Dissertations / Theses on the topic 'C-Fos'
To see the other types of publications on this topic, follow the link: C-Fos.
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 50 dissertations / theses for your research on the topic 'C-Fos.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse dissertations / theses on a wide variety of disciplines and organise your bibliography correctly.
1
Fleser, Angelica. "Resténose et expression des proto-oncogènes, c-myc, c-fos et c-jun." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/NQ35590.pdf.
Full text
2
Ferrari, Ana Luiza. "Expressão dos protooncogenes c-fos, c-myc e c-jun em miométrio e mioma humanos." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2006. http://hdl.handle.net/10183/6629.
Full text
3
Dalgleish, Gillian Denise. "Localisation signals within the c-myc and c-fos 3'untranslated regions." Thesis, University of Aberdeen, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.481826.
Full text
4
Pariat, Magali. "Dégradation des protéines c-fos, c-jun et p53 par les calpai͏̈nes." Montpellier 2, 1997. http://www.theses.fr/1997MON20092.
Full textAbstract:
Les genes des familles fos et jun codent pour des facteurs de transcription instables qui interagissent au sein du complexe transcriptionnel ap-1. La proteine p53 est aussi un facteur de transcription que l'on retrouve inactive par mutation dans 50% des tumeurs. Nous nous sommes interesses au catabolisme de ces proteines dans la mesure ou (i) il constitue un niveau cle de la repression de l'expression de ces genes, (ii) il est affecte dans le cas des formes virales mutees des proteines fos et jun vehiculees par des retrovirus oncogenes, (iii) la proteine p53 est stabilisee dans de nombreuses tumeurs. Nous avons mis en evidence une des voies proteolytiques agissant sur ces proteines : les calpaines, qui sont des cysteines proteases cytoplasmiques. Nous avons pu montrer que les differents membres des familles fos et jun etaient differentiellement sensibles aux calpaines. Par ailleurs, nous avons pu montrer que v-fosfbr, une des formes virales de c-fos etait resistant aux calpaines. Au cours de la caracterisation des motifs peptidiques impliques dans la reconnaissance de c-fos et c-jun par les calpaines, nous avons montre que les sequences pest n'etaient ni necessaires, ni suffisantes a la proteolyse par les calpaines, mais que les motifs impliques recouvraient plusieurs dizaines d'acides amines. L'etude de la degradation de p53 par les calpaines nous a permis de montrer que cette proteine est un substrat tres sensible de ces proteases in vitro et que cette sensibilite est conferee par des determinants d'ordre tertiaire. Certaines formes mutantes de p53 retrouvees dans des tumeurs se sont trouvees etre resistantes aux calpaines. Enfin, un certain nombre d'arguments experimentaux suggerent que les calpaines pourraient participer a la degradation de p53 in vivo.
5
Brown, Helen Jane. "Regulation of HOB1 activation domains in c-Fos." Thesis, University of Cambridge, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.390267.
Full text
6
Sariban, Eric. "Régulation des proto-oncogènes c-fms, c-fos et c-sis lors de la différenciation monocytaire." Doctoral thesis, Universite Libre de Bruxelles, 1988. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/213396.
Full text
7
Wilson, Timothy Craig. "The role of mRNA stability and Fos protein in transient c-fos mRNA accumulation." Thesis, University of Cambridge, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.304567.
Full text
8
MATSUI, NOBUO, HIROSHI TAKAGI, HIROOMI FUNAHASHI, YASUYUKI SATOH, NORIHIRO MIYAMOTO, YOSHIHARU MURATA, TSUNEO IMAI, HISAO SEO, and MOTOTSUGU OHNO. "ACTH Increases Expression of c-fos, c-jun and β-actin Genes in the Dexamethasone-treated Rat Adrenals." Thesis, The Japan Endocrine Society, 1992. http://hdl.handle.net/2237/16720.
Full text
9
Soster, Paula Rigon da Luz. "Imunorreatividade à proteína C-FOS após estimulação periférica nociva e tratamento com morfina no sistema nervoso central do caracol terrestre Megalobulimus abbreviatus." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2005. http://hdl.handle.net/10183/4935.
Full textAbstract:
Utilizando as técnicas de imunoistoquímica e densitometria óptica, foi investigada a localização e a expressão da proteína c-Fos no SNC do caracol Megalobulimus abbreviatus. Neurônios imunorreativos foram encontrados nos gânglios cerebrais, pedais, parietal direito e visceral de caracóis submetidos ao estímulo térmico aversivo (50oC), e sacrificados em diferentes tempos (3, 6, 12, 18 e 24 h) após a estimulação. A análise da imunorreatividade à c-Fos através do método de medida da densidade óptica (DO) revelou uma diferença significativa no sentido de apresentar uma maior expressão (p<0,05) na área do lobo pedal do pós-cérebro do gânglio cerebral em relação às outras regiões analisadas no mesmo gânglio (mesocérebro, pró-cérebro e lobo pleural do pós-cérebro). Além disso, também houve expressão significativamente maior (p<0,05) quando comparada a densitometria da região do mesocérebro em relação ao lobo pleural do pós-cérebro nos grupos controle, 3h e 18h. O lobo pleural do pós-cérebro apresentou uma expressão significativamente menor (p<0,05) na imunorreatividade da proteína c-Fos quando comparado ao pró-cérebro em animais sacrificados 12h e 24h após e estímulo aversivo. Em relação ao grupo controle, a DO da proteína c-Fos não variou nos diferentes tempos de sacrifício quando comparada a mesma região do gânglio (cerebral, pedal, parietal direito ou visceral) ao longo do tempo na maioria das regiões. A única diferença estatisticamente significativa (p<0,05) foi encontrada no mesocérebro do gânglio de animais sacrificados 12 h após o estímulo térmico aversivo, mostrando uma diminuição da imunorreatividade. Nos animais tratados com salina (1ml) ou morfina (20mg/kg) 15 min antes do estímulo térmico aversivo, os mesmos grupos neuronais nos gânglios do SNC de M. abbreviatus mostraram imunomarcação à proteína c-Fos. Em relação ao grupo controle, observou-se uma expressão significativamente menor (p<0,01) na DO da imunorreatividade da proteína c-Fos nos neurônios anteriores do gânglio pedal nos animais sacrificados 3 h e 6 h após o estímulo térmico aversivo. No momento em que a comparação foi feita entre os grupos salina e morfina de animais sacrificados ao mesmo tempo, na grande maioria dos grupos observou-se uma diminuição na imunorreatividade da proteína c-Fos. Esta diferença, porém, mostrou-se significativa (p<0,01) no mesocérebro de animais do grupo 3h, no lobo pedal do pós cérebro de animais dos grupos 3 h, 6 h e 18 h, nos neurônios anteriores do gânglio pedal nos grupos 6 h e 12 h, nos neurônios mediais do gânglio pedal do grupo 3 h, nos neurônios posteriores do gânglio pedal do grupo 6 h, nos neurônios da região anterior do gânglio parietal direito no grupo 12 h e nos neurônios do gânglio visceral no grupo experimental 12 h. A diferença na DO da proteína c-Fos apresentou uma diminuição extremamente significativa (p<0,001) nos neurônios mediais do gânglio pedal de animais sacrificados 12 h após o estímulo térmico aversivo, nos neurônios posteriores do gânglio pedal dos animais sacrificados 12 h após o estímulo e nos neurônios do gânglio visceral dos animais do grupo experimental 6 h. A partir destes dados e da correlação com estudos realizados em M. abbreviatus para detecção de mediadores químicos envolvidos na nocicepção, podemos concluir que as áreas imunorreativas que apresentaram estas variações na densidade óptica da imunorreatividade à proteína c-Fos em diferentes tempos de sacrifício e tratamento com morfina estão envolvidas no processo nociceptivo neste caracol.
10
TEYSSIER, MAGALI. "Expression des oncogenes c-fos et c-myc et immunomodulation de la lignee monocytaire." Paris 11, 1992. http://www.theses.fr/1992PA112239.
