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Journal articles on the topic 'Plasticità neuronale'

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Author: Grafiati

Published: 11 March 2023

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Chouard, Tanguy. "Plasticity & neuronal computation." Nature 431, no. 7010 (October 2004): 759. http://dx.doi.org/10.1038/431759a.

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12

Bading, Hilmar. "Transcription-dependent neuronal plasticity." European Journal of Biochemistry 267, no. 17 (September 2000): 5280–83. http://dx.doi.org/10.1046/j.1432-1327.2000.01565.x.

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13

Fitzgerald, Maria. "Neuronal growth and plasticity." Pain 23, no. 2 (October 1985): 211. http://dx.doi.org/10.1016/0304-3959(85)90068-5.

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14

Dubner, Ronald. "Neuronal plasticity and pain." Pain 41 (January 1990): S263. http://dx.doi.org/10.1016/0304-3959(90)92643-5.

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15

Nelson, Phillip G., and R. Douglas Fields. "Calcium and neuronal plasticity." Journal of Neurobiology 25, no. 3 (March 1994): 219. http://dx.doi.org/10.1002/neu.480250302.

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16

Matsumoto, Hiyori, Naoto Omata, Yasushi Kiyono, Tomoyuki Mizuno, Kayo Mita, and Hirotaka Kosaka. "Paradoxical changes in mood-related behaviors on continuous social isolation after weaning." Experimental Brain Research 239, no. 8 (June 18, 2021): 2537–50. http://dx.doi.org/10.1007/s00221-021-06149-x.

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AbstractContinuous social isolation (SI) from an early developmental stage may have different effects in youth and adulthood. Moreover, SI is reported to impair neuronal plasticity. In this study, we used post-weaning rats to compare the impact of continuous SI on depressive-like, anxiety-related, and fear-related behaviors and neuronal plasticity in puberty and adulthood. Furthermore, we assessed the effect of lithium on behavioral changes and neuronal plasticity. Continuous SI after weaning induced depressive-like behaviors in puberty; however, in adulthood, depressive-like and anxiety-related behaviors did not increase, but—paradoxically—decreased in comparison with the controls. The decreased expression of neuronal plasticity-related proteins in the hippocampus in puberty was more prominent in the prefrontal cortex and hippocampus in adulthood. In contrast, SI after weaning tended to decrease fear-related behaviors in puberty, a decrease which was more prominent in adulthood with increased neuronal plasticity-related protein expression in the amygdala. Lithium administration over the last 14 days of the SI-induced period removed the behavioral and expression changes of neuronal plasticity-related proteins observed in puberty and adulthood. Our findings suggest that the extension of the duration of SI from an early developmental stage does not simply worsen depressive-like behaviors; rather, it induces a behavior linked to neuronal plasticity damage. Lithium may improve behavioral changes in puberty and adulthood by reversing damage to neuronal plasticity. The mechanisms underlying the depressive-like and anxiety-related behaviors may differ from those underlying fear-related behaviors.

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17

Shefa, Ulfuara, Dokyoung Kim, Min-Sik Kim, Na Young Jeong, and Junyang Jung. "Roles of Gasotransmitters in Synaptic Plasticity and Neuropsychiatric Conditions." Neural Plasticity 2018 (2018): 1–15. http://dx.doi.org/10.1155/2018/1824713.

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Synaptic plasticity is important for maintaining normal neuronal activity and proper neuronal functioning in the nervous system. It is crucial for regulating synaptic transmission or electrical signal transduction to neuronal networks, for sharing essential information among neurons, and for maintaining homeostasis in the body. Moreover, changes in synaptic or neural plasticity are associated with many neuropsychiatric conditions, such as schizophrenia (SCZ), bipolar disorder (BP), major depressive disorder (MDD), and Alzheimer’s disease (AD). The improper maintenance of neural plasticity causes incorrect neurotransmitter transmission, which can also cause neuropsychiatric conditions. Gas neurotransmitters (gasotransmitters), such as hydrogen sulfide (H2S), nitric oxide (NO), and carbon monoxide (CO), play roles in maintaining synaptic plasticity and in helping to restore such plasticity in the neuronal architecture in the central nervous system (CNS). Indeed, the upregulation or downregulation of these gasotransmitters may cause neuropsychiatric conditions, and their amelioration may restore synaptic plasticity and proper neuronal functioning and thereby improve such conditions. Understanding the specific molecular mechanisms underpinning these effects can help identify ways to treat these neuropsychiatric conditions.

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18

Goh, EyleenL K., and EuniceW M. Chin. "Modulating neuronal plasticity with choline." Neural Regeneration Research 14, no. 10 (2019): 1697. http://dx.doi.org/10.4103/1673-5374.257516.

