Relevant bibliographies by topics / Plasticità neuronale

Academic literature on the topic 'Plasticità neuronale'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "Plasticità neuronale"

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Jardilino Maciel, Antonio Frank. "Uno sguardo sulla questione della temporalità." Perspectivas 4, no. 2 (March 23, 2020): 23–51. http://dx.doi.org/10.20873/rpv4n2-58.

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Nel contesto scientifico la plasticità e l’epigenesi sono divenuti due dei concetti più pregnanti del nostro tempo. Il primo, dislocato dal suo ambito originario, cioè l’estetica, continua a rivelare il suo potenziale filosofico, scientifico ed epistemologico. Nel pensiero di Catherine Malabou, la plasticità ha subito una vera e propria metamorfosi concettuale – dalla plasticità della temporalità alla plasticità cerebrale –, riferendosi alla capacità di ricevere e dare una forma. Allo stesso tempo, la “bomba al plastico” è una sostanza che provoca violentissime deflagrazioni. Nel primo caso, la plasticità ha una valenza positiva, venendo concepita come una sorta di lavoro “scultoreo” in senso biologico. La plasticità struttura l’identità, costituisce la sua storia, la temporalità e l’avvenire di una soggettività vivente. Nel secondo, la plasticità è una pura negazione. Nessuno pensa alla “plasticità cerebrale” come il lavoro radicale del negativo all’opera nelle lesioni cerebrali, nella deformazione o nella rottura delle connessioni neuronali, nelle sofferenze psichiche, nelle strutturazioni che avvengono nel vivente, nei traumi vari, nelle catastrofi naturali e politiche, nelle malattie neurodegenerative. Nella sua evoluzione teorica la plasticità verrà articolata in stretta relazione con lo sviluppo neuronale. La neuroplasticità, come concetto scientifico, ci consente di stabilire un ancoraggio biologico alla questione della formazione e decostruzione della soggettività e della temporalità. In questo senso, la plasticità non è il semplice riflesso del mondo, ma è frutto di un’istanza biologica conflittuale che rivela la forma di un altro mondo possibile. Da un lato, l’elaborazione di un pensiero dialettico in ambito neuronale, inteso come sviluppo neuroplastico, ci permette di uscire dalla stretta alternativa tra riduzionismo e antiriduzionismo, la quale è sempre rappresento il limite teorico della filosofia occidentale degli ultimi anni. Dall'altro, è possibile assumere il carattere trascendentale del pensiero totalmente connessa alla sua materialità. La nozione di epigenesi, in questo caso, si afferma come una “nuova forma di trascendentale”. Come figura biologica l’epigenesi si pone come condizione di possibilità della conoscenza e della razionalità rivelando, pertanto, la sua caratteristica a priori. Per mezzo delle nozioni di plasticità ed epigenesi il tempo può essere indagato in stretta connessione con la vita, con lo sviluppo organico del vivente, oltre che a permetterci una nuova visione della soggettività.
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Cardona, Mario. "Apprendere le lingue nella terza età è possibile ed è salutare. Il cervello ci dice perchè." Revista Italiano UERJ 12, no. 2 (July 13, 2022): 21. http://dx.doi.org/10.12957/italianouerj.2021.67581.

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ABSTRACT: L’invecchiamento della popolazione è un dato demografico mondiale che assume carattere rilevante in molti Paesi del cosiddetto “primo mondo”, Il concetto di anzianità oggigiorno non può più basarsi su dati misurabili che stabiliscono quando un individuo, nell’arco della sua vita, entra nella fase della vecchiaia. Si tratta di un concetto molto più ampio e articolato che riguarda dimensioni socio-sanitarie, psico-affettive, cognitive e culturali. È necessario dunque ripensare il ruolo attivo della popolazione anziana in una società complessa e plurilingue. Nell’ottica dell’invecchiamento di successo (succesful ageing) e in base al principio di cittadinanza attiva (active citizenship) l’apprendimento delle lingue diviene un aspetto educativo rilevante sia per la partecipazione attiva nella società, sia per i vantaggi cognitivi specifici che tale tipo di apprendimento comporta. Oggi la ricerca neuropsicologica dimostra come l’apprendimento possa avvenire lungo tutto l’arco della vita e come il nostro cervello sia in grado di attivare importati fenomeni di compensazione in grado di arginare il declino cognitivo. In questo contributo si prenderanno in considerazione alcuni aspetti neuropsicologici che dimostrano come l’apprendimento linguistico nell’anziano non solo sia possibile, ma sia auspicabile. Su questi presupposti è importante che la linguistica educativa sviluppi un adeguato modello glotto-geragogico.Parole chiave: Glotto-geragogia. Anziani. Linguistica educativa. Plasticità neuronale. Riserva cognitiva. Modello STAC (Scaffolding Theory of Aging and Cognition). RESUMO: O envelhecimento da população é um dado demográfico global que assume um caráter relevante em muitos países do chamado "primeiro mundo". Hoje o conceito de antiguidade não pode mais ser baseado em dados mensuráveis que estabelecem quando um indivíduo, durante sua vida, entra na fase da velhice. É um conceito muito mais amplo e articulado que diz respeito às dimensões sócio-saúde, psicoafetiva, cognitiva e cultural. É, pois, necessário repensar o papel ativo da população idosa numa sociedade complexa e multilingue. Com vista a um envelhecimento bem sucedido e com base no princípio da cidadania ativa, a aprendizagem de línguas torna-se um aspecto educativo relevante tanto para a participação ativa na sociedade como para as vantagens cognitivas específicas que tal tipo de aprendizagem acarreta. Hoje, a pesquisa neuropsicológica demonstra como o aprendizado pode ocorrer ao longo da vida e como nosso cérebro é capaz de ativar importantes fenômenos de compensação capazes de conter o declínio cognitivo. Neste artigo, serão levados em consideração alguns aspectos neuropsicológicos que demonstram como a aprendizagem de linguagem em idosos não é apenas possível, mas desejável. Com base nesses pressupostos, é importante que a linguística educacional desenvolva um modelo gloto-hieragógico adequado.Palavras-chave: Gloto-hieragogia. Idosos. Linguística educacional. Plasticidade neuronal. Reserva cognitive. Modelo STAC (Scaffolding Theory of Aging and Cognition). ABSTRACT: Population aging is a world demographic data which assumes a relevant character in many of the countries of the so called “first world”. The concept of aging, nowadays, cannot be anymore based on measurable data that establish when a human being, throughout his life, enters the stage of old age. It deals with a much wider and more complex concept that concerns socio-health, psycho-affective, cognitive and cultural dimensions. It is therefore necessary to rethink the active role of old population in a complicated and multilingual society. With a view to a successful aging and according to the principle of active citizenship, language learning becomes an educational aspect relevant both in order to achieve an active social participation and for the specific cognitive advantages that type of learning provides with. Nowadays, the neuropsychological research shows how learning could happen throughout the entire life and how our brain is capable to activate important cognitive compensation phenomena capable of stemming the cognitive decline. This essay will take into consideration some neuropsychological aspects that demonstrate how language learning in old people is not only possible, but desirable. On these assumptions it is important that educational linguistic develops an adequate foreign language learning geragogic model. Keywords: Foreign language learning geragogic model. Old age. Educational linguistics. Neural plasticity. Brain reserve. STAC Model (Scaffolding Theory of Aging and Cognition).
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COLEBROOK, ELAINE, and KEN LUKOWIAK. "Learning by the Aplysia Model System: Lack of Correlation Between Gill and Gill Motor Neurone Responses." Journal of Experimental Biology 135, no. 1 (March 1, 1988): 411–29. http://dx.doi.org/10.1242/jeb.135.1.411.