Full textAbstract:
The p388d1 murine macrophage cell line has been chosen to study events resulting from the transduction of immunomodulatory signals. Owing to the frequent implication of the c-myc gene in the tumorigenicity of hematopoietic cells, the normal c-myc status in this cell line is demonstrated by southern analysis. The early modulation of the c-fos and c-myc proto-oncogene expression has been studied by northern analysis and the dna synthesis by #3h-thymidine incorporation after treatment of p388d1 cells by tpa, calcium ionophore a23187, mdp and csf-1. No correlation could be evidenced in this cell line between the mitogenic effect and the c-fos and c-myc modulation induced by these immunomodifiers. The impact of lps, tpa and dibutyryl-cyclic amp on mhc class ii antigen (ia) has been revealed by radio-immuno-assay. These compounds inhibited constitutive or induced by interferon-gamma ia expression. This inhibition seemed to be in relation with c-fos expression. The ia expression was therefore analysed either after c-fos translation blockage by a dna antisense either after overexpression of c-fos by transfection of p388d1 cells with a plasmid containing the c-fos gene. The first results seemed to confirm an inverse correlation between the c-fos induction and the inhibition of ia expression
11
Salvat, Catherine. "Etude des mécanismes de la dégradation des proto-oncoprotéines c-Fos et c-Jun." Montpellier 2, 1998. http://www.theses.fr/1998MON20219.
Full textAbstract:
Les proto-oncogenes c-fos et c-jun definissent des familles multigeniques de facteurs de transcription impliques dans la regulation de la proliferation, de la differenciation cellulaire et de l'apoptose. Les proteines c-fos et c-jun sont metaboliquement instables. Des travaux in vitro et in vivo par differents groupes suggerent que plusieurs machineries proteolytiques, comprenant le proteasome, les calpaines ubiquitaires et les lysosomes, pourraient participer a leur degradation in vivo. Bien que le proteasome semble etre le systeme predominant, la contribution relative de chacune de ces machineries n'est pas connue et pourrait etre fonction du contexte cellulaire, de la localisation intracellulaire des proteines et/ou des conditions physiologiques. Au cours de ce travail, nous avons montre que : (i) c-fos et c-jun peuvent etre degradees par le proteasome in vitro en absence d'ubiquitination prealable et sans cofacteur autre que l'atp, (ii) c-fos et c-jun sont degradees par le proteasome in vivo lors de la transition g#0-s, (iii) durant la transition g#0-s, la degradation de c-jun, en accord avec des observations d'autres groupes, est dependante de la voie de l'ubiquitine. Nos resultats in vitro et in vivo soulevent la possibilite qu'il pourrait exister une degradation basale de c-jun independante de la voie de l'ubiquitine, acceleree apres ubiquitination comme cela a ete rapporte pour ikb, (iv) au contraire, la degradation de c-fos est apparemment independante de la voie de l'ubiquitine dans la lignee cellulaire que nous avons utilisee. Cela indique que au moins partiellement, lors de la transition g0-s, les mecanismes de ciblage de c-fos et c-jun au proteasome sont differents, (v) la degradation de c-fos est controlee par les cascades de signalisation intracellulaire impliquant les mapkinases. En parallele de ces observations, nous avons caracterise au niveau moleculaire, une lignee cellulaire thermosensible pour l'enzyme e1 de la voie de l'ubiquitine. De facon interessante nous avons observe que e1 est differentiellement limitante pour l'ubiquitination de differents substrats.
12
Williams, Timothy Simon Carl. "C-fos induction in spinal neurons by sensory stimulation." Thesis, University of Cambridge, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.239263.
Full text
13
Trouche, Didier. "Régulation transcriptionnelle du gène c-fos et différenciation cellulaire." Châtenay-Malabry, Ecole centrale de Paris, 1993. http://www.theses.fr/1993ECAP0306.
Full textAbstract:
Le gène c-Fos est le prototype des gènes formant la réponse nucléaire précoce de la cellule, lors de l'entrée en cycle prolifératif. La protéine c-Fos possède des propriétés transformantes, et son expression est contrôlée de manière extrêmement stricte au cours du cycle cellulaire. Les études sur les mécanismes responsables de ce contrôle ont été principalement menées dans des systèmes cellulaires modèles, en particulier dans les fibroblastes 3T3. Elles mettent en évidence le rôle primordial joué par le SRE (Serum Response Element) dans le contrôle de la transcription. Nos résultats permettent d'établir que, dans des modèles cellulaires issus du système hématopoïétique, la transcription du gène Fos est régulée d'une manière tout à fait similaire : le processus de la différenciation, non terminale, n'affecte pas directement les mécanismes régissant la transcription du gène c-Fos. La différenciation terminale s'accompagne souvent d'un arrêt de la prolifération cellulaire, et simultanément, on observe une diminution de l'activité du promoteur c-Fos. L'étude d'un système bien connu de différenciation terminale, la différenciation myoblastique, nous a permis de montrer que la protéine MyoD, élément-clé du processus, est capable de réprimer la transcription du gène c-Fos.
14
Stabile, Angelo Clodomiro. "Efeito do acetaminofeno e do celecoxib na distalização de incisivos e na ativação de regiões cerebrais relacionadas à nocicepção durante a movimentação ortodôntica em ratos." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/58/58137/tde-29102008-173257/.
Full textAbstract:
Antiinflamatórios podem diminuir a movimentação dentária (MD) em pacientes ortodônticos, fato este que leva à existência de poucas alternativas terapêuticas para o tratamento da dor. Acetaminofeno tem sido a medicação de escolha, mas não é tolerado por alguns pacientes. Este trabalho pesquisou a influência do celecoxib e do acetaminofeno na separação ortodôntica dos incisivos centrais superiores de ratos, assim como na ativação de estruturas relacionadas à nocicepção no núcleo espinhal do trigêmio, por meio da expressão de c-fos nos subnúcleos caudalis, interpolaris e oralis. Num primeiro momento, o peso do animal e a força ortodôntica foram variados, quando foi possível encontrar o relacionamento ideal entre estas duas variáveis, o qual permitiu movimentação dentária sem expansão da sutura palatina mediana. A aplicação de 35 g de força em animais de 400 g de peso distalizou os incisivos sem expandir a sutura palatina mediana, como pôde ser verificado em radiografias da maxila dos animais. Sendo assim, trinta ratos Wistar, machos, pesando cerca de 400 g, foram pré-tratados através de sonda gástrica (1 ml) com acetaminofeno (80mg/ml), celecoxib (20mg/ml) ou veículo (carboximetilcelulose 0,4%). Após 30 minutos, foram submetidos à movimentação dentária (35 g de força) ou deixados como controles. Ração moída foi fornecida e a cada 12 horas eles receberam, na mesma dosagem anterior, um dos medicamentos ou veículo. Depois de 48 horas, foram novamente anestesiados, fotografados e perfundidos com paraformaldeído 4%. Na seqüência, a maxilla foi radiografada e os cérebros removidos e processados para a imunohistoquímica para c-fos. A movimentação dentária induziu a distalização dos incisivos (p< 0.05), mas a distância inter-incisal não foi modificada pelos medicamentos. Adicionalmente, a movimentação dentária e o tratamento com as drogas não causaram qualquer alteração no número de neurônios Fos positivos nos subnúcleos interpolaris e oralis. No subnúcleo caudalis, entretanto, as duas drogas reduziram o número de neurônios Fos positivos devidos ao estímulo ortodôntico (p<0,05). Concluímos que os dois medicamentos reduzem a ativação neuronal de região nociceptiva e não afetam a movimentação dentária, sendo que o celecoxib seria uma possível alternativa ao acetaminofeno para o alívio de dor em pacientes ortodônticos, nos casos em que este for contra indicado.Anti-inflammatory drugs may slow dental movement in orthodontic patients, which leads to low therapeutic alternatives for pain control. Acetaminophen has been the first choice medication for the majority of patients, but it is not well tolerate for some. This work evaluated the influence of celecoxib and acetaminophen in the orthodontic separation of superior central incisor of rats, such as in the activation of nociceptive related structures in the spinal trigeminal nucleus, using c-fos expression in caudalis, interpolaris, and oralis sub nuclei. In a first moment, animal weigh and orthodontic force were varied, when it was possible to find the ideal relationship between these two variables, resulting in dental movement without median palate suture expansion. The application of 35 g of orthodontic force in animals weighing 400 g has been establish as the ideal experimental model, and this way, 30 male Wistar rats were pre-treated, by oral gavage (1 ml), with acetaminophen (80 mg/ml), celecoxib (20 mg/ml), or vehicle (carboxymethylcellulose 0,4%), and 30 minutes later, they were submitted or not to orthodontic stimulus. Animals received ground food, and one of the drugs or vehicle, every 12 hours. After 48 hours from the dental manipulation, they were anesthetized, photographed, and perfused with 4% paraformaldehyde. In the sequence, maxila was radiographed and brains were removed and processed for FOS immunocytochemistry. Dental movement induced incisor distalization (p<0,05), but interincisal gap was not modified by the drugs. Furthermore, no changes were found in FOS positive neurons in oralis and interpolaris subnuclei, following tooth movement, independently of whether medications were given or not. In caudalis subnucleus, however, both analgesics reduced the number of tooth movement induced FOS positive neurons. We conclude that neither celecoxib nor acetaminophen seems to affect tooth movement, but both may reduce pain caused by orthodontic appliance. Celecoxib, thus, may be a therapeutic alternative to acetaminophen when the latter was counter indicated.
