Пятое издание главной книги Л.С.Выготского (1896-1934)» принесшей ему посмертную мировую славу, воспроизводит первое (1934) издание. Восстановлены купюры, сделанные во втором (1956) и третьем (1982) изданиях, исправлены некоторые опечатки и неточности четвертого (1996) издания, возвращено первоначальное единство авторского замысла и стиля.
In 1978, Stephen Toulmin, on reviewing Vygotsky's book Mind in Society, called him "The Mozart of Psychology"stating that his work had immense contemporary relevance.
Я нахожу эту статью очень интересно - Воспоминание жизни Выготскаого, написала его дочка Гита: HisLife: byGitaVygodskaya. Возможно ли найти эту статью на русском языке (лучше на каком-нибудь российском вебсайте или в электронном файле)?
ВыгодскаяГ. Л. Егожизнь – отначаладоконца : памятиЛ. С. Выготского, 1896-1934 гг. / Г. Л. Выготская // ВестникМосковскогоун-та. Сер. 14, Психология. – 1994. – № 4. – С. 3-17.
Translated from the Russian language by Ilya Gindis
Published in School Psychology International (1994), Vol.16,
Vygotsky was born in 1896 inOrsha (О́рша), in the Russian Empire (today in Belarus). He was influenced by his cousin David Vygodsky and tutored privately by Solomon Ashpiz and graduated from Moscow State University in 1917. Later, he attended the Institute of Psychology in Moscow (1924–34), where he worked extensively on ideas about cognitive development, particularly the relationship of work that is still being explored. He died in Moscow of tuberculosis at the age of 37.
Researchers have long sought a factor that can trigger the brain’s ability to learn – and perhaps recapture the “sponge-like” quality of childhood. In the August 8 issue of the journal Cell, neuroscientists at Children's Hospital Boston report that they’ve identified such a factor, a protein called Otx 2.
Otx2 helps a key type of cell in the cortex to mature, initiating a critical period -- a window of heightened brain plasticity, when the brain can readily make new connections.
貴夫Takao K. Hensch, PhD, of the Neurobiology Program and Department of Neurology at Children’s, the study’s senior investigator, speculates that there may be similar factors from the auditory, olfactory and other sensory systems that help time critical periods.
Sensory experience in early life shapes the mammalian brain. An impairment in the activity-dependent refinement of functionalconnections within developing visual cortex was identified herein a mouse model. Gene-targeted disruption of one isoform of glutamicacid decarboxylase prevented the competitive loss of responsivenessto an eye briefly deprived of vision, without affecting cooperativemechanisms of synapse modification in vitro. Selective, use-dependentenhancement of fast intracortical inhibitory transmission withbenzodiazepines restored plasticity in vivo, rescuing the geneticdefect. Specific networks of inhibitory interneurons intrinsicto visual cortex may detect perturbations in sensory input todrive experience-dependent plasticity during development.
T. K. Hensch, M. Fagiolini, N. Mataga, Laboratory for Neuronal Circuit Development, Brain Science Institute RIKEN, 2-1 Hirosawa, Wako-shi, Saitama 351-0198, Japan. M. P. Stryker, Department of Physiology, University of California, San Francisco, CA 94143, USA. S. Baekkeskov and S. F. Kash, Department of Medicine and Microbiology/Immunology, Hormone Research Institute, University of California, San Francisco, CA 94143, USA.
* To whom correspondence should be addressed. E-mail: hensch@postman.riken.go.jp
TK Hensch, JA Gordon, EP Brandon, GS McKnight, RL … - Journal of Neuroscience, 1998 - Soc Neuroscience
The Journal of Neuroscience, March 15, 1998, 18(6):2108-2117
Developing sensory systems are sculpted by an activity-dependent strengthening and weakening of connections. Long-term potentiation(LTP) and depression (LTD) in vitro have been proposed to modelthis experience-dependent circuit refinement. We directly comparedLTP and LTD induction in vitro with plasticity in vivo in thedeveloping visual cortex of a mouse mutant of protein kinase A(PKA), a key enzyme implicated in the plasticity of a diversearray of systems.
In mice lacking the RI regulatory subunit of PKA, we observed three abnormalities of synaptic plasticity in layer II/IIIof visual cortex in vitro. These included an absence of (1) extracellularlyrecorded LTP, (2) depotentiation or LTD, and (3) paired-pulsefacilitation. Potentiation was induced, however, by pairing low-frequencystimulation with direct depolarization of individual mutant pyramidalcells. Together these findings suggest that the LTP defect inslices lacking PKARI lies in the transmission of sufficientnet excitation through the cortical circuit.
Nonetheless, functional development and plasticity of visual cortical responses in vivo after monocular deprivation did notdiffer from normal. Moreover, the loss of all responsiveness tostimulation of the originally deprived eye in most cortical cellscould be restored by reverse suture of eyelids during the criticalperiod in both wild-type and mutant mice. Such an activity-dependentincrease in response would seem to require a mechanism like potentiationin vivo. Thus, the RI isoform of PKA is not essential for oculardominance plasticity, which can proceed despite defects in severalcommon in vitro models of neural plasticity.
The moral weight of Human - AI interactions
-
I am passing on a document prepared for a meeting of the Chaos and Complex
Systems discussion group at the University of Wisconsin Madison. I attended
an...
regulatory subunit of PKA, we observed three abnormalities of synaptic plasticity in layer II/III of visual cortex in vitro. These included an absence of (1) extracellularly recorded LTP, (2) depotentiation or LTD, and (3) paired-pulse facilitation. Potentiation was induced, however, by pairing low-frequency stimulation with direct depolarization of individual mutant pyramidal cells. Together these findings suggest that the LTP defect in slices lacking 
發表文章
