Calcium elevation in the postsynaptic spine is a critical trigger for activity‑dependent synaptic plasticity.

Which ONE of the following outcomes is most directly initiated by increases in postsynaptic calcium at excitatory synapses?

Question

Calcium elevation in the postsynaptic spine is a critical trigger for activity‑dependent synaptic plasticity.

Which ONE of the following outcomes is most directly initiated by increases in postsynaptic calcium at excitatory synapses?

BlackTom AI · Accepted Answer

Increases in postsynaptic calcium directly activate intracellular signalling pathways that modify synaptic strength.

Relevant concepts: At excitatory glutamatergic synapses, Ca2+ is a key second messenger. NMDA-type glutamate receptors (and to a lesser extent voltage-gated Ca2+ channels) permit Ca2+ entry into the postsynaptic spine when the membrane is sufficiently depolarized. The amplitude and time course of that Ca2+ signal determine downstream activation of enzymes (kinases and phosphatases), cytoskeletal regulators, receptor trafficking machinery and transcription factors that together produce long-term changes in synaptic efficacy (LTP or LTD).

Step-by-step reasoning:
1. Glutamate release activates AMPA receptors and depolarizes the spine, relieving the Mg2+ block of NMDA receptors.
2. NMDA receptors open and allow Ca2+ influx into the spine, producing a local Ca2+ transient.
3. Elevated Ca2+ binds calmodulin and activates Ca2+/calmodulin-dependent kinases (notably CaMKII) and other kinases (PKA, PKC) or, with lower Ca2+ levels/longer duration, calcineurin (a phosphatase).
4. Activated kinases phosphorylate AMPA receptor subunits and associated proteins, promoting insertion of AMPA receptors into the postsynaptic membrane and increasing conductance; phosphatase activity can lead to AMPA removal (LTD).
5. Longer-term Ca2+-dependent signalling activates transcription factors (e.g., CREB) and structural remodeling of the spine, consolidating plasticity.

Why this answer is correct: The most immediate and direct consequence of postsynaptic Ca2+ elevation is intracellular signalling that changes receptor number/function and cytoskeletal state, thereby modifying synaptic strength — the defining mechanism of activity-dependent plasticity.

Why other options would be incorrect: Immediate generation of action potentials is primarily due to membrane depolarization and summation, not spine Ca2+ transients per se. Increased presynaptic release is a possible downstream or retrograde effect but is not the most direct postsynaptic-initiated outcome. Direct opening of unrelated ion channels or neurotransmitter synthesis are not the primary, direct result of the spine Ca2+ signal.

Confirmed final answer: Activation of intracellular signalling pathways that modify synaptic strength.

Calcium elevation in the postsynaptic spine is a critical trigger for activity‑dependent synaptic plasticity. Which ONE of the following outcomes is most directly initiated by increases in postsynaptic calcium at excitatory synapses?单项选择题

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