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19

Skrebitskii, V. G., and M. B. Shtark. "THE FUNDAMENTS OF NEURONAL PLASTICITY." Annals of the Russian academy of medical sciences 67, no. 9 (September 10, 2012): 39–44. http://dx.doi.org/10.15690/vramn.v67i9.405.

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Plasticity of the nervous system is determined by the modification of efficacy of synaptic transmission: long- term potentiation and long- term depression. Different modern technical approaches such as: registration of ionic currents in single neuron, molecular- genetic analysis, neurovisualization, and others reveal the molecular mechanisms of synaptic plasticity. The understanding of these mechanisms, in its turn, stimulates the development of methods of pharmacological correction of different forms of brain pathology such as Alzheimer disease, parkinsonism, alcoholism, aging and others.

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20

Santos, A. I., A. Martínez-Ruiz, and I. M. Araújo. "S-nitrosation and neuronal plasticity." British Journal of Pharmacology 172, no. 6 (September 5, 2014): 1468–78. http://dx.doi.org/10.1111/bph.12827.

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21

Emmons, Scott W. "Neuronal plasticity in nematode worms." Nature 553, no. 7687 (January 2018): 159–60. http://dx.doi.org/10.1038/d41586-017-09031-5.

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22

Debanne, Dominique. "Plasticity of neuronal excitabilityin vivo." Journal of Physiology 587, no. 13 (June 30, 2009): 3057–58. http://dx.doi.org/10.1113/jphysiol.2009.175448.

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23

Rossini, P. M. "NL3 Neuronal plasticity in human." Clinical Neurophysiology 121 (October 2010): S1. http://dx.doi.org/10.1016/s1388-2457(10)60004-1.

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24

Matus, Andrew. "Postsynaptic actin and neuronal plasticity." Current Opinion in Neurobiology 9, no. 5 (October 1999): 561–65. http://dx.doi.org/10.1016/s0959-4388(99)00018-5.

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25

Wolf, Marina E., Xiu Sun, Simona Mangiavacchi, and Steven Z. Chao. "Psychomotor stimulants and neuronal plasticity." Neuropharmacology 47 (January 2004): 61–79. http://dx.doi.org/10.1016/j.neuropharm.2004.07.006.

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26

Castrén, Eero, and René Hen. "Neuronal plasticity and antidepressant actions." Trends in Neurosciences 36, no. 5 (May 2013): 259–67. http://dx.doi.org/10.1016/j.tins.2012.12.010.

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27

Palikhova, T. A., and E. N. Sokolov. "Presynaptic plasticity in neuronal memory." International Journal of Psychophysiology 69, no. 3 (September 2008): 167. http://dx.doi.org/10.1016/j.ijpsycho.2008.05.431.

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28

Debanne, Dominique, Yanis Inglebert, and Michaël Russier. "Plasticity of intrinsic neuronal excitability." Current Opinion in Neurobiology 54 (February 2019): 73–82. http://dx.doi.org/10.1016/j.conb.2018.09.001.

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29

Mattson, Mark P. "Mitochondrial Regulation of Neuronal Plasticity." Neurochemical Research 32, no. 4-5 (October 6, 2006): 707–15. http://dx.doi.org/10.1007/s11064-006-9170-3.

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30

AGNATIC, L. F., F. BENFENATI, V. SOLFRINI, G. BIAGINI, K. FUXE, D. GUIDOLIN, C. CARANI, and I. ZINI. "Brain Aging and Neuronal Plasticity." Annals of the New York Academy of Sciences 673, no. 1 Physiopatholo (December 1992): 180–86. http://dx.doi.org/10.1111/j.1749-6632.1992.tb27451.x.

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31

Spitzer, Nicholas C. "New dimensions of neuronal plasticity." Nature Neuroscience 2, no. 6 (June 1999): 489–91. http://dx.doi.org/10.1038/9132.

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32

FRANKFURT, MAYA. "Gonadal Steroids and Neuronal Plasticity." Annals of the New York Academy of Sciences 743, no. 1 Hormonal Rest (November 1994): 45–59. http://dx.doi.org/10.1111/j.1749-6632.1994.tb55786.x.

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33

TICK, S., JF GIRMENS, JA SAHEL, and M. PAQUES. "Neuronal plasticity and macular edema." Acta Ophthalmologica 86 (September 2008): 0. http://dx.doi.org/10.1111/j.1755-3768.2008.6335.x-i1.

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34

ARAI, YASUMASA. "Neuronal plasticity to sex hormones." Juntendo Medical Journal 44, no. 2 (1998): 128–35. http://dx.doi.org/10.14789/pjmj.44.128.

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35

Anglade, P., S. Tsuji, Y. Agid, and E. C. Hirsch. "Neuronal plasticity and Parkinson disease." Molecular and Chemical Neuropathology 24, no. 2-3 (February 1995): 251–55. http://dx.doi.org/10.1007/bf02962152.

