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Binyamin Hochner

Researcher at Hebrew University of Jerusalem

Publications -  76
Citations -  6765

Binyamin Hochner is an academic researcher from Hebrew University of Jerusalem. The author has contributed to research in topics: Octopus & Aplysia. The author has an hindex of 37, co-authored 73 publications receiving 6047 citations. Previous affiliations of Binyamin Hochner include Interdisciplinary Center for Neural Computation & Columbia University.

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Injection of the cAMP-responsive element into the nucleus of Aplysia sensory neurons blocks long-term facilitation

TL;DR: In this article, a set of proteins, including one with properties similar to mammalian CREBPs, that specifically bind the mammalian CRE sequence were found to be required for long-term facilitation.
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Spatially resolved dynamics of cAMP and protein kinase A subunits in Aplysia sensory neurons

TL;DR: Cyclic adenosine monophosphate (cAMP)-dependent protein kinase, labeled with fluorescein and rhodamine on the catalytic and regulatory subunits, respectively, was injected into Aplysia sensory neurons either in culture or in intact cell clusters.
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Motor primitives in vertebrates and invertebrates.

TL;DR: This work has suggested that motor and movement primitives and modules might exist at the neural, dynamic and kinematic levels with complicated mapping among the elementary building blocks subserving these different levels of representation.
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An octopus-bioinspired solution to movement and manipulation for soft robots.

TL;DR: This study investigates the smart solution that the Octopus vulgaris adopts to perform a crawling movement, with the same limbs used for grasping and manipulation, with a suitable way to build a more complex soft robot that, with minimum control, can perform diverse tasks.
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Roles of PKA and PKC in facilitation of evoked and spontaneous transmitter release at depressed and nondepressed synapses in Aplysia sensory neurons.

TL;DR: The results suggest that whereas activation of PKA is sufficient to trigger the facilitation of nondepressed synapses, activation of both PKA and PKC is required to facilitate depressedsynapses, with the contribution of PKC becoming progressively more important as synaptic transmission becomes more depressed.