe, Wolfgang Rössler, Adrian Dyer." Würzburg : Universität Würzburg, 2016. http://d-nb.info/1137467711/34.
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27
Sim?es, Cristiano Soares. "Express?o de genes imediatos induzidos por vocaliza??es em sag?is-comuns (Callithrix jacchus)." Universidade Federal do Rio Grande do Norte, 2008. http://repositorio.ufrn.br:8080/jspui/handle/123456789/17261.
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Previous issue date: 2008-04-23Conselho Nacional de Desenvolvimento Cient?fico e Tecnol?gico
Immediate-early genes (IEGs) expression has been widely used as a valuable tool to investigate brain areas activated by specific stimuli. Studies of natural vocalizations, specially in songbirds, have largely benefited from this tool. Here we used IEGs expression to investigate brain areas activated by the hearing of conspecific common marmoset (Callithrix jacchus) vocalizations and/or utterance of antiphonal vocalizations. Nine adult male common marmosets were housed in sound-attenuating cages. Six animals were stimulated with playbacks of freely recorded natural long distance vocalizations (phee calls and twitters; 45 min. total duration). Three of them vocalized in response (O/V group) and three did not (O/n group). The control group (C) was composed by the remaining animals, which neither heard the playbacks nor spontaneously vocalized. After one hour of the stimulation onset (or no stimulation, in the case of the C group), animals were perfused with 0,9% phosphate-saline buffer and 4% paraformaldehyde. The tissue was coronally sectioned at 20 micro meter in a cryostat and submitted to immunohistochemistry for the IEGs egr-1 and c-fos. Marked immunoreactivity was observed in the auditory cortex of O/V and O/n subjects and in the anterior cingulate cortex, the dorsomedial prefrontal cortex and the ventrolateral prefrontal cortex of O/V subjects. In this study, brain areas activated by vocalizations of common marmosets were investigated using IEGs expression for the first time. Our results with the egr-1 gene indicate that potential plastic phenomena occur in areas related to hearing and uttering conspecific vocalizations.
A express?o de genes imediatos tem sido largamente utilizada na investiga??o de ?reas cerebrais ativadas por est?mulos espec?ficos. Estudos de comunica??o vocal, especialmente em aves canoras, t?m se beneficiado enormemente dessa ferramente. Neste trabalho, utilizamos a express?o de genes imediatos para identificar as ?reas corticiais ativadas pela audi??o e express?o de vocaliza??es co-espec?ficas de sag?is comuns (Callithrix jacchus). Nove sag?is comuns machos adultos foram mantidos em caixas de atenua??o ac?stica. Seis animais foram expostos a playbacks de vocaliza??es co-espec?ficas naturais (phee calls e twitters; total de 45 minutos). Tr?s deles vocalizaram em resposta, compondo o grupo que "ouviu e vocalizou" (O/V), e tr?s permaneceram em sil?ncio (grupo O/n). O grupo controle (C) foi composto pelos tr?s animais restantes, que n?o foram expostos ao est?mulo e nem vocalizaram espontaneamente. Depois de uma hora do in?cio do est?mulo, (ou nenhum est?mulo, no caso do grupo C), os animais foram perfundidos com solu??o salina 0,9%, seguida de paraformalde?do 4%. Os c?rebros foram removidos e cortados coronalmente a 20 micro metros com o aux?lio de um criostato e submetidos a imunohistoqu?mica para os genes imediatos egr-1 and c-fos. Maior imunorreatividade foi observada no c?rtex auditivo prim?rio dos animais dos grupos O/V e O/n e no c?rtex cingulado anterior, c?rtex pr?-frontal dorso-medial e c?rtex pr?-frontal ventro-lateral dos animais do grupo O/V. Este trabalho foi o primeiro a utilizar a express?o de genes imediatos no estudo das ?reas corticais envolvidas na comunica??o de sag?is comuns. Nossos resultados, especialmente em rela??o ao gene egr-1, indicam que eventos potencialmente pl?sticos ocorrem nas ?reas relacionadas ? audi??o e emiss?o de vocaliza??es co-espec?ficas.Express?o de genes imediatos induzidos por vocaliza??es em sag?is-comuns (Callithrix jacchus)
28
Lemos, Nelson Alessandretti de Mello. "Express?o de zif-268 durante a aquisi??o, evoca??o e extin??o de uma mem?ria aversiva." Universidade Federal do Rio Grande do Norte, 2008. http://repositorio.ufrn.br:8080/jspui/handle/123456789/17260.
