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J Grinberg-Zylberbaum

Researcher at National Autonomous University of Mexico

Publications -  13
Citations -  234

J Grinberg-Zylberbaum is an academic researcher from National Autonomous University of Mexico. The author has contributed to research in topics: Caudate nucleus & Extinction (psychology). The author has an hindex of 5, co-authored 13 publications receiving 228 citations.

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Journal ArticleDOI

The Einstein-Podolsky-Rosen Paradox in the Brain: The Transferred Potential

TL;DR: In this article, the brain-to-brain nonlocal EPR correlation between brains was studied to verify if the brain has a macroscopic quantum component, supporting the brain's quantum nature at the macrolevel.
Journal ArticleDOI

Patterns of interhemispheric correlation during human communication.

TL;DR: The interhemispheric correlation patterns for each subject were observed to become similar during the communication sessions as compared to the control situations, and these effects are not due to nonspecific factors such as habituation or fatigue.
Journal ArticleDOI

Suppression of motor conditioning by the injection of 3 M KCl in the caudate nuclei of cats.

TL;DR: Findings are consistent with the view that the CN activity is necessary for the motor regulation which subserves learned responses, and for the analysis and/or storage mechanisms of afferent information.
Journal ArticleDOI

Correlation of evoked potentials in the caudate nucleus and conditioned motor responses.

TL;DR: In cats with implanted electrodes in the CN the evoked potentials appeared and increased during the performance of an approaching conditioned response (CR) and the correct performance of the CR was positively correlated at the level of p.
Book ChapterDOI

Modulatory Effects of Acetylcholine and Catecholamines in the Caudate Nucleus During Motor Conditioning

TL;DR: The caudate nucleus seems to be an important part of the neuronal circuit which controls the motor conditioned responses (MCR), and facts suggest that in the CN exist both the necessary circuit to activate the elements for the performance of MCR and also neurones which are able to inhibit that activity.