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A semi-intact preparation of Aplysia californica was used to monitor simultaneously behavioural and motor neurone responses during classical conditioning of the gill withdrawal reflex. Gill motor neurone responses and gill withdrawal responses were both capable of enhancement in response to the conditioned stimulus after associative training. The neuronal and behavioural responses did not, however, correlate. In 32% of the conditioned (paired) preparations and 27% of the control (unpaired) preparations, the neuronal response was facilitated whereas the gill withdrawal response did not change, or decreased. In addition, amongst those preparations that showed behavioural enhancement, the acquisition of learning of gill withdrawal followed a different pattern from that displayed by the central neurones. This suggests that facilitation of the central sensory-motor neurone synapses is not primarily responsible for conditioning of the gill withdrawal reflex. The gill withdrawal response elicited by direct depolarization of the central motor neurones decreased following the unpaired (control) presentations of the conditioned and unconditioned stimuli, and remained unchanged following paired presentations, suggesting that there is a site of neuronal plasticity in the gill.
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Silver, Jerry, and AmandaPhuong Tran. "Cathepsins in neuronal plasticity." Neural Regeneration Research 16, no. 1 (2021): 26. http://dx.doi.org/10.4103/1673-5374.286948.

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Thoenen, H. "Neurotrophins and Neuronal Plasticity." Science 270, no. 5236 (October 27, 1995): 593–98. http://dx.doi.org/10.1126/science.270.5236.593.

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Gispen, Willem Hendrik. "Neuronal Plasticity and Function." Clinical Neuropharmacology 16 (1993): S5—S11. http://dx.doi.org/10.1097/00002826-199316001-00002.

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Klein, William L., James Sullivan, Annette Skorupa, and J. Santiago Aguilar. "Plasticity of neuronal receptors." FASEB Journal 3, no. 10 (August 1989): 2132–40. http://dx.doi.org/10.1096/fasebj.3.10.2546848.

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de Mendonça, Alexandre, and J. A. Ribeiro. "Adenosine and neuronal plasticity." Life Sciences 60, no. 4-5 (December 1996): 245–51. http://dx.doi.org/10.1016/s0024-3205(96)00544-9.

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Altar, C. A. "Neurotrophins and neuronal plasticity." European Neuropsychopharmacology 9 (September 1999): 183. http://dx.doi.org/10.1016/s0924-977x(99)80078-9.

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Schliebs, R. "Neuronal plasticity and degeneration." International Journal of Developmental Neuroscience 19, no. 3 (April 30, 2001): 229–30. http://dx.doi.org/10.1016/s0736-5748(01)00006-5.

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Dissertations / Theses on the topic "Plasticità neuronale"

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Alessandri, Marco <1976&gt. "Messa a punto di metodi per lo studio della plasticità neuronale del sistema nervoso enterico." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2008. http://amsdottorato.unibo.it/822/1/Tesi_Alessandri_Marco.pdf.

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Alessandri, Marco <1976&gt. "Messa a punto di metodi per lo studio della plasticità neuronale del sistema nervoso enterico." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2008. http://amsdottorato.unibo.it/822/.

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LEONE, LUCIA. "Ruolo del complesso distrofina-distroglicano e delle metalloproteasi nella plasticità neuronale e sinaptica del ganglio cervicale superiore di roditori." Doctoral thesis, La Sapienza, 2005. http://hdl.handle.net/11573/916857.

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OLLA, PIERLUIGI. "Effetti dell'isolamento sociale sull'assunzione di etanolo e sulla plasticità neuronale del recettore GABA_a nell'ippocampo di topi C57BL/6J." Doctoral thesis, Università degli Studi di Cagliari, 2011. http://hdl.handle.net/11584/266278.

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CAROSI, CHIARA. "Regolazione dell'espressione genica dell'mRNA di FMR1, responsabile della sindrome dell'X fragile: implicazioni nel ritardo mentale e nella plasticità sinaptica." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2008. http://hdl.handle.net/2108/427.