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Previous issue date: 2008-04-17Conselho Nacional de Desenvolvimento Cient?fico e Tecnol?gico
In the behavioral paradigm of discriminative avoidance task, both short and long-term memories have been extensively investigated with behavioral and pharmacological approaches. The aim of the present study was to evaluate, using the abovementioned model, the hippocampal expression of zif-268 - a calcium-dependent immediate early gene involved with synaptic plasticity process - throughout several steps of memory formation, such as acquisition, evocation and extiction. The behavioral apparatus consisted of a modified elevaated plus-maze, with their enclosed arms disposed in "L". A pre-exposure to the maze was made with the animal using all arms enclosed, for 30 minutes, followed by training and test, during 10 minutes each. The between sections interval was 24h. During training, aversive stimuli (bright light and loud noise) were actived whenever the animals entered one of the enclosed armas (aversive arm). Memory acquisiton, retention and extinction were evaluated by the percentage of the total time spent exploring the aversive arm. The parameters evaluated (time spent in the arms and total distance traveled) were estimated with an animal tracking software (Anymaze, Stoelting, USA). Learning during training was estimated by the decrease of the time spent exploring the aversive arm. One hour after the beginning of each section, animals were anaesthetized with sodium-thiopental (i.p.) and perfused with 0.9% heparinized saline solution followed by 4% paraformaldehyde. Brains were cryoprotected with 20% sucrose, separeted in three blocks and frozen. The middle block, containing the hippocampus, was sectioned at 20 micro meters in the coronal plane and the resutant sections were submitted to zif-268 immunohistochemistry. Our results show an increased expression of zif-268 in the dentate gyrus (DG) during the evocation and extinction stages. There is a distinct participation of the DG during the memory evocation, but not during its acquisition. Inaddition, all hippocampal regions (CA1, CA3 and DG) presented an increased zif-268 expression during the process of extinction.
No paradigma comportamental da esquiva discriminativa, as mem?rias de curto e de longo prazo t?m sido extensivamente estudadas tanto comportamental quanto farmacologicamente. O objetivo do presente estudo foi avaliar, usando o modelo supracitado, a express?o hipocampal de zif-268 - gene imediato dependente de c?lcio implicado em processos de plasticidade sin?ptica - ao longo das diversas etapas da forma??o da mem?ria, como aquisi??o, evoca??o e extin??o. O aparato comportamental consistiu de um labirinto em crum elevado modificado, com seus bra?os fechados dispostos em "L". Uma pr?-exposi??o ao labirinto foi feita com os animais usando os quatro bra?os fechados, com dura??o de 30 minutos, seguida de um treino e de um teste, cada qual com dura??o de 10 minutos. O intervalo entre as sess?es foi de 24 horas. Durante o treino, um est?mulo aversivo (luz e ru?do intensos) era acionado sempre que os animais entravam em um dos bra?os fechados (bra?o aversivo). A aquisi??o, reten??o e extin??o da mem?ria foram avaliados pelo percentual de tempo total gasto explorando o bra?o aversivo. Os par?metros avaliados (tempo nos bra?os e dist?ncia percorrida) foram registrados por um software de rastreamento de animais (Anymaze, Stoelting, USA). O aprendizado durante o treino foi estimado pelo decr?scimo do tempo gasto explorando o bra?o aversivo. Uma hora ap?s o in?cio de cada sess?o, os animais foram anestesiados com uma overdose de tiopental s?dico (i.p.) e perfundidos com solu??o salina heparinizada 0.9% seguida de paraformalde?do a 4%. Os enc?falos foram crioprotegidos com solu??o de sacorose a 20%, separados em tr?s blocos e congelados. O bloco do meio, contendo o hipocampo, foi seccionado a 20 micro metros no plano coronal e as sec??es resultantes foram ent?o submetidas ? imunohistoqu?mica para zif-268. Nossos resultados evidenciam um aumento da express?o de zif-268 no giro denteado (GD) durante asetapas de evoca??o e extins?o. H? uma participa??o distinta no GD durante a evoca??o e extin??o da mem?ria, mas n?o durante a aquisi??o. Al?m disso, todas as ?reas hipocampais (CA1, CA3 e GD) apresentam uma eleva??o da express?o de zif-268 durante o processo de extin??o
29
Wright, Edward. "Silencing of human cytomegalovirus immediate early gene expression." Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.620032.
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30
Vahid-Ansari, Faranak. "Antipsychotic-induced immediate-early gene expression in the limbic system." Thesis, University of Ottawa (Canada), 1995. http://hdl.handle.net/10393/10373.