15
Veyrune, Jean-Luc. "Devenir des ARNm c-fos et c-myc dans le cytoplasme : dégradation, traduction et localisation." Montpellier 2, 1996. http://www.theses.fr/1996MON20218.
Full textAbstract:
Les messagers des proto-oncogenes c-fos et c-myc font partie des arnm eucaryotes les plus instables. Cette instabilite a ete reliee a differentes sequences localisees soit dans la partie 3' non codante comprenant une region riche en au, soit dans les parties codantes du messager. Il a ete montre que la partie 3' non codante de ces messagers confere une tres mauvaise efficacite de traduction. De plus nous savons que l'utilisation de drogues bloquant la synthese des proteines (puromycine, cycloheximide) entraine le phenomene de super induction du a une stabilisation des messagers. Ces donnees experimentales suggeraient fortement un lien entre degradation et traduction. A l'aide du systeme ire/irp inspire de la regulation traductionnelle de l'arnm de la ferritine, nous avons montre l'existence d'une relation entre degradation et traduction de l'arnm de c-fos. La degradation du messager c-fos, qu'elle soit relayee par les elements d'instabilite de la region traduite ou 3' non traduite, semble etre dependante de sa traduction. En parallele, nous avons aborde l'etude de la localisation sub-cellulaire de l'arnm de c-myc. Deux techniques ont ete utilisees aux cours de ces travaux: l'hybridation in situ et le fractionnement biochimique des polysomes en fonction de leur association a des structures subcellulaires. Cela nous a permis de mettre en evidence une region de 85 nucleotides, incluse dans la region 3' non traduite du messager c-myc, necessaire et suffisante a la localisation perinucleaire du messager et a sa presence dans les polysomes lies au cytosquelette. Des mutations ponctuelles dans cette region ont revele l'importance de l'integrite du pentamere auuua pour une localisation canonique du messager
16
Yates, Samantha. "Differential induction of c-fos in wounded fetal rat skin /." Title page and abstract only, 1997. http://web4.library.adelaide.edu.au/theses/09SB/09sby34.pdf.
Full text
17
Zhao, Yuming. "Phenotypic analysis of osteoclast lineage in c-fos mutant mice." Thesis, King's College London (University of London), 2003. https://kclpure.kcl.ac.uk/portal/en/theses/phenotypic-analysis-of-osteoclast-lineage-in-cfos-mutant-mice(fafcec7f-6480-4f8c-87b6-3cca60a475fb).html.
Full text
18
Gentry, Aleksandra. "Growth control of chondrocytes by the c-fos proto-oncogene." Thesis, King's College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.399494.
Full text
19
Basset-Seguin, Nicole. "Role du proto-oncogene c-fos dans la physiopathologie cutanee." Montpellier 1, 1993. http://www.theses.fr/1993MON1T016.
Full text
20
Mirahmadi, Ramine. "Surexpression de c-fos dans la lignee murine monocytaire p388d1." Paris 5, 1996. http://www.theses.fr/1996PA05S018.
Full textAbstract:
La lignee monocytaire murine p388d1 presentant les caracteristiques de macrophages matures a ete choisie comme modele de l'etude d'evenements resultant d'une surexpression du proto-oncogene c-fos. La proteine fos est (avec jun) un composant du facteur de transcription ap-1 qui intervient dans la regulation de nombreux genes. L'analyse, dans le laboratoire, de l'expression des antigenes du cmh de classe ii induite par l'interferon (ifn) gamma en presence du dibutyryl ampcyclique montrait un paralele entre l'effet inhibiteur de cet agent sur cette induction et sa capacite a stimuler la transcription de c-fos. L'hypothese d'un role de c-fos dans l'expression du chm ii nous a conduit a transfecter de maniere permanente les cellules de la lignee par un plasmide contenant le gene c-fos murin sous controle du promoteur metallothioneine humain iia. Plusieurs clones ont ete selectionnes par la resistance a la geneticine. L'analyse par southern blot a permis d'evaluer les niveaux d'integration. Trois clones ont ete retenus en vue d'analyser l'expression de c-fos en presence ou en absence de l'inducteur (cl#2cd 5x10#-#6 m pendant 6 heures). La surexpression de fos s'accompagne d'un effet negatif sur l'entree en phase s et entraine une augmentation correlative de l'antigene i-a#d a la surface des cellules en presence d'ifn gamma. La presentation d'un peptide dans le contexte i-e#d a ete determinee par l'evaluation de l'il-2 secrete par l'hybridome t approprie. Apres l'induction par l'ifn gamma et aux basses concentrations du peptide, une diminution de la presentation est observee pour les clones surexprimant fos, sans correlation directe entre le niveau de fos et l'inhibition.
21
McQUADE, JILL MARIE SLANE. "THE INVOLVEMENT OF DFF45 AND c- fos IN HIPPOCAMPAL PLASTICITY AND FUNCTION." University of Cincinnati / OhioLINK, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1036088357.
Full text
22
Sato, Vinicius Antonio Hiroaki. "Substratos neurais envolvidos com o desenvolvimento do comportamento de desamparo em ratos: possível envolvimento do NO." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/17/17133/tde-20072016-091556/.
