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Susumu Tonegawa

Researcher at Massachusetts Institute of Technology

Publications -  419
Citations -  85400

Susumu Tonegawa is an academic researcher from Massachusetts Institute of Technology. The author has contributed to research in topics: Gene & T-cell receptor. The author has an hindex of 150, co-authored 416 publications receiving 79814 citations. Previous affiliations of Susumu Tonegawa include University of Zurich & RIKEN Brain Science Institute.

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Lack of kainic acid-induced gamma oscillations predicts subsequent CA1 excitotoxic cell death.

TL;DR: In this paper, the authors assessed the relationship between kainic acid (KA)-induced gamma oscillations and excitotoxicity in genetically engineered mice in which N-methyl-D-aspartic acid receptor deletion was confined to CA3 pyramidal cells.

Memory retrieval by activating engram cells in mouse models of early Alzheimer’s disease

TL;DR: It is shown that in transgenic mouse models of early AD, direct optogenetic activation of hippocampal memory engram cells results in memory retrieval despite the fact that these mice are amnesic in long-term memory tests when natural recall cues are used, revealing a retrieval, rather than a storage impairment.
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Competition from newborn granule cells does not drive axonal retraction of silenced old granule cells in the adult hippocampus.

TL;DR: The data demonstrate a remarkable stability in the face of a relatively prolonged period of altered synaptic competition between two populations of neurons within the adult brain.
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Phorbol ester effects at hippocampal synapses act independently of the gamma isoform of PKC.

TL;DR: It is demonstrated that the gamma isotype of PKC is not essential for phorbol ester-mediated synaptic facilitation, and limitations on the possible roles ofPKC in LTP are placed.
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Hybridization studies with an antibody heavy chain mRNA.

TL;DR: There are a very limited number possibly a single copy per subgroup of genes coding for the variable region of immunoglobulin polypeptides, and the results confirm and extend the previous finding that antibody diversity is generated in large part by somatic processes.