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The mechanism by which the atypical neuroleptic clozapine is able to relieve the symptoms of schizophrenia without causing extrapyramidal side effects that are characteristic of most other antipsychotic drugs is unclear. c-fos is a proto-oncogene that encodes a 55 kDa phosphoprotein, Fos, which is thought to be an activity marker in the central nervous system. Recently, it has been shown that clozapine and haloperidol produce distinct patterns of increased c-fos expression in the rat forebrain. Haloperidol induces Fos-like immunoreactivity (FLI) in the nucleus accumbens, dorsolateral striatum and lateral septal nucleus, whereas clozapine preferentially increases in FLI in limbic structures such as the prefrontal cortex, nucleus accumbens, mediolateral striatum and lateral septal nucleus. These findings suggest that clozapine's unique therapeutic profile may be related to its failure to induce FLI in the striatum as well as its idiosyncratic actions in the medial prefrontal cortex. Given the significant clinical implications of these results, the present study attempted to identify these receptors which mediate the different effects of clozapine and haloperidol on c-fos expression. (Abstract shortened by UMI.)
31
Rampersaud, Navita. "Role of the nuclear substructure in immediate-early gene induction." Thesis, University of Oxford, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.400439.
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32
Dalrymple, M. A. "The regulation of herpes simplex virus immediate early gene expression." Thesis, University of Glasgow, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.378173.
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33
Sokal, Nadia. "Defining the role of autographa californica multiple nucleopolyhedrovirus immediate early-0 and immediate early-1 proteins in viral genome replication and early gene transactivation." Thesis, University of British Columbia, 2012. http://hdl.handle.net/2429/42940.
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The immediate early-0 (IE0) and IE1 proteins of the baculovirus Autographa californica multiple nucleopolyhedrovirus (AcMNPV) are key transregulators in the viral replication cycle. If both proteins are absent, the virus is inactive. Either protein can support viral replication but both are required to achieve wildtype infection. Both IE0 and IE1 are involved in viral DNA replication and transcriptional transactivation of early genes. In this study, to analyze IE0 and IE1’s function, ie0, ie0MtoA or ie1 were placed under the control of identical promoters (ie1 or gp64) to achieve comparable levels of protein expression. The ie1 promoter produced higher levels of IE0, IE0MtoA and IE1 compared to the gp64 promoter. Time course assays of infected Spodoptera frugiperda 9 (Sf9) cells allowed examination of viral DNA replication and budded virus (BV) production. The results showed that when IE0 and IE1 protein levels were high, either IE0, IE1 or IE0 and IE1 together maintained DNA replication and BV production similar to wildtype levels. However, when IE0 and IE1 protein levels were low, only when IE0 and IE1 were present together was DNA replication and BV production similar to wildtype. These results suggest that during the virus replication cycle when cellular levels of IE0 or IE1 are low, for example at the beginning of infection, the presence of both proteins results in more efficient DNA replication. Transient transactivation studies were also performed to examine IE0 and IE1’s ability to activate nineteen viral early gene promoters. At low levels of IE0 and IE1 expression, a group of viral early gene promoters were found to be differentially transactivated by IE0 alone or when both IE0 and small amounts of IE1 were together. These results suggest that during early times post-infection, when cellular levels of viral proteins are low, IE0 in the presence of a small amount of IE1 results in rapid onset of viral DNA replication and efficient transactivation of a specific set of viral early gene promoters. In context of virus infection, rapid viral replication by IE0 and IE1 and transactivation of early genes by IE0 may counter the insect’s defense mechanisms like sloughing and apoptosis.
34
Gressier, Amélie. "Le rôle des noyaux reuniens et rhomboïde de la ligne médiane du thalamus ventral dans la consolidation d’un souvenir spatial chez le rat : approches comportementales et moléculaires." Thesis, Strasbourg, 2018. http://www.theses.fr/2018STRAJ010.