Full textAbstract:
Recentemente, o óxido nítrico (NO) tem sido relacionado com a depressão. A administração de inibidores da NO sintase (NOS) induz efeitos do tipo antidepressivo em modelos animais e há um aumento da expressão da NOS em estruturas do sistema límbico em indivíduos depressivos e em animais expostos a estresse. Além disso, sabe-se que o estresse causa um aumento da ativação de neurônios localizados em estruturas do sistema límbico e que o tratamento com antidepressivos bem como com inibidor da NOS, diminui essa marcação. Contudo, ainda não se sabe como o sistema nitrérgico dessas estruturas está relacionado com os comportamentos relacionados à depressão. Assim nosso objetivo é testar a hipótese de que o desenvolvimento do desamparo (comportamento relacionado à depressão) em ratos seria causado por um aumento de atividade de neurônios que contém nNOS em estruturas envolvidas com a resposta emocional ao estresse, e que os diferentes tratamentos induzem efeitos do tipo antidepressivo no modelo apresentando através de um efeito final comum de diminuir essa ativação e, portanto, diminuir os níveis de NO. Para isso, ratos foram submetidos ao modelo do desamparo aprendido e tratados com drogas antidepressivas. Após o teste, foi feita a imunohistoquímica com marcação para Fos (Fos-IR; marcador de atividade neuronal) e nNOS (nNOS-IR). O tratamento repetido com desipramina (DES, na dose de 25, mas não na de 12,5 mg/Kg), fluoxetina (FXT, na dose de 15, mas não na de 30 mg/Kg) e imipramina (IMI, 15mg/Kg) induziu efeito do tipo-antidepressivo no teste do desamparo aprendido (LH). O tratamento agudo apenas com imipramina, mas não com FXT ou IMI, induziu o mesmo tipo de efeito. O tratamento com DES, FXT ou IMI também aumentou o número de cruzamentos entre choques no LH, porém não induziu aumento de atividade locomotora no teste do campo aberto. O tratamento repetido com DES diminuiu a Fos-IR na amígdala basolateral (BlAm), amígdala lateral (LAm), córtex pré-frontal medial (mPFC), região CA1 e CA3 do hipocampo dorsal (dHPC) e região CA3 do hipocampo ventral (vHPC). O tratamento agudo com DES induziu um aumento de Fos-IR na amígdala central (CeAm), amígdala medial (MeAm) e CA1 e CA3 do dHPC. O tratamento repetido com FXT diminuiu Fos-IR na BlAm e LAm, enquanto o tratamento agudo aumentou Fos-IR na CeAm. O tratamento repetido com IMI aumentou nNOS-IR na MeAm e a dupla marcação no núcleo leito da estria terminal (BST); e diminuiu o Fos-IR na região CA1 do dHPC e na região parvocelular do núcleo paraventricular do hipotálamo (pPVN). Por fim, foram encontradas relações positivas entre o número de células Fos-IR e o número de falhas em fugir ou escapar dos choques no LH na BlAm, LAm, CA1 e CA3 do dHPC e CA3 do vHPC; i.e., quanto mais células ativadas nessas estruturas, maior o número de choques que os animais receberam sem consegui fugir. Os resultados aqui apresentados são, em parte, corroborados pela literatura, mostrando a participação das estruturas analisadas no comportamento do desamparo aprendido e no efeito das drogas antidepressivas. Nesse contexto, acredita-se que o BST funcionaria como um núcleo de processamento da informação vinda do mPFC, HPC e amígdala, enviando projeções para o PVN e regulando o funcionamento do eixo HPA. O trabalho abre caminho para a identificação de subpopulações específicas de neurônios que expressam a nNOS, buscando compreender o papel destas na modulação das respostas comportamentais numa situação de estresse, na busca pela formulação de um cenário cada vez mais completo da participação do sistema nitrérgico dentro do complexo neurocircuito que regula as emoçõesRecently, nitric oxide (NO) has been related with the neurobiology of depression. The NO synthase (NOS) inhibition induces antidepressant-like effects in animal models and there is an increase in the NOS expression in limbic structures of depressed patients or in stress exposed animals. Besides, it is well known that stressful events causes an increase in limbic structures neuronal activation and that antidepressant treatment as well as NOS inhibition attenuates this effect. However, it is still unknown how the limbic nitrergic system is related with depression-related behaviors. Then, the aim of this work is to test the hypothesis that the helplessness behavior development (a depression-related behavior) in rats would be induced by an increased activity of nNOS-containing neurons in structures related with the neurobiology of stress responses. Furthermore, the antidepressant-like effect induced by antidepressants treatment in this model would share a final effect, decreasing the activation of such neurons, and decreasing the levels of NO in these structures. For this aim, male rats were submitted to the learned helplessness model and treated with antidepressants. After the test, immunohistochemistry assay were performed, with double labeling for c-Fos (Fos-IR; neuronal activity marker) and nNOS (nNOS-IR). The repeated treatment with desipramine (DES, 25 mg/kg but not 12,5mg/kg), fluoxetine (FXT, 15 mg/Kg, but not 30 mg/Kg) and imipramina (IMI, 15 mg/KG) induced antidepressant-like effects in the learned helplessness test (LH). The acute treatment with IMI, but not with DES or FXT, induced the same effect. The repeated treatment with DES, FXT or IMI also increased the number of intertrial crossings in the LH, but not the locomotor activity score on the open field score. The repeated treatment with DES decreased the number of Fos-IR into the basolateral amygdala (BlAm), lateral amygdala (Lam), medial prefrontal cortex (mPFC), CA1 and CA3 regions of the dorsal hippocampus (dHPC), and CA3 region of the ventral hippocampus (vHPC). The acute treatment with DES increased the Fos-IR into the central amygdale (CeAm), medial amygdala (MeAm), and CA1 and CA3 regions of the dHPC. The repeated treatment with FXT decreases the number of Fos-IR into the BlAm and Lam, while the acute treatment increases the Fos-IR into the CeAm. The repeated treatment with IMI increased the nNOS-IR into the MeAm and the double- labeled cells into the bed nucleus of stria terminalis (BST); and decreased the Fos-IR into the CA1 region of the dHPC and into the parvocellular region of the paraventricular nucleus of the hypothalamus. Finally, positive correlations between the number of Fos-IR and the number of failures in escaping or avoiding the foot shocks on the LH were found into the BlAm, Lam, CA1 and CA3 of the dHPC, and CA3 of the vHPC, i.e., with more activated cells into these structures mentioned, more foot shocks the rats received. These results are (partially) corroborated with previous scientific papers, showing the analyzed structures participation in the learned helplessness behavior as well as in the antidepressant effect of antidepressant administration. Within this context, the BST would work as a relay center, processing the information coming from the mPFC, HPC and amygdaloid nuclei, and sending the output to the PVN, modulating the HPA axis. This work open some questions about the identification of specific nNOS-containing neuronal subpopulations, aiming to clarify their role in the stress response, and searching for the formulation of a more complete scenario of the nitrergic system participation in this complex emotion-regulating neurocircuit
23
Rossato, Daniele. "Imunorreatividade à proteína c-FOS na medula espinal lombossacral e no gânglio da raiz dorsal de râs Rana catesbeiana 3 dias após a secção nervosa periférica." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2006. http://hdl.handle.net/10183/7688.
Full textAbstract:
A dor constitui uma experiência complexa, mediada por distintos sistemas de transmissão sendo integrados por diversos mecanismos neurais. Um dos modelos mais empregados para o estudo da dor neuropática é a secção nervosa periférica, a qual resulta em alterações neuroquímicas e neuroanatômicas em neurônios sensoriais primários e em seus territórios de projeção. Após a secção do nervo ciático, os mamíferos apresentam um aumento na expressão de genes precocemente expressos, como o c-Fos e o c-Jun, no corno dorsal da medula espinal. Animais não mamíferos, como os anfíbios, também vem sendo utilizados como modelos para os estudos dos mecanismos acerca da nocicepção. No presente estudo foi analisado o padrão de imunorreatividade à proteína c-Fos na medula espinal lombossacral e no gânglio da raiz dorsal (GRD) de rãs Rana catesbeiana em condições basais, bem como de rãs submetidas à manipulação e à secção do nervo ciático. Para isso foram utilizados animais adultos, de ambos os sexos, sendo que os mesmos foram sacrificados 3 dias após o procedimento cirúrgico. A técnica imunoistoquímica utilizada foi a do anticorpo não marcado de Sternberger (1979), sendo utilizado anticorpo primário do tipo policlonal, na concentração de 1:700. As alterações no padrão de imunorreatividade a esta proteína no GRD dos três grupos experimentais foram quantificadas através das técnicas de densitometria óptica e contagem neuronal. Para a quantificação da proteína c-Fos na medula espinal lombossacral dos 3 grupos experimentais, utilizou-se a técnica de western blot. Em GRD, a imunorreatividade foi mais pronunciada no citoplasma de neurônios de pequeno (10-20μm), médio (25-35μm), e grande 40-50μm) diâmetro dos 3 grupos experimentais. A manipulação e a secção do nervo ciático provocou aumento no número de núcleos imunorreativos de células de pequeno diâmetro. A densitometria óptica foi significativamente maior no citoplasma das células dos GRDs localizados ipsilateralmente quando comparada com aquela das células pertencentes aos GRDs localizados contralateralmente à lesão. Todavia, não houve diferenças estatisticamente significativa entre a imunorreatividade nuclear nos GRDs entre os 3 grupos experimentais. O número de células imunorreativas nestes gânglios não mostrou mudanças significativas nos 3 grupos experimentais. Na medula espinal, a imunorreatividade à proteína c-Fos ocorreu predominantemente em núcleos localizados nos campos terminais dorsal e ventral, na banda mediolateral, na região ventral medial do corno ventral e nos funículos lateral e ventral medial. Os neurônios motores sempre foram imunorreativos. A manipulação e a secção do nervo ciático resultaram em um acréscimo no número de núcleos imunorreativos localizados nos campos terminais dorsal e ventral, e banda mediolateral, sendo este aumento maior na região do campo terminal dorsal. As demais regiões não mostraram modificações significantes no padrão de imunorreatividade da proteína c-Fos. A expressão desta proteína não modificou significativamente nos 3 grupos experimentais. Estes resultados mostram que, em rãs, similar ao que ocorre em mamíferos, a ativação de fibras aferentes primárias ativam a proteína c-Fos. No entanto, diferente de mamíferos, esta proteína ocorre no citoplasma de células sensoriais. Assim, apesar das rãs constituírem excelentes modelos para o estudo do papel do c-Fos nos mecanismos da transmissão nociceptiva, os estudos futuros abordando esta questão deverão considerar esta particularidade das rãs.
