Littérature scientifique sur le sujet « Plasticità neuronale »
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Articles de revues sur le sujet "Plasticità neuronale"
Jardilino Maciel, Antonio Frank. « Uno sguardo sulla questione della temporalità ». Perspectivas 4, no 2 (23 mars 2020) : 23–51. http://dx.doi.org/10.20873/rpv4n2-58.
Texte intégralCardona, Mario. « Apprendere le lingue nella terza età è possibile ed è salutare. Il cervello ci dice perchè ». Revista Italiano UERJ 12, no 2 (13 juillet 2022) : 21. http://dx.doi.org/10.12957/italianouerj.2021.67581.
Texte intégralCOLEBROOK, ELAINE, et 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 (1 mars 1988) : 411–29. http://dx.doi.org/10.1242/jeb.135.1.411.
Texte intégralSilver, Jerry, et AmandaPhuong Tran. « Cathepsins in neuronal plasticity ». Neural Regeneration Research 16, no 1 (2021) : 26. http://dx.doi.org/10.4103/1673-5374.286948.
Texte intégralThoenen, H. « Neurotrophins and Neuronal Plasticity ». Science 270, no 5236 (27 octobre 1995) : 593–98. http://dx.doi.org/10.1126/science.270.5236.593.
Texte intégralGispen, Willem Hendrik. « Neuronal Plasticity and Function ». Clinical Neuropharmacology 16 (1993) : S5—S11. http://dx.doi.org/10.1097/00002826-199316001-00002.
Texte intégralKlein, William L., James Sullivan, Annette Skorupa et J. Santiago Aguilar. « Plasticity of neuronal receptors ». FASEB Journal 3, no 10 (août 1989) : 2132–40. http://dx.doi.org/10.1096/fasebj.3.10.2546848.
Texte intégralde Mendonça, Alexandre, et J. A. Ribeiro. « Adenosine and neuronal plasticity ». Life Sciences 60, no 4-5 (décembre 1996) : 245–51. http://dx.doi.org/10.1016/s0024-3205(96)00544-9.
Texte intégralAltar, C. A. « Neurotrophins and neuronal plasticity ». European Neuropsychopharmacology 9 (septembre 1999) : 183. http://dx.doi.org/10.1016/s0924-977x(99)80078-9.
Texte intégralSchliebs, R. « Neuronal plasticity and degeneration ». International Journal of Developmental Neuroscience 19, no 3 (30 avril 2001) : 229–30. http://dx.doi.org/10.1016/s0736-5748(01)00006-5.
Texte intégralThèses sur le sujet "Plasticità neuronale"
Alessandri, Marco <1976>. « 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.
Texte intégralAlessandri, Marco <1976>. « 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/.
Texte intégralLEONE, 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.
Texte intégralOLLA, 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.
Texte intégralCAROSI, 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.
Texte intégralThe 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.
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.
Texte intégralHow 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
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.
Texte intégralSpatial 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
Higgins, David Conal. « A theoretical and numerical study of certain dynamical of synaptic plasticity ». Paris, Ecole normale supérieure, 2014. http://www.theses.fr/2014ENSURI01.
Texte intégralSynaptic 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
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.
Texte intégralSoula, Anaïs. « Rôle des microARNs cellulaires et vésiculaires dans la régulation transcriptomique du système nerveux ». Thesis, Bordeaux, 2017. http://www.theses.fr/2017BORD0794/document.
Texte intégralThis 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
Livres sur le sujet "Plasticità neuronale"
Glickstein, Mitchell, Christopher Yeo et John Stein, dir. Cerebellum and Neuronal Plasticity. Boston, MA : Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-0965-9.
Texte intégralTettamanti, Guido, Robert W. Ledeen, Konrad Sandhoff, Yoshitaka Nagai et Gino Toffano, dir. Gangliosides and Neuronal Plasticity. New York, NY : Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4757-5309-7.
