The molecular basis of CaMKII function in synaptic and behavioural memory¶
Lisman, S., & Cline. (2002). The molecular basis of CaMKII function in synaptic and behavioural memory.
Cited by¶
1 citation across 1 artifact.
Each citation links to the sentence it supports in the citing article.
Domain-specific¶
- Spike-Timing-Dependent Plasticity
- The biophysical mechanism is NMDA-receptor coincidence detection: the NMDA receptor requires both presynaptic glutamate binding and postsynaptic membrane depolarisation to admit calcium; the pre-then-post order reliably satisfies both conditions within the millisecond window, producing the calcium influx that recruits CaMKII and triggers LTP-related downstream cascades
This sourceCaMKII as the kinase activated by calcium entry through NMDA receptors and necessary and sufficient for LTP induction (the CaMKII step only, not the spike-timing logic).
Supported in partVerified against the source
- The biophysical mechanism is NMDA-receptor coincidence detection: the NMDA receptor requires both presynaptic glutamate binding and postsynaptic membrane depolarisation to admit calcium; the pre-then-post order reliably satisfies both conditions within the millisecond window, producing the calcium influx that recruits CaMKII and triggers LTP-related downstream cascades
Verification¶
Does it exist? Not checked yet. This work's DOI is recorded above but has not been resolved against an external catalogue, so nothing here confirms the work exists.
Does it back the claim? Read against the text for 1 of 1 citation: 1 supported in part. Each verdict is shown under its citation below, with what in the work backs the sentence.
Support is checked per citation rather than per work — the same source can be cited soundly in one article and wrongly in another. Per-citation recording began recently, so a citation with no recorded check is a gap in the record rather than evidence it went unchecked.
See how references were verified.
Registry ID ref:65205683ec8a · see in the full table