24
Coulon, Vincent. "Régulation intragénique de la transcription de c-fos : blocage de l'élongation et promoteur alterne." Phd thesis, Université Montpellier II - Sciences et Techniques du Languedoc, 2001. http://tel.archives-ouvertes.fr/tel-00007905.
Full textAbstract:
c-fos est un proto-oncogène et un gène de réponse précoce. Son activation transcriptionnelle est très rapide et transitoire, ce qui suggère un contrôle très strict.Au cours de ma thèse, nous avons abordé deux aspects de la régulation transcriptionnelle de c-fos par des séquences intragéniques. Le premier consiste en un blocage de l'allongement des transcrits dans le premier intron, dont nous avons montré qu'il intervient dans les fibroblastes Ltk-, comme cela avait été découvert dans les macrophages. Ce blocage est levé par l'augmentation de la concentration en calcium intracellulaire, et nous avons montré que ce phénomène est indépendant des CaM-Kinases et de la calcineurine, mais implique la calmoduline dans une nouvelle voie de signalisation.
Dans la seconde partie de mon travail de thèse, nous avons identifié, en aval de la région décrite ci-dessus, une nouvelle séquence intronique très fortement conservée qui possède les caractéristiques d'un promoteur. Nous avons montré que ce promoteur est fonctionnel en transfection transitoire, ce qui nous a encouragé à recourir aux souris transgéniques pour explorer ses territoires d'expression au cours du développement. Nos résultats préliminaires montrent que cette expression semble être limitée au système nerveux et aux glandes mammaires en développement.
Nous avons donc étudié deux régions régulatrices de la transcription de c-fos qui sont proches dans le gène, ce qui suggère un dialogue entre ces différentes fonctions.
25
Gill, Margaret J. "Effects of differential rearing on amphetamine-induced c-fos expression in rats." Thesis, Manhattan, Kan. : Kansas State University, 2008. http://hdl.handle.net/2097/987.
Full text
26
Zhang, Li Ping. "Investigations of C-FOS expression in rat spinal cord in vitro." Thesis, University of Southampton, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.242708.
Full text
27
Stokes, Christabel E. L. "Visualising functionally specific neurones in living brain using c-fos expression." Thesis, University of Bristol, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.289552.
Full text
28
Demoly, Pascal. "Expression du proto-oncogene c-fos dans l'epithelium bronchique de l'asthmatique." Montpellier 1, 1992. http://www.theses.fr/1992MON11169.
Full text
29
Salomon, Nina Schirin [Verfasser]. "Quantifizierung der c-fos Expression im Retinalen Pigmentepithel / Nina Schirin Salomon." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2009. http://d-nb.info/1023783053/34.
Full text
30
Goode, Nigel Thomas. "Protein Kinase "C" activity and c-fos expression in cellular proliferation control of a murine macrophage tumour." Thesis, Royal Veterinary College (University of London), 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.522534.
Full text
31
Tiniakos, Konstantina G. "Production, characterisation and clinical application of monoclonal antibodies to the human c-jun and c-fos oncoproteins." Thesis, University of Newcastle Upon Tyne, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.246089.
Full text
32
Appl, Thomas. "Neurochemical and functional characterisation of the melanin concentrating hormone system in the rat brain." Phd thesis, [S.l.] : [s.n.], 2007. http://opus.kobv.de/ubp/volltexte/2007/1460.
Full text
33
Clément, Olivier. "L'hypothalamus latéral contiendrait le générateur principal du sommeil paradoxal : arguments neuroanatomiques et pharmacologiques chez le rat." Phd thesis, Université Claude Bernard - Lyon I, 2011. http://tel.archives-ouvertes.fr/tel-00739636.
Full textAbstract:
Les mécanismes neurologiques responsables du déclenchement et de l'homéostasie du sommeil, et du sommeil paradoxal (SP) en particulier, sont l'objet d'un nombre toujours plus important d'études du fait notamment de l'attention croissante portée aux pathologies associées. Les travaux rapportés dans cette thèse s'inscrivent parfaitement dans cette dynamique puisqu'ils ont pour objectif de mieux caractériser les populations neuronales mises en jeu dans la régulation du SP ainsi que leurs interactions. Dans cette optique, nous avons combiné différentes approches techniques complémentaires à savoir : neuroanatomie fonctionnelle, polysomnographie et pharmacologie sur animal libre de se mouvoir. Nous avons ainsi pu démontrer pour la première fois la nature glutamatergique des neurones du SLD, région pontique jouant un rôle central dans la mise en place du SP. De plus, s'il est généralement admis que ces neurones du SLD sont sous le contrôle de neurones GABAergiques situés au niveau de la partie ventrolatérale de la substance grise périaqueducale (VLPAG), le contrôle de ces derniers est encore soumis à controverse. Les résultats que nous avons obtenus suggèrent fortement que l'aire latérale de l'hypothalamus (LH) serait responsable de ce contrôle et donc de celui du SP. En effet, la LH est l'afférence majeure à la VLPAG activée lors d'une hypersomnie de SP. En outre, son inactivation par application locale de muscimol entraine la disparition totale du SP et l'activation des neurones GABAergiques de la VLPAG projetant sur le SLD. En parallèle, nous avons étudié le rôle du noyau réticulé paragigantocellulaire dorsal (DPGi) dans la genèse du SP. Bien que le DPGi fût déjà connu pour être responsable de l'inhibition du locus coeruleus (LC) durant les phases de SP, nous apportons ici un certain nombre d'arguments suggérant que le DPGi pourrait être responsable de l'inhibition, non seulement du LC, mais également de l'ensemble des neurones adrénergiques et noradrénergiques. Cela suggère donc que ce noyau joue également un rôle majeur dans la régulation du SP. Les données rapportées dans cette thèse permettent donc de mieux appréhender les mécanismes neuronaux contrôlant la survenue et la régulation du SP. En particulier, ils apportent de nouvelles données en faveur d'un rôle central de l'hypothalamus dans la régulation du SP puisqu'il constituerait le générateur principal de cet état.
34
Okada, Elaine Machado Pingueiro. "Efeito do laser de baixa potência após a expansão rápida da maxila, na ativação de regiões cerebrais relacionadas à nocicepção." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/58/58135/tde-12072012-093209/.