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La formation des souvenirs repose sur un dialogue entre l’hippocampe et le cortex préfrontal médian (CPFm) qui se met en place progressivement et durablement après l’encodage de l’information. La lésion des noyaux reuniens et rhomboïde (ReRh), relai anatomo-fonctionnel entre ces deux structures, perturbe la consolidation à long terme d’un souvenir spatial. A ce jour, les mécanismes mis en jeu ne sont, pas connus. Nous avons donc étudié les processus moléculaires impliqués dans la formation d’un souvenir spatial, au sein de l’hippocampe et du CPFm, et les conséquences induites par la lésion des noyaux ReRh. Pour cela, nous avons lésé les noyaux ReRh de rats, puis nous les testés dans une tâche de piscine de Morris pendant trois jours. Nous avons alors effectué un séquençage des ARNm des sous-régions hippocampiques CA1 dorsale et ventrale, une analyse par RT-qPCR des ARNm du CPFm, ainsi qu’une analyse de l’activation de ces structures par quantification de la protéine issue du gène immédiat c-fos. Nos résultats montrent que la lésion des noyaux ReRh modifie les processus transcriptionnels et traductionnels qui prennent place dans l’hippocampe et le CPFm, dès trois jours d’apprentissage spatial. Ces résultats pourraient expliquer la non persistance d’un souvenir spatial et les déficits comportementaux qui en résultent à la suite d’une lésion des noyaux ReRhMemorization relies on a dialogue between the hippocampus and the medial prefrontal cortex (mPFC). This dialog takes place progressively after the encoding of an event. Given their connectivity, the thalamic nuclei named reuniens and rhomboid (ReRh) may modulate the functional loop between these two structures. Indeed, a lesion of these nuclei impairs the persistence of a spatial memory. The mechanisms underlying this process are still unknown. Therefore, we analyzed the molecular mechanisms underlying spatial memory consolidation within the hippocampus and the mPFC, and the consequences of a lesion of the ReRh nuclei. After a stereotaxic lesion of the ReRh nuclei, rats were subjected to three days of a spatial training in the Morris water maze. We then performed a RNA sequencing of the dorsal and ventral hippocampus (CA1 regions), RT-qPCR analysis of the mPCF, and a quantification of the expression of c-fos in these two structures. Results show that ReRh nuclei lesion impairs the transcriptional and translational mechanisms within the hippocampus and the mPFC as soon as after three days of a spatial learning. These alterations could lead to the retrieval deficit observed after a long post-acquisition delay
35
Kaouane, Nadia. "Mémoire émotionnelle normale et pathologique : implication des glucocorticoïdes intra-hippocampiques." Thesis, Bordeaux 1, 2010. http://www.theses.fr/2010BOR14203/document.
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Une mémoire émotionnelle normale se base sur la sélection de stimuli prédictifs d’un événement important pour l’individu. Cependant, ce processus de sélection peut être compromis en situation de forte intensité émotionnelle. En particulier, la sélection d’un élément saillant non nécessairement prédictif, associée à une amnésie de type déclaratif pour les éléments contextuels, caractérise les altérations mnésiques de l’état de stress post-traumatique (ESPT). Les données de la littérature suggèrent que l’action de glucocorticoïdes dans l’hippocampe serait l’une des causes possibles du développement de troubles mnésiques de type ESPT. Nos travaux ont porté sur les conditions dans lesquelles les glucocorticoïdes dans l’hippocampe peuvent altérer les fonctions mnésiques chez la souris.En utilisant des procédures de conditionnement classique aversif, nous montrons que l’injection post-apprentissage de corticostérone dans l’hippocampe dorsal, en situation de forte intensité émotionnelle, conduit (1) à une sélection incorrecte du stimulus saillant non prédictif du choc électrique au détriment des éléments contextuels (2) et à des dysfonctionnements d’activité neuronale au sein du circuit hippocampo-amygdalien (expression de c-Fos). De façon intéressante, par une action sur le même type de récepteurs (aux glucocorticoïdes, GR), l’injection de corticostérone dans l’hippocampe ventral conduit également à un processus incorrect de sélection du stimulus prédictif mais en faveur des éléments contextuels. Enfin, un apprentissage en labyrinthe radiaire révèle que l’injection de corticostérone dans l’hippocampe dorsal altère spécifiquement la mémoire relationnelle, analogue de la mémoire déclarative humaine, uniquement chez les animaux ayant été au préalable exposés à un stress.L’ensemble de nos données révèlent qu’un excès de glucocorticoïdes dans l’hippocampe contribue (1) à des déficits de mémoires émotionnelle et relationnelle, (2) à la sélection inadaptée de stimuli non prédictifs d’un événement aversif (3) reposant sur des dysfonctionnements du circuit hippocampo-amygdalien, le tout, correspondant à des altérations mnésiques de type ESPTNormal emotional memory is based on the selection of cues predicting threatening events. However, exposure to extreme threatening situation can compromise the selection of the correct cues. In particular, selection of a salient not necessarily predictive cue, associated with declarative amnesia for peritraumatic contextual cues, characterizes the memory disturbances of posttraumatic stress disorder (PTSD). Accumulating evidence suggest that action of glucocorticoids into the hippocampus could be a potential mechanism for PTSD-related memory disturbances. Hence, we studied the conditions for which glucocorticoids into the hippocampus can alter memory functions in mice.Using Pavlovian fear conditioning, we showed that post-training infusion of glucocorticoids in the dorsal hippocampus, in stressful situation, resulted in (1) selection of a salient non predictive cue instead of contextual cues and in (2) dysfunctions of neural activity of the hippocampal-amygdalar circuit (c-Fos expression). Interestingly, via action on the same receptor subtype (glucocorticoid receptors, GR), infusion of glucocorticoids in the ventral hippocampus also resulted in incorrect selection of predictive cue but in favor of contextual cues. Finally, using radial-maze task, we showed that infusion of glucocorticoids in the dorsal hippocampus specifically impaired relational declarative-like memory, only in mice previously exposed to stress.Altogether, our findings reveal that excess glucocorticoids in the hippocampus contributes to (1) deficits in emotional and relational memories, (2) incorrect selection of predictive cues (3) based to dysfunctions of the hippocampal-amygdalar circuit, all, corresponding to PTSD-related memory disturbances
36
Jian, Ming. "Dopaminergic regulation of immediate-early gene expression in the central nervous system." Thesis, University of Ottawa (Canada), 1995. http://hdl.handle.net/10393/9781.
