Synaptic Plasticity and Molecular Memory Mechanisms
How synapses change over time
Plasticity rules
Synaptic plasticity emerges from activity-dependent changes in receptor trafficking, phosphorylation state, spine morphology, and gene expression. Hebbian and anti-Hebbian forms of plasticity can be implemented by calcium-dependent thresholds and feedback loops.
Molecular memory
Long-term plasticity requires coordinated changes at the synapse and in the nucleus, often involving transcription, translation, and structural remodeling.
LTP and LTD
Long-term potentiation often involves NMDA receptor-dependent calcium entry, CaMKII activation, AMPA receptor insertion, and actin remodeling. Long-term depression can involve phosphatase activation, receptor removal, and spine shrinkage. The balance between kinase and phosphatase signaling is central.
Which receptor is classically required for many forms of hippocampal LTP induction?
NMDA receptors permit calcium entry that triggers LTP-related signaling.
Correct answer: NMDA receptor
Name one molecular event associated with long-term potentiation.
Increased synaptic AMPA receptor number strengthens excitatory transmission.
Correct answer: AMPA receptor insertion
Short-term versus long-term plasticity
Short-term plasticity
- Seconds to minutes
- Often presynaptic and vesicle-based
Long-term plasticity
- Hours to years
- Requires transcription and structural remodeling
Molecular substrates of memory
A major molecular signature of LTD is often the removal of which receptor from the postsynaptic membrane?
Many LTD paradigms involve AMPA receptor endocytosis.
Correct answer: AMPA receptor
Designing a plasticity experiment
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1
Step 1: Establish a baseline synaptic response.
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Step 2: Induce plasticity with an appropriate stimulation paradigm.
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Step 3: Verify receptor trafficking or spine changes.
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Step 4: Block candidate signaling nodes to test mechanism.
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Step 5: Confirm durability with delayed readouts.