Full textAbstract:
O laser de baixa potência vem sendo utilizado em Odontologia com diversos objetivos, como diminuir o tempo de reparação de tecidos moles e duros e, atualmente, alguns profissionais tem utilizado esta ferramenta para o controle clínico da dor. O presente trabalho in vivo teve como objetivo avaliar quantitativamente os efeitos do laser de baixa potência (LBP) com diodo de GaAlAs (Gálio-alumínioarsenieto) no controle da dor após a expansão rápida da maxila (ERM), analisando a ativação de regiões cerebrais relacionadas à nocicepção, por meio da expressão de c-fos nos subnúcleos caudalis, interpolaris e oralis. Utilizou-se 75 ratos Wistar, machos, pesando em média 220g, que foram distribuídos em 4 grupos: Grupo Controle (n=5) animais não tratados (sem ERM e sem aplicação do LBP) e no período zero foram submetidos à eutanásia; Grupo Experimental I (n=20) animais submetidos apenas à aplicação do LBP no período zero e à eutanásia nos períodos 12, 24 48 e 72 horas após a aplicação do LBP; Grupo Experimental II (n=25) animais submetidos apenas à ERM e à eutanásia nos períodos 6, 12, 24 48 e 72 horas após a ERM; Grupo Experimental III (n=25) animais submetidos à ERM e logo em seguida o LBP no período zero; Os animais deste grupo foram submetidos à eutanásia nos mesmos períodos que o Grupo Experimental II. Após a eutanásia, os cérebros foram coletados e realizou-se secções coronais de 40 micrômetros. Os cortes foram processados para a imunohistoquímica para c-fos e analisados com o auxilio de um microscópio óptico. As células imunorreativas à proteína Fos foram contadas através do auxilio de um sistema de imagem (Image J). O teste de variância (ANOVA) foi usado seguido pelo pós-teste de Tukey, com nível de significância de 5%. O grupo que teve ERM apresentou um aumento significativo do número de neurônios Fos positivos nos subnúcleos interpolaris e caudalis 6 horas após a expansão maxilar, o que diminuiu expressivamente a partir de 12 horas, com um segundo pico no período de 24 horas (p<0,001). O grupo que teve aplicação do LBP teve redução expressiva do número de neurônios Fos positivos em todos os subnúcleos 12 horas após a aplicação da força (p<0,001). Os resultados sugerem que o LBP reduz a ativação neuronal de região nociceptiva e o mesmo seria uma possível alternativa para o alívio de dor em pacientes ortodônticos.Low-level laser therapy (LLLT) has been used in Dentistry with many objectives, especially to decrease the time needed for bone and soft healing. Currently, some professionals have applied this tool for clinical management of pain. The aim of the present iin vivo study was to quantitatively evaluate the effects of Gallium-Aluminum- Arsenide (GaAlAs) low-level laser therapy (LLLT) on pain control after rapid maxillary expansion (RME) in young rats, by means of c-fos quantification in nociceptive related structures (caudalis, interpolaris and oralis subnuclei). A total of 75 male rats, weighting 220g, were assigned to 4 groups: Control Group (n=5) with no treatment (no RME and no LLLT); Experimental I (n=20) with LLLT without RME, evaluated at 12, 24, 48 and 72 hours; Experimental II (n=25) with RME without LLLT, evaluated at 6, 12, 24, 48 and 72 hours after RME; Experimental III (n=25) with RME and LLLT (54J/cm2), evaluated at 6, 12, 24, 48 and 72 hours after RME. The animals were euthanized, brain tissues were collected and coronal sections were cut at 40m, through the spinal trigeminal caudalis, spinal trigeminal interpolaris, and spinal trigeminal oralis subnuclei. The sections were processed for c-fos immunohistochemistry and were analyzed in light microscopy. The Image J software was used to quantify Fos immunoreactive neurons in sections of the rat brains. Statistical analysis was performed using ANOVA and Tukey tests with a significance level of 5%. In the experimental group I, Fos expression significantly increased in neurons in oralis and interpolaris subnuclei 6 hours after the maxillary expansion, then significantly decreased at 12 hours, and increased again at 24 hours (p<0.001). In experimental group III, Fos significantly decreased in neurons in all subnucleis 12 hours after force application (p<0.001). These results suggest that LLLT decrease cfos expression in neurons of nociceptive regions and it may be used as a therapeutic alternative to reduce pain in orthodontic patients.
35
Hagemeier, Christian. "Transactivation of the hsp70 gene and protooncogenes c-fos and c-myc by human cytomegalovirus immediate early proteins." Thesis, University of Cambridge, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.316643.
Full text
36
Tourkine, Nicolai͏̈. "Présence d'éléments intragéniques potentiellement impliqués dans le contrôle de la transcription des gènes c-fos et c-myc." Montpellier 2, 1990. http://www.theses.fr/1990MON20043.
Full textAbstract:
Les elements intrageniques qui participent au controle de la regulation de l'expression des genes c-fos et c-myc murins ont ete recherches. La jonction entre le premier intron de c-myc impliquee dans un blocage de la progression des arn polymerases est differentiellement accessible aux enzymes de restriction dans les noyaux des cellules de friend. Cette accessibilite est correlee avec un fort blocage ainsi qu'avec une structure normale de la chromatine. Nous avons mis en evidence la presence d'un complexe adn-proteines in vitro et in situ et caracterise les sites d'interaction sur l'adn. Nous avons egalement decouvert un element intragenique de la regulation de la regulation transcriptionnelle negative du gene c-fos (fire). Il contient une sequence palindromique et interagit avec des facteurs proteiques. Le blocage de l'elongation de c-fos s'installe pendant l'adhesion des macrophages a un support solide et semble dependre de la presence de facteurs nucleaires qui interagissent avec fire. Il semblerait que calcium joue un role central dans ce phenomene
37
Bauters, Christophe. "Expression des oncogenes nucleaires c-myc et c-fos dans les surcharges hemodynamiques du coeur de rat adulte." Lille 2, 1990. http://www.theses.fr/1990LIL2M006.
Full text
38
Hamlin, Adam Scott. "Functional Neuroanatomy of Morphine-Induced Abstinence, Tolerance, and Sensitisation." University of Sydney, 2006. http://hdl.handle.net/2123/1164.
Full textAbstract:
Doctor of Philosophy (PhD)The investigation into the relationship between neural plasticity in the rat forebrain associated with opiate-induced behaviours yielded two major results. The major finding of the functional neuroanatomy of acute morphine dependence was that doses of naloxone that induced hyperalgesia following a brief exposure to morphine, in previously drug-naïve rats, caused a specific induction of the inducible transcription factor (itf) proteins c-Fos and zif268 in the extended amygdala. Moreover, doses of naloxone that caused a simple reversal in morphine analgesia failed to induce itf proteins in these same brain regions. This increase in itf proteins was specific to regions of the extended amygdala that receive and process nociceptive information relayed via the spino-parabrachio-amygdaloid pathway and was not observed in other regions that are involved in supraspinal pain modulation such as the rostral ventromedial medulla and the periaqueductal gray. We also found that acute morphine increased c-Fos protein in the basolateral amygdala and the major output nucleus of the central amygdala the medial subdivision. Acute morphine also up-regulated c-Fos protein in striatal, midbrain, and hypothalamic nuclei. A unique finding of the current study was that prolonged exposure to morphine was required to induce c-Fos in these brain regions, as the subsequent administration of naloxone 30-minutes after morphine either reversed or blocked this induction. These results indicate the potential role of the amygdala in analgesia following systemic morphine and in pain facilitation during acute morphine abstinence. Investigation into the neurons and circuitry that undergo long-term neuroplasticity in response to repeated morphine exposure revealed that network-level changes in the distribution of Fos protein in the nucleus accumbens and striatum predicted both tolerance to catalepsy and psychomotor sensitisation. Drug-naïve rats became profoundly cataleptic following morphine, an effect that rats with a drug-history became tolerant. Rats with a history of morphine exposure showed an increase in stereotyped behaviours compared to drug-naïve rats. The major finding of this study was that a shift in the induction of c-Fos protein from a matrix predominance in drug-naïve rats toward a patch predominance in drug-sensitised rats in the accumbens core predicted both tolerance to catalepsy and sensitisation of oral stereotyped behaviours. Acute injection of morphine in a drug-naïve rat induced catalepsy and increased the number of c-Fos-positive neurons in matrix striatopallidal projection neurons of the rostral accumbens core. An increase in activity of striatopallidal projection neurons, which give rise to the indirect pathway, could potentially increase inhibitory drive to the pedunculopontine nucleus (PPN). The PPN, long known as a site of termination for basal ganglia output, is thought to direct the outflow of incentive-motivational and sensorimotor information from the nucleus accumbens to pons, medullary, and spinal cord nuclei translating the incentive impact of the stimuli into appropriate motor, autonomic and emotive responses (Winn et al., 1997). Inhibition of this nucleus would cause the animal to be unable to initiate a movement and in effect lock up, which is precisely what cataleptic postures look like. In contrast c-Fos-positive neurons were decreased in the rostral matrix and increased in patch striatonigral projection neurons along the rostro-caudal extent of the accumbens core when morphine was administered to drug-sensitised rats. Striatonigral neurons located in the patch give rise to the direct pathway innervating the dopaminergic neurons in both substantia pars compacta and the dopamine rich islands in the substantia nigra pars reticulata (Berendse et al., 1992; Gerfen, 1992; Furuta et al., 2002). Activity of this pathway is thought to be involved in the initiation of movement (Gerfen, 1992; Gerfen and Wilson, 1996), however, when this pathway is overstimulated as is the case when morphine is injected in drug-sensitised rats this could potentially cause increased activity of PPN neurons leading to repetitive psychomotor behaviours or stereotypy. This data adds to the growing body of evidence that suggests that long-term neuroadaptations induced by drugs of abuse including morphine that lead to behavioural sensitisation involves the circuitry that includes the nucleus accumbens.