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Le regioni non tradotte localizzate al 5’ ed al 3’ degli mRNA maturi sono di particolare importanza nella regolazione genica. Nel promotore del gene FMR1, responsabile della sindrome dell’X fragile, ci sono siti di inizio della trascrizione multilpli sia nelle cellule linfoblastoidi sia nelle linee cellulari neuronali; questa caratteristica è tipica dei promotori, come quello di FMR1, che mancano della sequenza nota come TATA box. In questo studio ho analizzato la regione 5’UTR del gene FMR1 del cervello umano e di quello di topo. Nel caso delle regioni dell’ippocampo e del cervelletto umane ho identificato l’uso di quattro siti alternativi di inizio della trascrizione, ognuno dei quali co-localizza con delle sequenze chiamate Inr-like (initiator like sequences), comunemente presenti nei promotori che mancano della TATA box. La presenza del quarto sito di inizio non è rilevabile nelle linee cellulari linfoblastoidi indicando una selezione tessuto specifica dei siti di inizio. Dati preliminari indicavano la presenza di trascritti più lunghi, cioè con l’uso dei siti di inizio più distanti, correlati con un incremento delle ripetizioni CGG, lasciando ipotizzare un modello in cui la lunghezza delle ripetizioni influenzi direttamente la trascrizione del gene e in un modo tessuto specifico. Per completare la mia analisi ho diretto la mia attenzione sul promotore del gene FMR1 di topo. Ho studiato la regione 5’UTR in cervelletto e in ippocampo di topi selvatici e di topi modificati geneticamente, CGG ki, in cui sono state annesse circa 100 ripetizioni CGG derivanti dalla corrispondente regione umana. Nel topo però, pur avendo evidenziato l’uso di siti di inizio della trascrizione alternativi, non ho evidenziato nessuna dipendenza dell’uso dei siti dalla lunghezza delle espansioni. In ultimo ho completato lo studio analizzando la poliadenilazione alternativa nella regione 3’UTR del gene umano di FMR1, dal momento che tale meccanismo è spesso associato con la localizzazione tessuto specifica di alcuni mRNA. Usando la tecnica della 3’ RACE ho identificato cinque trascritti con poliadenilazione alternativa, uno contenente la sequenza canonica e gli altri con sequenza non canonica. Da questi dati possiamo dedurre che il gene FMR1 possiede poliadenilazione alternativa ma che questa non sembra essere tessuto specifica. In questo studio ho poi analizzato gli effetti del trattamento antidepressivo sulla espressione genica, in particolare analizzando la regione 3’UTR nel messaggero per αCaMKII (la subunità α della chinasi II Calcio calmodulina dipendente). Gli antidepressivi sono il terzo gruppo di farmaci più venduto nel mondo. Molti di essi sono basati su molecole che, come la fluoxetine, hanno come bersaglio una singola molecola , il trasportatore della serotonina (5-HT). Gli effetti di tali farmaci sono localizzati sia nella pre che nella post-sinapsi, suggerendo che dei cambiamenti nella struttura sinaptica sono correlati alle modificazioni della plasticità sinaptica osservate nei pazienti depressi. Sulla base di queste osservazioni , le molecole chiave del trattamento degli antidepressivi sono recettori, chinasi, neurotrofine e proteine coinvolte nella neurogenesi e nella funzione sinaptica come per esempio αCaMKII. Avvalendomi della metodologia della 3’RACE, ho analizzato se un trattamento acuto con fluoxetina su cellule corticali primarie potesse influenzare l’espressione del mRNA della αCaMKII. Ho evidenziato che, dopo trattamento, si assiste ad una modulazione della poliadenilazione del trascritto di αCaMKII come anche ad un incremento della proteina stessa. Questo indica un cambiamento della sua espressione dopo antidepressivo, lasciando ipotizzare che tale terapia agisce sulla poliadenilazione alternativa del messaggero della αCaMKII per aumentare poi l’efficienza di traduzione della proteina.
The 5’ and 3’ untranslated regions (UTRs) play important roles in regulating gene activity. Within the promoter of the human FMR1 gene, responsible for the Fragile X syndrome, there are multiple transcription start sites in both lymphoblastoid and neuronal cell lines, a common feature of other promoters that lack the TATA box initiator element. In this study I have identified a fourth transcription initiation site in human brain tissue, including hippocampus and cerebellum. All four sites co-localize with an initiator (Inr)-like sequence, commonly found at transcriptional start sites within TATA-less promoters. No detectable activity of the fourth site was observed in lymphoblastoid lines, suggesting a tissue-specific determinants of start site selection. Preliminary data indicate that the longer transcripts (upstream Inrs) are expressed at higher levels with increasing CGG repeat number, providing further support for an initiation model in which the CGG repeat element in the FMR1 gene directly modulates upstream initiation, and in a tissue-specific manner. I have also analyzed the presence of alternative transcription start sites in the promoter of mouse FMR1 gene. I compared the wild type mouse with the transgenic mouse CGG ki, that including in the 5’UTR of FMR1 100 CGG repeats of human gene. In mouse analysis I find several multiple initation sites but I did not find any differences in their usage between wild-type and the CGG ki mice. I have also studied alternative polyadenylation usage in the 3’UTR of the human FMR1 gene, since, the presence of alternative polyadenylation sites has been associated with tissue specific localization of other mRNA species. Using 3’RACE methodology, I have identified five polyadenylation sites, one canonical and four non canonical. These preliminary analysis indicates that transcripts containing the different polyadenylation sites are expressed in both human cell lines and human brain tissues. In this study I also investigated the role of UTRs in antidepressants treatment. Antidepressants are the third most commonly sold group of therapeutic agents worldwide. Most of them are based on molecules, such as fluoxetine, that target a single protein in the brain, the serotonin (5-HT) transporter. Effects of depression are probably localized at both pre- and postsynaptic compartments suggesting that changes in synaptic structure are related to the impaired modification in synaptic strength observed in patients with depression. Based on these hypothesis/observations, key target molecules of the antidepressant treatment are receptors, kinases, neurotrophic factors and protein involved in neurogenesis as well as synaptic function such as αCaMKII. I used the 3’RACE to determine if acute treatment of neurons with fluoxetine would change the αCaMKII mRNA expression in mouse neuronal cortical culture. I obtained that fluoxetine treatment induces a shift in the alternative polyadenylation site usage of αCaMKII mRNA as well as an increase in the total αCaMKII protein in cortical primary culture. These results show that the dendritically localized αCaMKII mRNA changes its pattern of expression after antidepressant treatment. They also show that this treatment affects the use of alternative polydenylation allowing neurons to achieve different levels of protein, possibly translating αCaMKII with a higher efficiency. Key Words: 5’ UTR, 3’ UTR, transcription start site, polyadenylation, dendritic mRNAs, neuronal gene expression, synaptic plasticity, fluoxetine.
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Ménardy, Fabien. "Reconnaissance des signaux de communication chez le diamant mandarin : étude des réponses des neurones d’une aire auditive secondaire." Thesis, Paris 11, 2012. http://www.theses.fr/2012PA11T049/document.