Texte intégralMaiese, Kenneth, dir. Neuronal and Vascular Plasticity. Boston, MA : Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0282-1.
Texte intégralCollege), NATO Advanced Research Workshop on Cerebellum and Benavioral Plasticity (1986 Magdalen. Cerebellum and neuronal plasticity. New York : Plenum Press, 1987.
Trouver le texte intégralGuido, Tettamanti, et International Society for Neurochemistry. Meeting., dir. Gangliosides and neuronal plasticity. Padova : Liviana Press, 1986.
Trouver le texte intégralMeerlo, Peter, Ruth M. Benca et Ted Abel, dir. Sleep, Neuronal Plasticity and Brain Function. Berlin, Heidelberg : Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-46878-4.
Texte intégralBen-Ari, Yehezkel, dir. Excitatory Amino Acids and Neuronal Plasticity. Boston, MA : Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5769-8.
Texte intégralEuropean 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.
Trouver le texte intégralRaphael, Pinaud, Tremere Liisa A et De Weerd Peter, dir. Plasticity in the visual system : From genes to circuits. New York : Springer, 2005.
Trouver le texte intégralAnsermet, François. A chacun son cerveau : Plasticité neuronale et inconscient. Paris : Odile Jacob, 2004.
Trouver le texte intégralChapitres de livres sur le sujet "Plasticità neuronale"
Andrews, Anne M., Greg A. Gerhardt, Lynette C. Daws, Mohammed Shoaib, Barbara J. Mason, Charles J. Heyser, Luis De Lecea et al. « Neuronal Plasticity ». Dans Encyclopedia of Psychopharmacology, 855. Berlin, Heidelberg : Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_3426.
Texte intégralRahmann, Hinrich, et Mathilde Rahmann. « Neuronal Plasticity ». Dans 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.
Texte intégralMaiese, Kenneth, Zhao Zhong Chong et Jing-Qiong Kang. « Transformation into Treatment : Novel Therapeutics that Begin within the Cell ». Dans Neuronal and Vascular Plasticity, 1–26. Boston, MA : Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0282-1_1.
Texte intégralChong, Zhao Zhong, Jing-Qiong Kang et Kenneth Maiese. « G-Protein Mediated Metabotropic Receptors Offer Novel Avenues in Neuronal and Vascular Cells for Cytoprotective Strategies ». Dans Neuronal and Vascular Plasticity, 257–98. Boston, MA : Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0282-1_10.
Texte intégralMcKinney, Michael, Karen Baskerville, David Personett, Katrina Williams et John Gonzales. « Cholinergic Plasticity and the Meaning of Death ». Dans Neuronal and Vascular Plasticity, 27–74. Boston, MA : Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0282-1_2.
Texte intégralWei, Ling, Kejie Yin, Jin-Moo Lee, James Y. Chao, Shan Ping Yu, Teng-Nan Lin et Chung Y. Hsu. « Restorative Potential of Angiogenesis after Ischemic Stroke ». Dans Neuronal and Vascular Plasticity, 75–94. Boston, MA : Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0282-1_3.
Texte intégralDuckles, Sue Piper, et Diana N. Krause. « Vascular Endothelial Function : Role of Gonadal Steroids ». Dans Neuronal and Vascular Plasticity, 95–115. Boston, MA : Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0282-1_4.
Texte intégralXu, Zao C. « Alterations of Synaptic Transmission Following Transient Cerebral Ischemia ». Dans Neuronal and Vascular Plasticity, 117–34. Boston, MA : Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0282-1_5.
Texte intégralMaynard, Kenneth I. « The Future of Brain Protection : Natural Alternatives ». Dans Neuronal and Vascular Plasticity, 135–63. Boston, MA : Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0282-1_6.
Texte intégralHenderson, Rebecca J., et James R. Connor. « Iron S Involvement in the Molecular Mechanisms and Pathogenesis of Alzheimers Disease ». Dans Neuronal and Vascular Plasticity, 165–88. Boston, MA : Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0282-1_7.