Full textAbstract:
Alterations in dopaminergic neurotransmission have profound effects on neuronal expression of the putative activity marker, Fos, in both the dorsal and ventral striatum. In the dorsal striatum, D1-like receptor agonists elevates Fos-like immunoreactivity predominantly in neurons projecting to the midbrain (substantia nigra), whereas D2-like receptor antagonist enhances Fos-like immunoreactivity principally in neurons projecting to the pallidum (globus pallidus). Since the nucleus accumbens (largest component of the ventral striatum) also sends projections to the midbrain (ventral tegmental area and substantia nigra) and pallidum (ventral pallidum), the present study utilized retrograde tract tracing techniques to determine if there was a similar segregation of D1-like receptor agonist- and D2-like receptor antagonist-induced $\rm Fos\sb{2{-}16}$-like immunoreactivity in these accumbal projections. Like in the dorsal striatum, D1-like receptor agonists but not D2-like receptor antagonists, increased $\rm Fos\sb{2{-}16}$-like immunoreactivity in accumbal neurons projecting to the midbrain. Also like in the dorsal striatum, D2-like receptor antagonist-induced $\rm Fos\sb{2{-}16}$-like immunoreactivity was located preferentially in accumbal neurons projecting to the pallidum (ventral pallidum). However, unlike in the dorsal striatum where the vast majority of neurons which display D1-like receptor agonist-induced $\rm Fos\sb{2-16}$-like immunoreactivity project to the midbrain, nearly 50% of those neurons in the nucleus accumbens which were $\rm Fos\sb{2{-}16}$ immunoreactive after d-amphetamine or CY 208-243 administration projected to the ventral pallidum. Thus, a similar number of accumbal neurons which expressed D1-like receptor agonist-induced $\rm Fos\sb{2{-}16}$-like immunoreactivity were retrogradely labelled from the midbrain and ventral pallidum. (Abstract shortened by UMI.)
37
Cardiff, James W. "Experienced-induced immediate early gene expression in hippocampus after granule cell loss." Thesis, Lethbridge, Alta. : University of Lethbridge, Dept. of Neuroscience, c2012, 2012. http://hdl.handle.net/10133/3356.
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Adrenalectomy
(ADX)
has
been
shown
to
cause
selective
degeneration
of
granule
cells
in
the
dentate
gyrus
(DG).
This
occurs
due
to
the
reduction
of
corticosterone
(CORT)
and
behavioural
deficits
are
associated
with
the
loss
of
these
neurons.
Dentate
lesions
and
cell
loss
associated
with
ADX
have
been
shown
to
effect
behaviour
in
a
number
of
spatial
tasks.
In
contras,
it
has
been
shown
granule
cell
loss
does
not
affect
the
specificity
of
place
cells
in
CA3
and
CA1.
We
used
the
ADX
model
to
examine
the
role
of
DG
granule
cells
plays
in
representing
space
using
immediate
early
gene
(IEG)
activation
in
the
principal
hippocampal
subfields
after
exploration
of
novel
environments.
Rats
were
allowed
to
free
explore
multiple
novel
environments
and
then
the
mRNA
for
the
IEG
Homer
1a
(H1a)
was
used
as
a
marker
of
neural
activity.
After
degeneration
of
approximately
half
of
the
DG
granule
cells
we
found
a
significant
increase
in
number
of
active
cells
in
the
DG,
CA3
and
CA1
in
ADX
animals.
The
results
indicate
a
reduction
in
granule
cells
causes
a
dramatic
increase
in
the
proportion
of
remaining
DG
granule
cells
in
response
to
exploration.
