Memories can persist and be reinstated in the absence of learning-induced synaptic alterations, supporting cell-intrinsic storage¶

Claim · All claims
Evidence · 1 study · review r3 · q2
Currency · newest study 2019 · not yet checked against its sources · not reviewed by a person

Subclaims¶

q2 i? Contextual fear memory can be induced by optogenetic stimulation of training-active hippocampal neurons despite post-training protein synthesis inhibitor that caused retrograde amnesia and eliminated conditioning-induced hippocampal LTP at perforant path-dentate gyrus synapses; Aplysia sensitization memory can be reinstated by abbreviated training after reconsolidation blockade despite apparent elimination of synaptic growth. → Wickliffe C. Abraham 2019

Evidence¶

Wickliffe C. Abraham 2019¶

Wickliffe C. Abraham, Owen D. Jones and David L. Glanzman. (2019). Is plasticity of synapses the mechanism of long-term memory storage? npj Science of Learning 4:9. https://doi.org/10.1038/s41539-019-0048-y

q2 · i? · review · r3

Narrative review attributing this optogenetic experiment to Ryan et al. The review reports memory induction succeeded despite protein synthesis inhibition that "eliminated conditioning-induced hippocampal LTP" at potentiated perforant path-dentate gyrus synapses, which the review says supports cell-intrinsic storage.

"the long-term memory for contextual fear conditioning in mice can be induced by optogenetic stimulation of hippocampal neurons that were active during behavioural training, even though the mice had received post-training injections of a protein synthesis inhibitor, a treatment that caused retrograde amnesia and eliminated conditioning-induced hippocampal LTP"

Discussion¶

Related Claims¶

• DNMT inhibitors block memory formation and/or consolidation and disrupt well-consolidated memory, implicating DNA methylation in memory processes — related
• LTP exhibits electrophysiological properties that make it an attractive candidate memory mechanism, including rapid induction, persistence up to at least a year, and greater persistence with spaced than massed induction protocols — reports the opposite
• Retrograde intervention experiments—reversing LTP or depotentiating learning-strengthened synapses—cause memory loss, lending strong support to the synaptic plasticity and memory hypothesis — reports the opposite
• Transfer of memory via RNA injection in Aplysia—trained donor RNA enhanced the siphon-withdrawal reflex in untrained recipients—offers the strongest challenge to date to the synaptic plasticity hypothesis — related
• Evidence challenges protein-synthesis sufficiency for memory: memory formation is reported in a variety of tasks even during more than 90% reduction of protein — related