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A l’heure actuelle, il reste largement à étudier comment le codage sensoriel des signaux vocaux de communication contribue à leur détection et à leur reconnaissance. Peu d’études se sont, en effet, penchées sur le codage des vocalisations au niveau des régions auditives en fonction de l’individu qui les produit et du degré de familiarité avec cet individu. Dans ce cadre, les oiseaux chanteurs sont un bon modèle parce qu’ils utilisent des vocalisations pour interagir et reconnaître leurs congénères et qu’ils possèdent, de plus, un ensemble de régions auditives. Parmi ces régions, le nidopallium caudomedian (NCM), une aire auditive analogue du cortex auditif secondaire chez les mammifères, est actuellement considérée comme une région spécialisée dans le traitement des vocalisations (chants et cris) de l’espèce : les neurones du NCM répondent plus fortement aux vocalisations de l’espèce qu’à celles d’une autre espèce. À partir de là, parce que chez le diamant mandarin, le cri de distance permet aux individus, mâles ou femelles, de reconnaître leur partenaire sexuel, nous avons cherché à savoir si, chez les femelles comme chez les mâles, les neurones du NCM montraient une discrimination dans leurs réponses auditives entre le cri d’individus connus (parmi lesquels figurait le partenaire sexuel) et ceux d’individus inconnus et si ces réponses reflétaient le degré de familiarité de ces vocalisations. Les enregistrements de l’activité des neurones du NCM, chez des diamants mandarins vigiles (grâce à un système de télémétrie) ou anesthésiés, lors de la présentation de cris de distance, ont révélé, chez les femelles vivant en couple et ayant été familiarisées avec un autre couple de diamants mandarins, une plus forte augmentation de l’activité lors de la diffusion des cris d’individus connus, mâles ou femelles, qu’aux cris d’individus inconnus. Une telle augmentation n’a pas été, en outre, observée chez des femelles contrôles qui n’avaient jamais entendu ces mêmes cris auparavant. De plus, ils ont indiqué que le nombre de neurones montrant un fort degré de sélectivité ainsi que la quantité d’information portée par les trains de potentiels d’action étaient plus importants chez les femelles vivant en couple que chez les femelles contrôles. En revanche, chez les mâles, bien que la plupart des neurones montrait des réponses lors de la diffusion des cris, aucune différence n’a été mise en évidence entre les cris d’individus connus et ceux d’inconnus. Nous avons alors cherché à savoir comment, d’un point de vue acoustique, les cris de distance étaient représentés au sein du NCM. En se basant sur une étude comportementale ayant déterminé quelles étaient les caractéristiques acoustiques qui contribuaient à la reconnaissance de ces cris, nous avons cherché à savoir si les neurones du NCM étaient sensibles à ces mêmes caractéristiques acoustiques. Les résultats ont montré que, chez les femelles, la suppression de la fréquence fondamentale et la modification du timbre du cri du partenaire sexuel ou du propre cri de l’oiseau provoquaient une forte diminution des réponses au sein du NCM alors que, chez les mâles, les réponses variaient selon le paramètre modifié et le type de cri présenté. Nos résultats suggèrent donc que, chez le diamant mandarin, le NCM est impliqué dans le codage du cri de distance. Cependant, ils mettent en évidence des différences dans ce codage entre les mâles et les femelles. Chez les femelles, ce codage permet de discriminer entre les cris d’individus connus et ceux d’individus inconnus alors que chez les mâles, son rôle reste à être déterminé. Chez les femelles, l’expérience sociale au travers de la mémorisation des signaux de communication des individus peut donc façonner les propriétés fonctionnelles des neurones d’une aire auditive secondaire. Ces propriétés pourraient donc continuellement subir des changements pour s'adapter à l’environnement social de l’individu
How sensory signals are encoded in the brain and whether their behavioural relevance affects their encoding are central questions in sensory neuroscience. Studies have consistently shown that behavioural relevance can change the neural representation of sounds in the auditory system, but what occurs in the context of natural acoustic communication where significance could be acquired through social interaction remains to be explored. The zebra finch, a highly social songbird species that forms lifelong pair bonds and uses a vocalization, the distance call, to identify its mate offers an opportunity to address this issue. One auditory area in the songbird telencephalon, the caudo-medial nidopallium (NCM) that is considered as being analogous to the secondary mammalian auditory cortex, has recently emerged as part of the neural substrate for sensory representation of species-specific vocalizations: the activation of NCM neurons is greatest when birds are exposed to conspecific song, as compared to heterospecific song or artificial stimuli. This led us to investigate whether, in the zebra finch, NCM neurons could contribute to the discrimination among vocalizations that differ in their degree of familiarity: calls produced by the mate, by familiar individuals (males or females), or by unfamiliar individuals (males or females). In females, behaviourally relevant calls, i.e. the mate’s call and familiar calls, evoked responses of greater magnitude than unfamiliar calls. This distinction between responses was seen both in multiunit recordings from awake freely moving mated females (using a telemetric system) and in single unit recordings from anesthetized mated females. In contrast, control females that had not heard them previously displayed response of similar magnitude to call stimuli. In addition, more cells showed highly selective responses in mated than in control females suggesting that experience-dependent plasticity in call-evoked responses resulted in enhanced discrimination of auditory stimuli. In males, as in females, call playback evoked robust auditory responses. However, neurons in males did not appear capable of categorizing the calls of individuals (males or females) as ‘‘familiar’’ or ‘‘unfamiliar’’. Then, we investigated how calls are represented in the NCM of zebra finches by assessing whether certain call-specific acoustic cues drove NCM neurons to a greater degree than others. Behavioural studies had previously identified call-specific acoustic cues that are necessary to elicit a vocal response from male and female zebra finches. Single-unit recordings indicated that NCM neurons in females were particularly sensitive to call modifications in the spectral domain: suppressing the fundamental frequency of call stimuli or modifying the relative energy levels of harmonics in call caused a marked decrease in response magnitude of NCM neurons. In males, NCM neurons also appear to be sensitive to call modifications in the spectral domain, however changes in magnitude of responses (increase or decrease) depended on the acoustic cue that had been modified.Our results provide evidence that the NCM is a telencephalic auditory region that contributes to the processing of the distance call, in females as well in males. However, how the distance call is processed and represented in the NCM appears to differ between males and females. In females, the NCM could be involved in dicrimination between call stimuli whereas, in males, its functional role in call-processing remains to be determined. Our results also suggest that, in females, social experience with the call of individuals, by affecting the degree to which neurons discriminated between these calls, may shape the functional properties of neurons in a telencephalic auditory area. The functional properties of auditory neurons may therefore change continuously to adapt to the social environment
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Hilal, Muna. "Role of Scribble1 in hippocampal synaptic maturation, bidirectional plasticity and spatial memory formation in mice." Thesis, Bordeaux 2, 2013. http://www.theses.fr/2013BOR22037/document.