The
change
in
DG
activation
disrupts
the
representations
in
CA3
and
CA1
and
thereby
affects
behaviour.vii, 60 leaves : ill. (some col.) ; 29 cm
38
Rose, Sally Louisa. "Phosphorylation and acetylation of histone H3 concomitant with immediate early gene induction." Thesis, King's College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251624.
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McKibbon, Valerie Lynn. "Dopaminergic and glutamatergic mechanisms influence immediate-early gene expression in rodent brain." Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283934.
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Bastide, Matthieu. "Approche expérimentale de la physiopathologie des dyskinésies L-Dopa induites dans la maladie de Parkinson : comparaison de la cible classique, le striatum avec l’ensemble du cerveau." Thesis, Bordeaux, 2014. http://www.theses.fr/2014BORD0132/document.
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Le traitement de référence de la maladie de Parkinson (MP) reste l’utilisation du précurseurdirect de la dopamine: la L-3,4-dihydroxyphenylalanine (L-Dopa). Le traitement chroniquedes patients parkinsoniens à la L-Dopa induit, en revanche, systématiquement desmouvements involontaires anormaux que l’on qualifie de dyskinésies induites par la L-Dopa(DIL). L’étude de l’expression des dyskinésies s’est essentiellement focalisée sur lesdysfonctions neuronales engendrées dans les régions motrices des ganglions de la base et apermis de révéler une surexpression significative de gènes de réponse précoce (GRP) tels que: ΔFosB, ARC, Zif268 et FRA2 dans le striatum de rats dyskinétiques traités chroniquement à la L–Dopa. En revanche, plusieurs autres régions dopaminoceptives, probablement affectées par la dopamine exogène nouvellement synthétisée, ont été négligées alors qu’elles pourraient jouer un rôle clé dans l’expression des dyskinésies. Par conséquent, nous avons quantifié l’expression de ΔFosB, ARC, FRA2 et Zif268 dans l’ensemble du cerveau de rats dyskinétiques que nous avons comparée à des rats non-dyskinétiques. Cette approche nous a permis d’identifier 9 structures, localisées en dehors des ganglions de la base, présentant une surexpression d’au moins 3 des GRPs cités ci-dessus. Parmi ces structures, le domaine dorsolatéral du « bed nucleus of the stria terminalis » (dlBST) et l’habenula latérale (LHb) montrent une corrélation significative entre l’expression de ΔFosB et la sévérité des dyskinésies. Nous avons donc fait l’hypothèse que ces 2 structures pouvaient être impliquées dans l’expression des dyskinésies. Par conséquent, pour évaluer le rôle potentiel du dlBST et de la LHb dans les dyskinésies, nous avons inhibé l’activité électrique des neurones exprimant FosB/ΔFosB en utilisant la méthode d’inactivation sélective du Daun02/ß-galactosidase que nous avons précédemment validée dans une structure bien connue pour être impliquée dans les dyskinésies: le striatum. Nous avons démontré que l’inhibition de ces neurones, à la fois dans le dlBST et la LHb, diminuait la sévérité des dyskinésies sans affecter l’effet bénéfique de la L-Dopa chez les rats dyskinétiques. Nous avons ensuite pu confirmer l’implication du dlBST grâce au model de référence des dyskinésies: le macaque dyskinétique lésé au MPTP. L’ensemble de ces résultats nous a ainsi permis de montrer, pour la première fois, l’implication fonctionnelle de 2 structures externes aux ganglions de la base dans l’expression des dyskinésies, offrant de nouvelles perspectives thérapeutiquesThe gold standard treatment for Parkinson’s disease (PD) remains the dopamine precursor L- 3,4-dihydroxyphenylalanine (L-Dopa). Long-term L-Dopa treatment systematically leads to abnormal involuntary movements (AIMs) called L-Dopa-induced dyskinesia (LID). These manifestations first led to investigate the neuronal dysfunctions in the motor regions of thebasal ganglia and unravelled an overexpression of ΔFosB, ARC, Zif268 and FRA2 immediate-early genes (IEG) in the dopamine-depleted striatum of dyskinetic rats. However, other several dopaminoceptive structures, likely affected by the exogenously produced dopamine, have been neglected although they might play a key role in mediating LID. Hence, we assessed the expression of ΔFosB, ARC, FRA2 and Zif268 IEGs in the whole brain of dyskinetic rats compared to non-dyskinetic ones. Such approach shed light notably upon 9 structures located outside of the basal ganglia displaying an IEG overexpression. Among them, the dorsolateral bed nucleus of the stria terminalis (dlBST) and the lateralhabenula (LHb) displayed a significant correlation between ΔFosB expression and LID severity. We therefore postulated that these structures might play a role in LID manifestation. Therefore, to assess dlBST and LHb causal roles upon LID severity, we inhibited the electrical activity of FosB/ΔFosB-expressing neurons using the selective Daun02/β- galactosidase inactivation method that we previously validated in a well known structure involve in LID: the striatum. Interestingly, the inactivation of dlBST and LHb ΔfosBexpressing neurons alleviated LID severity and increased the beneficial effect of L-Dopa in dyskinetic rats. Remarkably, BST involvement in LID was confirmed in the gold standard model of LID, the dyskinetic MPTP-lesioned macaque. Altogether, our results highlight for the first time the functional involvement of 2 structures
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Bonelli-Salvadori, Aurélie. "Sensibilité aux ondes électromagnétiques (4G) du cerveau de rat à différents âges : impact sur la persistance d'un souvenir spatial et sur l'expression des gènes." Thesis, Strasbourg, 2018. http://www.theses.fr/2018STRAJ105.
