Synaptic Plasticity
The ability of synapses (connections between neurons) to strengthen or weaken over time based on activity. Synaptic plasticity is the cellular basis of learning and memory. Long-term potentiation (LTP) and long-term depression (LTD) are its primary mechanisms.
Technical Context
Synaptic plasticity forms: LTP (long-term potentiation — persistent strengthening, lasting hours to lifetime; the cellular mechanism of memory formation), LTD (long-term depression — persistent weakening, involved in memory flexibility and motor learning), spike-timing-dependent plasticity (STDP — strengthening or weakening depends on precise timing of pre- and post-synaptic firing), and homeostatic plasticity (synaptic scaling — global adjustment of all synaptic strengths to maintain stable network activity). LTP molecular mechanism (hippocampal CA1): glutamate release → AMPA receptor activation (depolarisation) + NMDA receptor activation (requires coincident depolarisation to relieve Mg²⁺ block) → Ca²⁺ influx through NMDA receptor → CaMKII activation → AMPA receptor phosphorylation (enhanced conductance) + AMPA receptor insertion (more receptors at synapse) → strengthened synaptic transmission. BDNF is required for late-phase LTP (protein synthesis-dependent, lasting >3 hours). Disrupted synaptic plasticity is implicated in cognitive decline and is a theoretical target for nootropic peptide research.