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Related Experiment Videos

Silent memory engrams as the basis for retrograde amnesia.

Dheeraj S Roy1, Shruti Muralidhar1, Lillian M Smith1

  • 1RIKEN-Massachusetts Institute of Technology Center for Neural Circuit Genetics at the Picower Institute for Learning and Memory, Department of Biology and Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139.

Proceedings of the National Academy of Sciences of the United States of America
|October 29, 2017
PubMed
Summary

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This summary is machine-generated.

Memory engrams, the neuronal basis of memory, persist even when protein synthesis is inhibited. These "silent engrams" can be recalled via optogenetics, revealing memory storage relies on cell connectivity.

Area of Science:

  • Neuroscience
  • Memory Research
  • Cellular Biology

Background:

  • Specific neuronal ensembles (memory engrams) store memory information.
  • Engrams persist under protein synthesis inhibition-induced amnesia, forming
  • "silent engrams".
  • Silent engrams are recallable via optogenetics but not natural cues, suggesting retrieval deficits.

Purpose of the Study:

  • Investigate the long-term retention and retrieval mechanisms of silent engrams.
  • Determine the role of engram cell connectivity in memory recall under amnesia.
  • Explore methods to convert silent engram cells into active ones.

Main Methods:

  • Utilized optogenetics for memory recall stimulation in rodents.
  • Administered protein synthesis inhibitors to induce retrograde amnesia.
Keywords:
amnesiaengramepisodichippocampusmemory

Related Experiment Videos

  • Assessed engram cell connectivity and synaptic plasticity.
  • Manipulated engram cell connectivity and gene expression (α-p-21-activated kinase 1).

    • Main Results:

    • Optogenetic recall of silent engrams persisted for at least 8 days under amnesia.
    • Long-term memory retention correlated with persistent functional engram cell-to-engram connectivity.
    • Inactivating downstream engram cell connectivity abolished optogenetic recall.
    • Recall strength was dependent on stimulation intensity, indicating reliance on synaptic function.
    • Overexpression of α-p-21-activated kinase 1 converted silent to active engram cells, increasing spine density.

    Conclusions:

    • Memory information is retained in silent engrams during amnesia.
    • Memory storage is hypothesized to depend on specific engram cell connectivity.
    • Downstream connectivity is crucial for memory retrieval from silent engrams.
    • Synaptic plasticity and structure are essential for effective memory recall.