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36

Mikkonen, Mia, Mikko Matto, Irina I. Alafuzoff, Hikka Soininen, and Riitta Miettinen. "Neuronal plasticity in Alzheimer's disease." Neurobiology of Aging 21 (May 2000): 113. http://dx.doi.org/10.1016/s0197-4580(00)82305-2.

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37

Duman, Ronald S., and Samuel S. Newton. "Epigenetic Marking and Neuronal Plasticity." Biological Psychiatry 62, no. 1 (July 2007): 1–3. http://dx.doi.org/10.1016/j.biopsych.2007.04.037.

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38

Thoenen, H. "102 Neurotrophins and neuronal plasticity." International Journal of Developmental Neuroscience 14 (July 1996): 75. http://dx.doi.org/10.1016/0736-5748(96)80293-0.

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39

Groth, Rachel D., Robert L. Dunbar, and Paul G. Mermelstein. "Calcineurin regulation of neuronal plasticity." Biochemical and Biophysical Research Communications 311, no. 4 (November 2003): 1159–71. http://dx.doi.org/10.1016/j.bbrc.2003.09.002.

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40

FRIEDRICH, P. "Protein structure and neuronal plasticity." Cell Biology International Reports 14 (September 1990): 11. http://dx.doi.org/10.1016/0309-1651(90)90155-r.

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41

Sims, Robert E., John B. Butcher, H. Rheinallt Parri, and Stanislaw Glazewski. "Astrocyte and Neuronal Plasticity in the Somatosensory System." Neural Plasticity 2015 (2015): 1–12. http://dx.doi.org/10.1155/2015/732014.

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Changing the whisker complement on a rodent’s snout can lead to two forms of experience-dependent plasticity (EDP) in the neurons of the barrel cortex, where whiskers are somatotopically represented. One form, termed coding plasticity, concerns changes in synaptic transmission and connectivity between neurons. This is thought to underlie learning and memory processes and so adaptation to a changing environment. The second, called homeostatic plasticity, serves to maintain a restricted dynamic range of neuronal activity thus preventing its saturation or total downregulation. Current explanatory models of cortical EDP are almost exclusively neurocentric. However, in recent years, increasing evidence has emerged on the role of astrocytes in brain function, including plasticity. Indeed, astrocytes appear as necessary partners of neurons at the core of the mechanisms of coding and homeostatic plasticity recorded in neurons. In addition to neuronal plasticity, several different forms of astrocytic plasticity have recently been discovered. They extend from changes in receptor expression and dynamic changes in morphology to alteration in gliotransmitter release. It is however unclear how astrocytic plasticity contributes to the neuronal EDP. Here, we review the known and possible roles for astrocytes in the barrel cortex, including its plasticity.

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42

Chang, Hung-Ming, Wen-Chieh Liao, Ji-Nan Sheu, Chun-Chao Chang, Chyn-Tair Lan, and Fu-Der Mai. "Sleep Deprivation Impairs Ca2+ Expression in the Hippocampus: Ionic Imaging Analysis for Cognitive Deficiency with TOF-SIMS." Microscopy and Microanalysis 18, no. 3 (April 12, 2012): 425–35. http://dx.doi.org/10.1017/s1431927612000086.

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AbstractSleep deprivation causes cognitive dysfunction in which impaired neuronal plasticity in hippocampus may underlie the molecular mechanisms of this deficiency. Considering calcium-mediated NMDA receptor subunit 1 (NMDAR1) and neuronal nitric oxide synthase (nNOS) activation plays an important role in the regulation of neuronal plasticity, the present study is aimed to determine whether total sleep deprivation (TSD) would impair calcium expression, together with injury of the neuronal plasticity in hippocampus. Adult rats subjected to TSD were processed for time-of-flight secondary ion mass spectrometry, NMDAR1 immunohistochemistry, nNOS biochemical assay, cytochrome oxidase histochemistry, and the Morris water maze learning test to detect ionic, neurochemical, bioenergetic as well as behavioral changes of neuronal plasticity, respectively. Results indicated that in normal rats, strong calcium signaling along with intense NMDAR1/nNOS expression were observed in hippocampal regions. Enhanced calcium imaging and neurochemical expressions corresponded well with strong bioenergetic activity and good performance of behavioral testing. However, following TSD, both calcium intensity and NMDAR1/nNOS expressions were significantly decreased. Behavioral testing also showed poor responses after TSD. As proper calcium expression is essential for maintaining hippocampal neuronal plasticity, impaired calcium expression would depress downstream NMDAR1-mediated nNOS activation, which might contribute to the initiation or development of TSD-related cognitive deficiency.