39
GOMEZ, GOMEZ YVETTE MAGALY 863445, ROMERO ARACELI 392910 ROMERO, LEYVA MICHAEL ESPERANZA 596705 GASCA, and BOTELLO FELISA YAERIM 596703 LOPEZ. "Inmunoreactividad de c-Fos en el hipotálamo y el sistema de recompensa asociada a la novedad social en ratas jóvenes." Tesis de Licenciatura, Universidad Autónoma del Estado de México, 2017. http://hdl.handle.net/20.500.11799/65168.
Full textAbstract:
Inmunoreactividad de c-Fos en Ratas para evaluar la conducta socialInmunoreactividad de c-Fos en el hipotálamo y el sistema de recompensa asociada a la novedad social en ratas jóvenes El ambiente social, en un gran número de especies de mamíferos, incluyendo los humanos, es necesario para el bienestar y la supervivencia, especialmente durante periodos críticos del desarrollo, como la niñez y la juventud. Dentro del Circuito del Comportamiento Social, el área que ha causado mayor interés es el núcleo paraventricular (PVN) del hipotálamo, productor de las hormonas pro-sociales vasopresina y oxitocina. Sin embargo, otras áreas han quedado un poco olvidas, como es el caso del núcleo supraóptico (SON) del hipotálamo, que también es productor de oxitocina y vasopresia, y las áreas del sistema de recompensa que participan en la asignación del valor hedónico de los estímulos, como es el caso del núcleo accumbens (Nacc) y del pálido ventral (VP). Debido a que las interacciones sociales durante la juventud determinan en gran medida la calidad del desarrollo, la hipótesis de este trabajo plantea que, durante la juventud, la socialización representa un estímulo altamente recompensante, por lo que la novedad social podría poseer mayor valor hedónico que la familiaridad social y que la novedad ambiental. Para comprobarlo se expuso a ratas jovenes a diferentes estímulos socioambientales y se comparó el número de neuronas inmunoreactivas a la proteína c-Fos (un marcador de actividad neuronal) en el PVN y SON del hipotálamo, en el Nacc (Shell y Core), y en el VP. Los resultados arrojaron que en el PVN se presenta más producción de c-Fos ante estímulos sociales novedosos, mientras que en el SON no se enconrtaron diferencias en la producción de está proteína ante estímulos novedosos, sociales o físicos, ni ante estimulos sociales familiares. En cuanto al sistema de recompensa se observó un mayor número de neuronas inmunoreactivas en el grupo expuesto a novedad social en Nacc Core, Nacc Shell y VP. De acuerdo a los datos obtenidos, se puede concluir que la actividad del PVN, responde al carácter novedoso de las relaciones sociales, probablemente por el papel que juega la oxitocina en la formación de lazos afectivos. Por otra parte, el SON, a pesar de que produce las mismas hormonas que el PVN, no parece ser afectado especialmente por los estímulos sociales. En cuanto al sistema de recompensa se observó mayor incremento de la producción de c-Fos en Nacc Core, Shell, y en VP ante la novedad social, posiblemente por la conexión que poseen estas áreas con el PVN, lo que sugiere que este circuito ayuda a que el sistema de recompensa le asigne un mayor valor hedónico a los etimulos sociales novedosos ya que son importantes y necesarios para el desarrollo y bienestar las especies sociales.
40
Hamon, Martial. "Expression des oncogenes nucleaires dans l'aorte de lapin apres angioplastie : influence de l'heparine sur l'expression de c-myc, c-fos et c-jun." Lille 2, 1991. http://www.theses.fr/1991LIL2M347.
Full text
41
Ding, Wei. "Induction of c-fos and activation of parallel MAPK cascades by cadmium." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/MQ54074.pdf.
Full text
42
Armstrong, Johanna. "C-fos, response to injury and local drug delivery in vascular models." Thesis, University of Sheffield, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312781.
Full text
43
Lange, Claudia Maren Ruth Susanne. "The role of intragenic sequences in calcium regulation of c-fos transcription." Thesis, University of Cambridge, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.621786.
Full text
44
Ramírez, Sandra. "Role du coactivateur cbp dans l activite du sre de c-fos." Paris 12, 1999. http://www.theses.fr/1999PA120092.
Full textAbstract:
La proteine cbp, connue pour etre un coactivateur de plusieurs facteurs de transcription dependants du signal est un integrateur des differents voies de signalisation et elle est aussi impliquee dans la regulation de la transcription du proto-oncogene c-fos. Nous avons partie de la hypothese que cbp cooperer avec srf pour la l'activation transcriptionnelle en reponse au serum l'element sre. Dans une premiere etude faite dans la lignee cellulaire f9 nous avons montre que cbp stimule de facon dose dependante l'activite du gene rapporteur luciferase sous le controle de l'element sre du promoteur de c-fos. La partie amino-terminale de la proteine cbp est suffisante pour activer cette transcription. De plus nos resultats montrent que l'activation est independant du motif reconnu par les proteines ets, la boite ets dans sre. Par ailleurs, nous avons montre que la proteine cbp forme un complexe in vivo avec la proteine srf dans des cellules u20s. Tous ces resultats montrent que cbp joue un role de coactivateur de la transcription du facteur de transcription srf dans l'activation du proto-oncogene c-fos via le sre. Un de mecanismes par lesquels cbp peut cooperer dans l'activation de la transcription est en faisant le pont entre les facteurs de transcription et la machinerie basale de transcription. Il est connu que cbp interagit avec certaines facteurs generaux de la transcription, tels que tbp et tfiib. Un deuxieme mecanisme pourrait etre la modulation de la structure chromatinienne grace a l'activite hat intrinseque de cbp ou a une activite hat recrute par elle meme ou de facon independant de cbp. Nous avons montre que cbp est phosphorylee pendant la transition g1/s du cycle cellulaire et que pendant cette meme periode l'activite hat de cbp est maximale. Nous avons egalement demontre que cbp peut etre phosphorylee, dans sa region carboxyterminale, en dehors de son domaine a activite hat, par les mapks et particulierement par erk2. Avec l'aide du test hat mis au point par mr. Ait-si-ali dans notre laboratoire, nous avons trouve que cette phosphorylation stimule de facon significative l'activite hat de la proteine cbp. Ces donnees permettent de mieux comprendre le role important de la proteine cbp dans le controle de la transcription et son implication dans le bon deroulement de la proliferation et de la differentiation cellulaires.
45
Vanhille, Laurent. "Les complexes MafB/MaffB et MafB/c-Fos : dualité dans la prolifération." Aix-Marseille 2, 2009. http://www.theses.fr/2009AIX22044.
Full text
46
McQuade, Jill M. Slane. "The involvement of DFF45 and c-fos in hippocampal plasticity and function." Cincinnati, Ohio : University of Cincinnati, 2002. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=ucin1036088357.
Full text
47
Hooper, Michele Leigh. "Infusion into the brain of an antisense oligodeoxynucleotide to c-fos suppresses production of Fos and produces a behavioral effect." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/mq24969.pdf.
Full text
48
Whitelaw, Philippa F. "The expression of cellular oncogenes c-myc and c-fos in rat skeletal muscle : changes during development and hypertrophy." Thesis, University of Aberdeen, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295585.