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Avec l'avènement de la téléphonie et des réseaux mobiles, l'impact des radiofréquences (RF) sur la santé humaine est plus que jamais un sujet d'actualité. Les résultats des recherches Homme et animal restent controversés et ne permettent pas de conclusion définitive sur l’existence ou non d’effets des RF, notamment sur le cerveau. Ainsi, nos résultats montrent que chez le rat, jeune, adulte et âgé, une exposition de 3 mois à un signal LTE 4G (900 MHz, 61V/m, DAS = 0,33 W/kg) n’a aucun effet sur l’apprentissage et la mémoire spatiale récente et ancienne, ni sur l’anxiété ou la locomotion. L’expression des gènes a été étudiée par séquençage haut débit des ARNm, en conditions "Basal" et "Apprentissage" dans l’hippocampe dorsal et le cortex préfrontal médian. Nos résultats montrent que des gènes appartenant à des regroupements fonctionnels spécifiques sont modulés en réponse à l’exposition aux RF dans l'hippocampe dorsal en condition "Basal" et dans le cortex préfrontal médian, pendant et suite à un apprentissage spatial. Cependant, il est important de noter que ces modulations génétiques n'impactent pas le rappel d'un souvenir récent ou ancien. En perspective, il sera important de connaître les possibles répercussions que ces régulations peuvent avoir à plus long terme sur le fonctionnement cérébralThe increasing development of mobile phone technology and networks raises the question of the impact of electromagnetic fields in the radiofrequency range (RF) on human health and well-being. However, data from humans and animal scientific research remain controversial and do not allow to conclude about potential harmful effects of RF, particularly on the brain. Thus, our results showed that, in young, adult and aged rats, a chronic exposure (3 months) to a 4G LTE signal (900 MHz, SAR = 0.33 W/kg, 61V/m) had no impact on spatial learning and long-term memory, nor on anxiety and locomotion. Gene expression was studied using high throughput RNA sequencing in the dorsal hippocampus and medial prefrontal cortex, both in "Basal" and "Learning" conditions. Our results show that some genes belonging to specific functional groups were modulated by RF in the dorsal hippocampus in "Basal" condition and, in the median prefrontal cortex during and after spatial learning. However, it is to note that these gene expression modulations have no impact on recent or remote memory. In perspective, it will be important to explore the potential effects of such changes in brain functioning
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McGahan, Lynda. "Expression of immediate-early gene proteins in the rat hippocampus following transient global ischemia." Thesis, University of Ottawa (Canada), 1996. http://hdl.handle.net/10393/10454.
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The temporospatial expression patterns of the immediate-early gene (IEG) proteins Fos, FosB, $\Delta$FosB, Jun, JunB, JunD, and NGFI-A were investigated in rat hippocampus by immunonohistochemistry 2 h, 12 h, 24 h, and 48 h after forebrain ischemia. Transient global ischemia (20 min), produced by four vessel occlusion (4-VO), elicited different patterns of IEG expression in vulnerable CA1 and more resilient CA3 neurons. Cell counts revealed that initially, ischemia elevated immunoreactivity in both CA1 and CA3 hippocampal subfields for all IEGs examined, with the exception of JunD and NGFI-A. However, distinct patterns of IEG expression became evident in these regions at later time points following recirculation of blood flow. The pivotal difference was the persistence of ischemia-induced elevations of FosB and Jun expression in the CA1 region of the hippocampus. Unlike CA3 neurons where IEG immunoreactivity had subsided to basal levels by 24 h-48 h after reperfusion, CA1 neurons continued to display increased FosB- and Jun-like immunoreactivity 48 h post-ischemia. In contrast to FosB and Jun, JunB expression declined significantly below basal levels in CA1 neurons at 48 h, while JunB-like immunoreactivity remained unaltered in CA3 neurons. Given that JunB has been shown to inhibit the transactivating properties of Jun, decreased JunB levels may contribute to the apoptotic death of CA1 neurons by enhancing the transcriptional regulating activity of Jun. Also notable at 48 h was the complete loss of constitutive NGFI-A expression from CA1 neurons of ischemic animals. In summary, these findings suggest that persistent elevations in FosB and Jun expression coupled with reductions in JunB and NGFI-A levels may play a role in the apoptotic death of CA1 neurons following transient global ischemia. (Abstract shortened by UMI.)