Texte intégralActes de conférences sur le sujet "Plasticità neuronale"
de Arcangelis, L., H. J. Herrmann, C. Perrone-Capano, Sumiyoshi Abe, Hans Herrmann, Piero Quarati, Andrea Rapisarda et Constantino Tsallis. « Neuronal avalanches and brain plasticity ». Dans COMPLEXITY, METASTABILITY, AND NONEXTENSIVITY : An International Conference. AIP, 2007. http://dx.doi.org/10.1063/1.2828739.
Texte intégralGoldsteen, 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 et R. Gosens. « IL33 regulates airway neuronal plasticity in vitro ». Dans ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.5035.
Texte intégralFernando, Chrisantha. « Neuronal replicators solve the stability-plasticity dilemma ». Dans the 12th annual conference. New York, New York, USA : ACM Press, 2010. http://dx.doi.org/10.1145/1830483.1830511.
Texte intégralChurchland, Paul M. « Conceptual and neuronal plasticity in visual processing ». Dans OSA Annual Meeting. Washington, D.C. : Optica Publishing Group, 1988. http://dx.doi.org/10.1364/oam.1988.tud2.
Texte intégralHILLMAN, DEAN, et JAMES WOLFE. « Neuronal plasticity in relation to long-duration spaceflight ». Dans Space Programs and Technologies Conference. Reston, Virigina : American Institute of Aeronautics and Astronautics, 1990. http://dx.doi.org/10.2514/6.1990-3811.
Texte intégralGoldsteen, P., L. van der Koog, L. E. M. Kistemaker, Y. S. Prakash, A. M. Dolga et R. Gosens. « IL-33 Regulates Airway Neuronal Plasticity In Vitro ». Dans 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.
Texte intégralMettler, Henrik D., Maximilian Schmidt, Walter Senn, Mihai A. Petrovici et Jakob Jordan. « Evolving neuronal plasticity rules using cartesian genetic programming ». Dans GECCO '21 : Genetic and Evolutionary Computation Conference. New York, NY, USA : ACM, 2021. http://dx.doi.org/10.1145/3449726.3459420.
Texte intégralOhno, Shuhei, Hideyuki Kato et Tohru Ikeguchi. « Neuronal avalanche induced by multiplicative spike-timing-dependent plasticity ». Dans 2011 International Joint Conference on Neural Networks (IJCNN 2011 - San Jose). IEEE, 2011. http://dx.doi.org/10.1109/ijcnn.2011.6033405.
Texte intégralMiguel-Aliaga, Irene. « Endocrine and neuronal control of intestinal plasticity inDrosophila melanogaster ». Dans 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.105318.
Texte intégralSheikhattar, Alireza, Jonathan B. Fritz, Shihab A. Shamma et Behtash Babadi. « Adaptive sparse logistic regression with application to neuronal plasticity analysis ». Dans 2015 49th Asilomar Conference on Signals, Systems and Computers. IEEE, 2015. http://dx.doi.org/10.1109/acssc.2015.7421406.
Texte intégralRapports d'organisations sur le sujet "Plasticità neuronale"
Brown, Thomas H. Long-Term Synaptic Plasticity and Learning in Neuronal Networks. Fort Belvoir, VA : Defense Technical Information Center, juillet 1986. http://dx.doi.org/10.21236/ada173170.
Texte intégralVogt, Brent A. Receptor Subtype Alterations : Bases of Neuronal Plasticity and Learning. Fort Belvoir, VA : Defense Technical Information Center, décembre 1990. http://dx.doi.org/10.21236/ada232655.
Texte intégralTam, 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, juin 1992. http://dx.doi.org/10.21236/ada257221.
Texte intégralTam, 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, décembre 1990. http://dx.doi.org/10.21236/ada230477.
Texte intégral