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La formation de la mémoire spatiale est un mécanisme complexe qui transforme les informations récemment acquises en traces mnésique robustes à long terme. D’un point de vue moléculaire, ces phénomènes sont dépendants de l’expression de deux formes opposées de plasticité synaptique ; la potentialisation à long terme (LTP) et la dépression à long terme (LTD). L’induction de la LTP/LTD dépend de la fine régulation entre des kinases et des phosphatases sensibles au Ca2+ qui vont activer respectivement la LTP et la LTD dans la densité postsynaptique (PSD). Cette régulation met également en jeu des interactions en avale entre les récepteurs et des protéines d’échafaudages spécialisées au sein de la PSD. Scribble1 (Scrib1) est une de ces protéines d’échafaudage appartenant à la famille des LAP (leucine-rich repeats & PDZ domains) avec 16 répétitions riches en leucine et 4 domaines PDZ (PSD-95/Dlg/ZO-1). Lors de cette étude, nous avons développé de souris « knock-out » conditionnelles avec une délétion complète de la Scrib1 dans les principaux neurones de l’encéphale antérieur, dont les neurones excitateurs de l’hippocampe, grâce au système Cre-lox (Scrib1f/f,CaMKII-cre). Les souris Scrib1f/f,CaMKII-cre présentent une altération de la morphologie des dendrites apicales sans modification de la morphologie ni de la densité des épines dans la région CA1 de l’hippocampe. Sur le plan fonctionnel, les neurones du CA1 des souris Scrib1f/f,CaMKII-cre présentent une augmentation du nombre de synapses silencieuses (non-fonctionnelles). Ceci réduit le nombre de synapses actives et entraine une diminution globale de la transmission basale des synapses CA3-CA1 comparée aux synapses Scrib1f/f. Les souris Scrib1f/f,CaMKII-cre montrent une augmentation de la LTP mais sont incapables d’exprimer une LTD ni la depotentiation à long terme. De plus, des protocoles de LTD induisent une LTP chez ces souris. Au niveau moléculaire, nous avons mis en évidence une interaction directe au sein des synapses entre Scrib1 et la phosphatase PP2A impliquée dans la LTD. De plus, l’absence de Scrib1 entraine une réduction des niveaux de PP2A dans la PSD chez les souris Scrib1f/f,CaMKII-cre. Ceci implique une diminution de l’activation de la voie de signalisation de la LTD via PP2A au profit de celle de la CAMKII et la LTP, ce qui pourrait expliquer l’induction d’une LTP à la place d’une LTD chez les souris Scrib1f/f,CaMKII-cre. Sur le plan cognitif, les souris Scrib1f/f,CaMKII-cre présentent des déficits dans la flexibilité de l’apprentissage spatial comparées aux souris Scrib1f/f. Chez les souris Scrib1f/f,CaMKII-cre, la la mémoire spatiale à court terme n’était pas altérée tandis que la mémoire à long terme était déficiente. Ainsi, ces données révèlent un rôle majeur de Srib1 dans consolidation de la mémoire spatiale. Lors de cette étude, nous avons montré un rôle pour Scrib1 dans les connections et la morphologie des neurones CA1, ainsi que la conversion fonctionnelle des synapses silencieuses en synapses actives. D’une manière importante, Scrib1 permet l’expression de la plasticité synaptique bidirectionnelle à travers une interaction avec PP2A et module la formation de la mémoire spatiale à long terme
Spatial memory formation is a complex process that transforms newly-acquired information into long-lasting and solid memories. Molecularly, these phenomena rely on the expression of two opposite forms of synaptic plasticity; long-term potentiation (LTP) and long-term depression (LTD). LTP/LTD induction relies on a fine balance between Ca2+-sensitive kinases and phosphatases that activate specific pathways of either LTP or LTD, respectively. This regulation also involves downstream interactions between receptors and highly specialized scaffold proteins, at the PSD. Scribble1 (Scrib1) is a scaffold protein that belongs to the LAP (leucine-rich repeats and PDZ domains) protein family, with 16 leucine rich repeats and 4 PDZ (PSD-95/Dlg/ZO-1) domains. Here, we developed conditional knock-out mice with a complete loss of Scrib1 expression in the major neurons of the postnatal forebrain, including hippocampal excitatory neurons, using the Cre-Lox system (Scrib1f/f,CaMKII-cre). Scrib1f/f,CaMKII-cre presented altered morphology of apical dendrites but intact spine density and spine morphology in the CA1 region. Functionally, we found increased number of silent (non-functional) synapses that decreases the number of active synapses in Scrib1f/f,CaMKII-cre CA1 neurons leading to a global decrease in basal glutamatergic synaptic transmission at CA3-CA1 synapses compared to Scrib1f/f synapses. Scrib1f/f,CaMKII-cre synapses displayed enhanced LTP but were unable to express LTD or long-term depotentiation. More strikingly, LTD-inducing protocols generated LTP in Scrib1f/f,CaMKII-cre synapses. Molecularly, we revealed a direct interaction between Scrib1 and the phosphatase PP2A that signals LTD at the synapse. Moreover, we found that the absence of Scrib1 results in a reduction of synaptic PP2A levels in Scrib1f/f,CaMKII-cre mice. This probably leads to a decrease in PP2A signaling pathway activation which favors the competing pathway downstream CaMKII resulting in LTP induction instead of LTD in Scrib1f/f,CaMKII-cre mice. On the cognitive level, we found that spatial learning was slower and inflexible in Scrib1f/f,CaMKII-cre compared to Scrib1f/f mice. Short-term spatial memory was intact while long-term memory was impaired. These results argue for an important role of Scrib1 in spatial memory consolidation. We here report that Scrib1 is important for appropriate neuronal shaping and wiring of CA1 neurons as well as functional conversion of silent synapses into active ones. Importantly, it allows bidirectional synaptic plasticity through interaction with PP2A and modulates long-term spatial memory formation
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Higgins, David Conal. "A theoretical and numerical study of certain dynamical of synaptic plasticity." Paris, Ecole normale supérieure, 2014. http://www.theses.fr/2014ENSURI01.