Full textAbstract:
A study has been made on the expression of cellular oncogenes c-myc and c-fos in rate skeletal muscle both in vitro in cell lines and primary culture and in vivo during development and after the induction of two models of hypertrophy. Using the technique of Northern hybridisation, results showed that the pattern of expression of c-myc and c-fos mRNA in primary myoblast cells and in established myoblast and fibroblast cells in culture were similar; stimulation of quiescent cells to proliferate induced expression from the c-fos gene within 30 minutes and the c-myc gene by 2 hours. The findings demonstrate that c-myc and c-fos mRNA levels are increased in terminally differentiated rat skeletal muscle both in vitro and in vivo. They confirm work which showed that c-myc is not exclusively connected with cell proliferation (Endo and Nadal-Ginard 1986) and extend previous work into the increased expression of c-myc and c-fos mRNA in cardiac muscle induced to hypertrophy (Mulvagh et al., 1987; Izumo et al., 1988; Komuro et al., 1988). The possible location of the elevated expression within the muscle after hypertrophy and the relative contributions from an inflammatory response, satellite cells and myofibres are discussed. Elevation of c-myc and c-fos mRNA in hypertrophy induced both surgically by tenotomy and pharmocologically with clenbuterol argue against a significant contribution from infiltrating fibroblasts, while from the literature, the activation of satellite cells appears to occur later. It is concluded that the elevated expression of c-myc in skeletal muscle is probably located within the myofibres and may be linked to mechanisms of cell enlargement. However further confirmation with in situ hybridisation and immunohistochemistry is required.
49
Valencia, Garcia Sara. "Décryptage du réseau neuronal responsable de l’atonie musculaire pendant le sommeil paradoxal chez le rat : création d’un modèle rongeur du RBD (REM sleep Behavior Disorder)." Thesis, Lyon 1, 2014. http://www.theses.fr/2014LYO10324.
Full textAbstract:
Les circuits neuronaux responsables du sommeil paradoxal (SP) et de l'atonie musculaire qui le caractéristique sont l'objet de nombreuses recherches expérimentales, notamment en raison de l'existence de plusieurs pathologies invalidantes associées. Cette thèse de Neurobiologie s'inscrit plus spécifiquement dans la description anatomique et fonctionnelle du réseau neuronal responsable de l'atonie musculaire et son potentiel dysfonctionnement dans les troubles comportementaux en SP (RBD, REM sleep Behavior Disorder). Pour ce faire, nous avons combiné plusieurs techniques faisant appel à la neuroanatomie fonctionnelle, au traçage rétrograde de voies nerveuses, à l'hybridation in situ à la polysomnographie et à l'inactivation irréversible de populations neuronales ciblées moléculairement à l'aide de virus adéno-associés contenant des short hairpin RNAs (AAV-shRNA) chez le rat libre de ses mouvements. Nous avons ainsi montré que, contrairement à l'hypothèse généralement admise, le noyau sublatérodorsal pontique (SLD) n'est pas le générateur du SP. En effet, l'inactivation neurochimique de ses neurones glutamatergiques ou sa lésion totale diminuent les quantités de SP sans le supprimer, indiquant que le SLD n'est pas suffisant pour la genèse du SP. En revanche, ces expériences démontrent son implication directe dans la mise en place de l'atonie musculaire lors du SP. En effet, la déconnexion neurochimique des neurones glutamatergiques du SLD provoque pendant le SP l'apparition intermittente de tonus musculaire accompagné de comportements moteurs anormaux. En parallèle, nos travaux de thèse ont permis d'apporter des données expérimentales nouvelles sur la localisation, au sein de la formation réticulée bulbaire ventrale et non dans la moelle épinière, des interneurones GABA/glycine responsables de l'hyperpolarisation des motoneurones somatiques pendant le SP. En effet, ces neurones réticulaires sont exclusivement recrutés pendant le SP et envoient des projections monosynaptiques inhibitrices vers les motoneurones somatiques lombaires. De plus, leur déconnexion neurochimique ciblée déclenche des comportements moteurs anormaux sous-tendus par le maintien d'un tonus musculaire irrégulier pendant le SP. L'analyse actimétrique de ces comportements moteurs oniriques induits expérimentalement montre qu'ils sont très semblables à ceux observés après l'inactivation du SLD et à ceux décrits chez les patients RBD. Les données rapportées dans cette thèse permettent de mieux comprendre les mécanismes neurobiologiques générant le SP et ceux contribuant au contrôle moteur pendant le SP. Par la même occasion, nos travaux ont permis de valider deux modèles rongeurs du RBD humain, ouvrant ainsi des perspectives expérimentales pour l'élaboration de traitements ciblés de cette pathologie affectant le SPA growing number of studies investigate the neuronal network responsible for paradoxical (PS) (or REM) sleep genesis and muscle atonia specific of this sleep state. The aim of this thesis was to characterize at the anatomical and functional levels the populations of neurons involved in generating muscle atonia during PS and their potential failure in REM sleep Behavior Disorder (RBD). For this purpose, we combined a large panel of experimental techniques such as functional neuroanatomy, retrograde tract-tracing, in situ hybridization, polysomnography and irreversible inactivation of genetically-targeted neurons with short-hairpin RNAs introduced in viral adenovectors (AAV-shRNA) in freely moving rats. We thus demonstrated for the first time that, in contrast to the currently admitted hypothesis, the pontine sublaterodorsal nucleus (SLD) is not the PS generator, since genetic inactivation of its glutamatergic neurons or its whole lesion diminish the quantities of but do not eliminate PS. This indicates that the SLD is not sufficient for PS generation. In contrast, our experiments clearly show that the SLD is responsible for muscle atonia because the specific inactivation of its glutamatergic neurons induces an irregular muscle tone concomitant to atypical motor behaviors during PS. In addition, we achieved original data about the location within the ventral medullary reticular formation, and not at spinal levels as often believed, of the glycine/GABA interneurons managing the sustained hyperpolarization of somatic motoneurons during PS. We indeed observed that these medullary neurons are selectively recruited during PS and send monosynaptic inhibitory efferents to the lumbar somatic motoneurons. Furthermore, their genetic inactivation is followed by an increase of abnormal motor behaviors underpinned by a sustained, although irregular, muscle tone. The actimetric analysis of these oneiric experimentally induced behaviors reveals that they are very similar to those observed after SLD inactivation or those reported in RBD patients. Taken together, data harvested during this Thesis help us to better understand the complex neurobiological mechanisms generating PS or specifically contributing to the control of the motor system during PS. At the same time, we validated two rodent models closely mimicking human RBD and thus opening new research fields for the development of targeted treatments for this pathology affecting REM sleep
50
de, Belle Ian D. "Characterization of c-fos promoter binding proteins in normal and neoplastic liver cells." Thesis, University of Ottawa (Canada), 1995. http://hdl.handle.net/10393/10392.
Full textAbstract:
The ability of the c-fos gene to respond to a variety of stimuli reflects the complexity of its regulation. Indeed, aberrant regulation can lead to cellular transformation. The fine regulation of the gene relies on the interaction of protein factors interacting with a set of regulatory elements present within the promoter of the gene in a cooperative fashion. In these studies, multiprotein complexes capable of binding to the serum response element, the cAMP response element, and sis-conditioned medium response element, were identified in liver cell nuclei. A subset of these proteins was able to interact with multiple regulatory elements and might be able to direct functional cooperation between them. These multiple factors could be targeted by different signalling pathways. The behavior of these multiprotein complexes was analyzed under physiological conditions of transient c-fos expression in regenerating rat liver and under pathological conditions of chemically induced hepatocarcinogenesis and in solid 5123tc Morris hepatomas whereby constitutive expression of the gene occurs. Elevated expression of the c-fos gene in both normal and in transformed cells correlated with the loss and/or complete absence of the 47 kDa CRE-binding activity. The 47 kDa CRE-binding protein was characterized as highly CRE-specific and distinct from the other members of the CREB/CREM/ATF family of proteins. The 47 kDa CREB factor displayed DNA-binding activity in the dephosphorylated form. The functional importance of the c-fos promoter binding proteins was assessed by in vitro transcription which suggested the presence of a transcriptional block in quiescent liver cells which was relieved in proliferating hepatocytes. The results are consistent with the identification of the 47 kDa CRE-specific DNA-binding protein as a transcriptional repressor in quiescent liver cells.