Retrograde intervention experiments—reversing LTP or depotentiating learning-strengthened synapses—cause memory loss, lending strong support to the synaptic plasticity and memory hypothesis¶

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? Treatments known to reverse LTP (ZIP, dominant-negative PKMζ, optogenetic depotentiation) cause memory loss or amnesia across a range of tasks, including selective effects on one of two memories sharing overlapping ensembles. → 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 retrograde intervention findings to multiple cited studies. The review reports that LTP-reversing treatments "cause memory loss across a range of tasks", and that input-specific LTP occurs in the amygdala during discriminative fear learning with depotentiation of those synapses causing memory loss.

"administration of zeta-inhibitory-peptide (ZIP) as well as over-expression of a dominant-negative PKM ζ, treatments known to reverse LTP, cause memory loss across a range of tasks"

Discussion¶

Related Claims¶

• 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 — related
• Memories can persist and be reinstated in the absence of learning-induced synaptic alterations, supporting cell-intrinsic storage — 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 — reports the opposite
• DNMT inhibitors block memory formation and/or consolidation and disrupt well-consolidated memory, implicating DNA methylation in memory processes — related