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L'efficacité synaptique quantifie la capacité d'un neurone présynaptique à influer sur le potentiel de membrane d'un neurone postsynaptique. La plasticité synaptique, regroupant tous les processus d'altération de l'efficacité synaptique, est considérée comme le mécanisme fondamental de mémorisation et d'apprentissage dans le cerveau. Dans ce travail nous examinons des règles d'apprentissage formelles aux synapses chimiques et leurs conséquences sur la mémorisation de patrons appris. La plasticité de la synapse entre les fibres parallèles du cervelet et la cellule de Purkinje n'est pas de type Hobbien et dépend de la fréquence et de la durée de l'activité présynaptique. Nous avons développé un modèle qui prenne en compte les caractéristiques de cette règle d'apprentissage spécifique. Ce modèle, basé sur l'interaction entre des variables de signalisation par le calcium et l'oxyde nitrique (NO) reproduit un large corpus de données expérimentales publiées. La relative simplicité de ce modèle permettra son utilisation dans des simulations nunmériques faisant intervenir un grand nombre de synapses dans une architecture de réseau. En parallèle nous avons étudié une règle de plasticité plus typique, telle qu'observée aux synapses corticales, et avons développé des outils analytiques prédisant le comportement de cette synapses modèle dans le contexte de régimes d'activité présynaptique et postsynaptique poissonniens. Nous étendons cette analyse formelle à un réseau de neurones « leaky integrate and fire » (LIF) et développons des outils théoriques qui décrivent la réponse du réseau à des entrées externes bruitées d'amplitude constante ou transitoirement augmentée. Nous utilisons ces outils pour mesurer la durée de rétention de mémoires synaptiques dans un régime de décharge de fond à 1/sec soit dans des neurones indépendants soit dans un réseau récurrent. Nous trouvons que l'abaissement de la concentration de calcium extracellulaire augmente les constantes de temps de rétention do la mémoire. L'introduction d'une bistabilité dans la règle d'apprentissage synaptique rallonge le temps de mémorisation de plusieurs ordres de grandeur. Dans tous les cas nous fournissons des prédictions théoriques sur les échelles de temps de rétention de mémoire qui s'accordent aux résultats de simulations numériques. Les deux parties de cette étude traitent des processus régissant l'apprentissage et sa rétention dans les circuits cérébraux. Les doux modèles montrent l'importance de la fréquence de décharge et des corrélations temporelles entre potentiels d'action dans l'induction d'apprentissage au niveau synaptique. L'ajustement des variables du modèle pour mimer les conditions physiologiques in vivo permet d'allonger la rétention d'apprentissage, dans un réseau soumis à une décharge moyenne continue, sur des échelles de temps biologiquement significative. Notre travail présente une tentative d'unification entre les règles biophysiques détaillées régissant l'apprentissage et une approche analytique en champ moyen
Synaptic efficacy measures the ability of a presynaptic neuron to influence the membrane potential of a postsynaptic neuron. The process of changing synaptic efficacy, via plasticity, is thought to underlie learning and memory in the brain. Focusing on chemical synapses, we examine tho abstract rules of synaptic plasticity which determine how changes in synaptic efficacy occur. Beginning with an atypical, non-Hobbian synapse, the parallel fibre to Purkinje cell synapse, we develop a model which explains the burst frequency and length dependence of this particular synaptic plasticity rule. We present a model based on underlying calcium and NO pathways which accurately unifies much of the experimental literature. This model will be useful in future studios of synaptic plasticity for this synapse and its simplicity will allow for numerical studios involving large numbers of synapses in a network architecture. We also examine a more typical plasticity rule for neocortical synaptic plasticity, developing analytical tools which accurately predict the behaviour of this synapse model under pre- and postsynaptic Poisson spiking. Building on this analysis we extend the theory to leaky integrate-and-fire (LIF) neurons in a network. We develop theoretical tools which can accurately describe the network response to both constant and transiently elevated noisy external inputs. Utilising those tools we examine the duration of synaptic memories under ongoing background (1/sec) spiking activity both in independent neurons and in a recurrent network. We find that lowering tho extracellular calcium concentration extends memory time scales and that the further introduction of a bistability to tho synaptic plasticity rule extends this memory time scale by several orders of magnitude. In al! cases we providc theoretical predictions of memory time scales which match subsequent simulation comparisons. Both sets of investigations reveal insights into the processes of learning and subsequent forgetting in the brain. Both models reveal the joint importance of burst frequency and relative spike timing in the induction of memory changes at the synaptic level. Adjustment of model parameters to more closely mimic in vivo conditions extends the retention time of memories, under ongoing activity, to biologically relevant time scales. Our work represents a coherent development right through from the biophysical processes of synaptic plasticity to the analytical mean-field level
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Daouzli, Adel Mohamed Renaud Sylvie Saïghi Sylvain. "Systèmes neuromorphiques étude et implantation de fonctions d'apprentissage et de plasticité /." S. l. : Bordeaux 1, 2009. http://ori-oai.u-bordeaux1.fr/pdf/2009/DAOUZLI_ADEL_MOHAMED_2009.pdf.