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43

Дегтерев, А. А., and A. A. Degterev. "Simulation of Spontaneous Activity in Neuronal Cultures with Long-Term Plasticity." Mathematical Biology and Bioinformatics 10, no. 1 (June 22, 2015): 234–44. http://dx.doi.org/10.17537/2015.10.234.

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Existence of spontaneous population bursts is a widely studied phenomenon observed in neuronal cultures in vitro. Recent models of neuronal cultures network activity consist of a number of burst generating mechanisms such as synaptic noise and presence of pacemaker neurons in the network. In the previous simulations of bursting in neuronal cultures synaptic weights change in accordance with the rule of short-term plasticity whereas the long-term values of them, and hence the network structure, remain unchanged. In this paper we reproduce neuronal network models with static synapses, and then investigate spontaneous activity changes in neuronal networks with long-term plasticity defined by STDP rule. Our results demonstrate that introduction of long-term plasticity in the model leads to discrepancy with the experimental data.

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44

Dhuriya, Yogesh Kumar, and Divakar Sharma. "Neuronal Plasticity: Neuronal Organization is Associated with Neurological Disorders." Journal of Molecular Neuroscience 70, no. 11 (June 6, 2020): 1684–701. http://dx.doi.org/10.1007/s12031-020-01555-2.

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45

Dykes, RW. "Acétylcholine et plasticité neuronale du cortex somatosensoriel." médecine/sciences 6, no. 9 (1990): 870. http://dx.doi.org/10.4267/10608/4253.

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46

Bonfanti, Luca, and Sébastien Couillard-Després. "Neuronal and Brain Maturation." International Journal of Molecular Sciences 23, no. 8 (April 15, 2022): 4400. http://dx.doi.org/10.3390/ijms23084400.

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47

Bailey, Rowan. "Sculptural Plasticity." Philosophy Today 63, no. 4 (2019): 1093–109. http://dx.doi.org/10.5840/philtoday2020128313.

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This essay explores “sculptural plasticity” through neuronal matterings of the brainbody in philosophy, literature, and art. It focuses on Socrates’s cataleptic condition as evidenced in Plato’s Symposium, the plasticities at work in Jean-Paul Sartre’s Nausea, and morphogenetic acts of cell formation in the sculptural installation of Pierre Huyghe’s After ALife Ahead.

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48

Zagrebelsky, Marta. "Molekulare Regulation der neuronalen Plastizität und Lernprozesse." BIOspektrum 26, no. 6 (October 14, 2020): 600–602. http://dx.doi.org/10.1007/s12268-020-1466-3.

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Abstract Activity-dependent plastic changes at synapses are essential for learning, but maintaining memory traces requires stable neuronal networks. The balance between plasticity and stability of the brain circuitry is tightly regulated. Among the mechanisms involved in regulating neuronal plasticity is the modulation of excitation and inhibition. Nogo-A was recently described for its ability to limit synaptic plasticity and to reciprocally regulate excitatory and inhibitory synaptic transmission.

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Ansermet, François. "Traccia e oggetto, tra neuroscienze e psicoanalisi." ATTUALITŔ LACANIANA, no. 9 (April 2009): 13–20. http://dx.doi.org/10.3280/ala2009-009003.

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- 003 Il dato psichico e quello biologico non hanno una misura comune ma si incontrano intorno alla questione della traccia e della plasticitŕ neuronale. L'esperienza lascia una traccia nella rete neuronale, la plasticitŕ dimostra che l'accadimento psichico finisce per modificare l'organismo e rimette sulla scena delle neuroscienze il problema della traccia, che Freud ha dimostrato essere determinata dall'esperienza di soddisfacimento. Č l'oggetto (a) il supporto della traccia, mentre il significante nascerebbe al contrario dalle tracce cancellate. Il paradosso del fenomeno della plasticitŕ sta nel fatto che l'iscrizione dell'esperienza separa dall'esperienza, rendendo il soggetto libero da quest'ultima. Il posto del soggetto, dell'atto del soggetto, si impone al di lŕ del biologico, a causa di un difetto stesso di determinazione insita nel biologico. Parole chiave : traccia - plasticitŕ - oggetto (a) - esperienza - libertŕ del soggetto.

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50

Hasegawa, Yoshitaka, Keisuke Hotta, Hideo Mukai, Bon-chu Chung, Yuuki Ooishi, Yasushi Hojo, and Suguru Kawato. "3P234 Acute Modulation of Synaptic Plasticity of Pyramidal Neurons by Hippocampal-derived Sex Steroids(16. Neuronal Circuit & Information processing,Poster)." Seibutsu Butsuri 53, supplement1-2 (2013): S250. http://dx.doi.org/10.2142/biophys.53.s250_5.

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