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Huff, Nicole C. "Amygdala modulation of hippocampus-dependent memories and the influence on immediate early gene expression." Diss., Connect to online resource, 2005. http://wwwlib.umi.com/dissertations/fullcit/3178346.
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Dyson, Mark. "Site-specificity and targeting of histone H3 phosphorylation concomitant with immediate-early gene induction." Thesis, University of Oxford, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404116.
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Albasser, Mathieu M. "Use of immediate-early gene expression to map relationships between limbic structures supporting memory." Thesis, Cardiff University, 2009. http://orca.cf.ac.uk/55876/.
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This thesis explores the influence of brain regions within the "extended hippocampal memory system" on the activity of the retrosplenial cortex in the rat. One of the first goals was to use lesion studies to improve the understanding of the vulnerability of the retrosplenial cortex, especially in the context of diencephalic and temporal lobe amnesia. The second was to assess what are the brain areas within the temporal lobe involved in object recognition and how they interact. These two objectives were made possible by visualising immediate-early gene expression. By combining this technique with lesions, distal effects of different lesions (hippocampus, mammillothalamic tract and fornix) on the activity of the retrosplenial cortex were measured. For object recognition, the immediate-early gene imaging enabled the assessment of normal brain activity in rats associated with behavioural discrimination of novelty. The lesion studies provide information about the specific and common vulnerability of the retrosplenial cortex, as all three distal lesions resulted in a decrease of immediate-early gene activity in the retrosplenial cortex. In addition, these findings unify diencephalic amnesia with temporal amnesia, and emphasize the need to study networks or systems instead of individual structure. The immediate-early gene/object recognition experiment implicated the caudal part of the perirhinal cortex (and Te2) and of the hippocampus in object recognition, and highlighted the importance of mapping brain region relationships within a connected system. Taken together, these experiments provide clear support for the concept of an extended hippocampal memory system, but also show how this system may interact with other structures involved in different forms of memory. The findings underlie the potential afforded by use of immediate-early gene expression techniques in animal studies.
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Crump, Nicholas T. "The role of p300/CBP in dynamic acetylation of histone H3K4me3 and immediate-early gene regulation." Thesis, University of Oxford, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.534164.
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Chu, William. "Apoptosis in human CNS neurons, effect on immediate early gene expression and key neuron-specific proteins." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0002/MQ44085.pdf.
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Chu, William 1970. "Apoptosis in human CNS neurons: effect on immediate early gene expression and key neuron-specific proteins." Thesis, McGill University, 1997. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=20228.
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Apoptosis has been proposed as the mechanism of neuronal cell death, while altered levels of amyloid precursor protein (APP) and the amyloid beta peptide, a proteolytic cleavage product of APP, are believed to contribute to the neurodegeneration in AD. Thus, defining the molecular mechanisms regulating these events are of interest. The expression of the immediate early genes (IEG), in particular c-jun, has been shown to be a requirement for neuronal apoptosis. Due to the presence of activator protein-1 (AP-1) consensus sequences in the promoter of the APP gene, which has been shown to be responsive to regulation by immediate early genes, we set out to determine whether expression of the immediate early genes resulted in a correlated increase in the expression of APP during neuronal apoptosis. Apoptosis was induced in highly purified human primary neuron cultures by serum deprivation and characterized by propidium iodide and TUNEL (terminal transferase mediated dUTP nick end labeling) staining to detect condensed chromatin and fragmented nuclei, distinct morphological features of apoptotic cells. Immediate early gene, c-fos and c-jun, expression was assessed at the transcriptional level by RT-PCR and immunoblotting at the protein level. (Abstract shortened by UMI.)
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Haghgoo, Hojjat Allah [Verfasser]. "Immediate early gene expression in the rat accessory olfactory system in social recognition / Hojjat Allah Haghgoo." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2009. http://d-nb.info/1023497263/34.
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Aston, James. "The pharmacology of MDMA and methylphenidate, as revealed by immediate-early gene expression in rat brain." Thesis, De Montfort University, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.413755.
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