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Soula, Anaïs. "Rôle des microARNs cellulaires et vésiculaires dans la régulation transcriptomique du système nerveux." Thesis, Bordeaux, 2017. http://www.theses.fr/2017BORD0794/document.

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Ce travail consiste à étudier l’expression, le rôle et l’échange des microARNs (miARNs), dans le système nerveux (SN). Les microARNs (miARNs) sont des petits ARNs endogènes non-codants qui exercent une régulation négative sur l’expression desgènes, en s’hybridant sur la région 3’ non-codante des ARNm cibles.Dans un premier, nous avons dévoilé le rôle spécifique du miR-92a, dans lecontrôle de l’expression de la sous-unité GluA1 des récepteurs AMPA, dans un paradigme de plasticité synaptique homéostatique, dans lequel la plasticité synaptique est inhibée.Nous avons ensuite montré, par RNA-Seq que les miARNs sont différentiellement exprimés entre les structures du SN. Cette technologie nous a aussi permis de révéler la présence de nouvelles espèces de miARNs. De plus les résultats suggèrent que l’expression des miARNs (connus et nouveaux) participe à la signature transcriptomique singulière de chacune des structures.Dans un troisième temps, notre travail montre que les miARNs peuvent être échangés entre les cellules du système nerveux via les vésicules extracellulaires (EVs). Le contenu des EVs en miARNs varie en fonction de l’activité neuronale, et ces derniers ont pour cibles prédictives des protéines impliquées dans la régulation de la plasticité neuronale. Nos résultats suggèrent donc que l’échange de miARNs via les EVs est un nouveau mécanisme de modulation de la plasticité neuronale.Enfin, nous proposons un nouvel outil de purification des EVs, qui à l’avenir permettrait de purifier les EVs du SNC selon leur origine cellulaire.Pour conclure, ce travail apporte une meilleure compréhension du rôle des miARNs dans la régulation de la physiologie du SNC
This work consists in stuying the expression, the role and the transport of microRNAs (miRNAs) in the central nervous system (CNS). microRNAs (miRNAs) are small endogenous non coding RNAs, exerting a negative regulation on gene expression.They inhibit protein translation by hybridization on the 3’ untranslated region of mRNA.First, we have revealed the specific role of miR-92a in the control of the expressionof GluA1, in an homeostatic plasticity paradigm in which the synaptic plasticity is inhibited.Second, by using RNA-Seq technology, we showed that miRNAs are differentially expressed in the different structures of the CNS. Moreover, we have discovered new species of miRNAs. Finally, our results suggest that the miRNA expression (of known and new miRNAs) participate in the singular transcriptomique signature of each structure.Third, we have shown that miRNAs are transported into EVs, and can be exchanged between the cells of the CNS. The miRNA content of EVs varies depending on neuronal activity. Target prediction of these miRNAs includes genes involved in the regulation of neuronal plasticity. Together, our results suggest that the exchange of miRNAs through EVs is a new mechanism involved in the modulation of neuronal plasticity. Finally, we propose a new tool for purifiying EVs depending on their cellular origin.To conclude, this study allows a better understanding of the role of miRNAs in the regulation of the physiology of the CNS
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Books on the topic "Plasticità neuronale"

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Glickstein, Mitchell, Christopher Yeo, and John Stein, eds. Cerebellum and Neuronal Plasticity. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-0965-9.

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Tettamanti, Guido, Robert W. Ledeen, Konrad Sandhoff, Yoshitaka Nagai, and Gino Toffano, eds. Gangliosides and Neuronal Plasticity. New York, NY: Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4757-5309-7.

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Maiese, Kenneth, ed. Neuronal and Vascular Plasticity. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0282-1.

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College), NATO Advanced Research Workshop on Cerebellum and Benavioral Plasticity (1986 Magdalen. Cerebellum and neuronal plasticity. New York: Plenum Press, 1987.

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Guido, Tettamanti, and International Society for Neurochemistry. Meeting., eds. Gangliosides and neuronal plasticity. Padova: Liviana Press, 1986.

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Meerlo, Peter, Ruth M. Benca, and Ted Abel, eds. Sleep, Neuronal Plasticity and Brain Function. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-46878-4.

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Ben-Ari, Yehezkel, ed. Excitatory Amino Acids and Neuronal Plasticity. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5769-8.

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European Neuroscience Association Satellite Symposium on Excitatory Amino Acids and Neuronal Plasticity (1989 Fillerval, France). Excitatory amino acids and neuronal plasticity. New York: Plenum Press, 1990.

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Raphael, Pinaud, Tremere Liisa A, and De Weerd Peter, eds. Plasticity in the visual system: From genes to circuits. New York: Springer, 2005.

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Ansermet, François. A chacun son cerveau: Plasticité neuronale et inconscient. Paris: Odile Jacob, 2004.

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Book chapters on the topic "Plasticità neuronale"

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Andrews, Anne M., Greg A. Gerhardt, Lynette C. Daws, Mohammed Shoaib, Barbara J. Mason, Charles J. Heyser, Luis De Lecea, et al. "Neuronal Plasticity." In Encyclopedia of Psychopharmacology, 855. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_3426.

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Rahmann, Hinrich, and Mathilde Rahmann. "Neuronal Plasticity." In The Neurobiological Basis of Memory and Behavior, 187–217. New York, NY: Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4612-2772-4_9.

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Maiese, Kenneth, Zhao Zhong Chong, and Jing-Qiong Kang. "Transformation into Treatment: Novel Therapeutics that Begin within the Cell." In Neuronal and Vascular Plasticity, 1–26. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0282-1_1.

