Reference library
A critical time window for dopamine actions on the structural plasticity of dendritic spines.
Paper summary
Separate glutamate uncaging, postsynaptic spiking and optogenetic dopamine manipulations in mouse nucleus-accumbens D1 medium spiny neurons identify a short timing window for dopamine-promoted spine enlargement after conditioning. Activity-specific local processes interact with dopamine/cyclic-AMP/PKA/CaMKII mechanisms. Dopamine did not simply increase the calcium transient in the reported tests; broader PKA and local CaMKII-related effects were distinguishable.
Relevance to the project
A mechanistic lead for associating recent local parameter-dependent activity with later modulation. Raw output history is not automatically a per-synapse eligibility trace, and the biological timing window does not select an updater history length or import external reward into the design.
Specific mouse slice/cell conditions and predominantly structural plasticity. Supplementary Materials and Methods, raw data and independent functional/behavioral reproduction were not read. Supports a delayed local learning component, not literal multilayer gradient backpropagation.
Source record
- Reference ID
- pmc-pmc4225776
- Archived version
- PMC article HTML; manuscript/publication label retained in source
- Summary provenance
- reference-library/papers/pmc-pmc4225776/metadata.json · summary
- Review status
- Targeted main-text mechanistic review; supplements and reproduction excluded
- Reading scope
- Existing original HTML and its verified extract reused. Main text, main experimental results, Figures 1–4 captions, pharmacological controls and Discussion read on 2026-10-09; supplementary Materials and Methods and raw data not read. Earlier 2026-10-02 orientation summary preserved in reading_history.