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Chong, Zhao Zhong, Jing-Qiong Kang, and Kenneth Maiese. "G-Protein Mediated Metabotropic Receptors Offer Novel Avenues in Neuronal and Vascular Cells for Cytoprotective Strategies." In Neuronal and Vascular Plasticity, 257–98. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0282-1_10.

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McKinney, Michael, Karen Baskerville, David Personett, Katrina Williams, and John Gonzales. "Cholinergic Plasticity and the Meaning of Death." In Neuronal and Vascular Plasticity, 27–74. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0282-1_2.

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Wei, Ling, Kejie Yin, Jin-Moo Lee, James Y. Chao, Shan Ping Yu, Teng-Nan Lin, and Chung Y. Hsu. "Restorative Potential of Angiogenesis after Ischemic Stroke." In Neuronal and Vascular Plasticity, 75–94. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0282-1_3.

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Duckles, Sue Piper, and Diana N. Krause. "Vascular Endothelial Function: Role of Gonadal Steroids." In Neuronal and Vascular Plasticity, 95–115. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0282-1_4.

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Xu, Zao C. "Alterations of Synaptic Transmission Following Transient Cerebral Ischemia." In Neuronal and Vascular Plasticity, 117–34. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0282-1_5.

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Maynard, Kenneth I. "The Future of Brain Protection: Natural Alternatives." In Neuronal and Vascular Plasticity, 135–63. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0282-1_6.

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Henderson, Rebecca J., and James R. Connor. "Iron S Involvement in the Molecular Mechanisms and Pathogenesis of Alzheimers Disease." In Neuronal and Vascular Plasticity, 165–88. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0282-1_7.

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Conference papers on the topic "Plasticità neuronale"

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de Arcangelis, L., H. J. Herrmann, C. Perrone-Capano, Sumiyoshi Abe, Hans Herrmann, Piero Quarati, Andrea Rapisarda, and Constantino Tsallis. "Neuronal avalanches and brain plasticity." In COMPLEXITY, METASTABILITY, AND NONEXTENSIVITY: An International Conference. AIP, 2007. http://dx.doi.org/10.1063/1.2828739.

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Goldsteen, Pien A., L. Van Der Koog, L. E. M. Kistemaker, Y. S. Prakash, B. Ditz, M. Van Den Berge, G. H. Koppelman, M. C. Nawijn, A. M. Dolga, and R. Gosens. "IL33 regulates airway neuronal plasticity in vitro." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.5035.

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Fernando, Chrisantha. "Neuronal replicators solve the stability-plasticity dilemma." In the 12th annual conference. New York, New York, USA: ACM Press, 2010. http://dx.doi.org/10.1145/1830483.1830511.

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Churchland, Paul M. "Conceptual and neuronal plasticity in visual processing." In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1988. http://dx.doi.org/10.1364/oam.1988.tud2.

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The substantial dependents of perceptual processing on one’s prior conceptual set is by now a familiar theme. I here explore the possibility of radical changes in the character and content of one’s perceptual processing, changes occasioned by radical changes in one’s background conceptual framework. Recent research into learning, categorization, and perception in artificial and neural nets provides new ground for this exploration and new insights into the nature of both conceptual and perceptual plasticity in living creatures.
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HILLMAN, DEAN, and JAMES WOLFE. "Neuronal plasticity in relation to long-duration spaceflight." In Space Programs and Technologies Conference. Reston, Virigina: American Institute of Aeronautics and Astronautics, 1990. http://dx.doi.org/10.2514/6.1990-3811.

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Goldsteen, P., L. van der Koog, L. E. M. Kistemaker, Y. S. Prakash, A. M. Dolga, and R. Gosens. "IL-33 Regulates Airway Neuronal Plasticity In Vitro." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a7407.

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Mettler, Henrik D., Maximilian Schmidt, Walter Senn, Mihai A. Petrovici, and Jakob Jordan. "Evolving neuronal plasticity rules using cartesian genetic programming." In GECCO '21: Genetic and Evolutionary Computation Conference. New York, NY, USA: ACM, 2021. http://dx.doi.org/10.1145/3449726.3459420.

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Ohno, Shuhei, Hideyuki Kato, and Tohru Ikeguchi. "Neuronal avalanche induced by multiplicative spike-timing-dependent plasticity." In 2011 International Joint Conference on Neural Networks (IJCNN 2011 - San Jose). IEEE, 2011. http://dx.doi.org/10.1109/ijcnn.2011.6033405.

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Miguel-Aliaga, Irene. "Endocrine and neuronal control of intestinal plasticity inDrosophila melanogaster." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.105318.

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Sheikhattar, Alireza, Jonathan B. Fritz, Shihab A. Shamma, and Behtash Babadi. "Adaptive sparse logistic regression with application to neuronal plasticity analysis." In 2015 49th Asilomar Conference on Signals, Systems and Computers. IEEE, 2015. http://dx.doi.org/10.1109/acssc.2015.7421406.

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Reports on the topic "Plasticità neuronale"

1

Brown, Thomas H. Long-Term Synaptic Plasticity and Learning in Neuronal Networks. Fort Belvoir, VA: Defense Technical Information Center, July 1986. http://dx.doi.org/10.21236/ada173170.

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Vogt, Brent A. Receptor Subtype Alterations: Bases of Neuronal Plasticity and Learning. Fort Belvoir, VA: Defense Technical Information Center, December 1990. http://dx.doi.org/10.21236/ada232655.

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Tam, David C. A Study of Neuronal Properties, Synaptic Plasticity and Network Interactions Using a Computer Reconstituted Neuronal Network Derived from Fundamental Biophysical Principles. Fort Belvoir, VA: Defense Technical Information Center, June 1992. http://dx.doi.org/10.21236/ada257221.

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Tam, David C. A Study of Neuronal Properties, Synaptic Plasticity and Network Interactions Using a Computer Reconstituted Neuronal Network Derived from Fundamental Biophysical Principles. Fort Belvoir, VA: Defense Technical Information Center, December 1990. http://dx.doi.org/10.21236/ada230477.

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