Which statement best describes spike-timing–dependent plasticity (STDP) and its primary cellular mechanism?

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BlackTom AI · Accepted Answer

The question asks about spike-timing–dependent plasticity (STDP) and its primary cellular mechanism, so we should evaluate what each option claims about timing rules and the intracellular signaling that follows.
Option 1 states that STDP depends only on presynaptic firing rate and that precise timing relative to the postsynaptic spike is irrelevant. This is inaccurate because STDP is defined by the relative timing between presynaptic and postsynaptic spikes, with the direction and magnitude of synaptic change strongly dependent on whether the presynaptic event precedes or follows the postsynaptic event within a narrow time window. Simply relying on firing rate ignores the critical timing dependence.
Option 2 claims that when a postsynaptic spike precedes a presynaptic spike, LTP is induced due to back-propagating action potentials inserting AMPA receptors. While back-propagating action potentials can contribute to synaptic changes under certain conditions, the classic STDP rule emphasizes that postsynaptic-spike–preceding presynaptic spike typically leads to LTD within the canonical timing window, and LTP is more reliably associated with presynaptic-before-postsynaptic timing. Moreover, the mechanism described (back-propagating APs inserting AMPA receptors) is an oversimplification and not the standard STDP rule.
Option 3 explicitly describes the canonical STDP timing rule: if a presynaptic spike precedes a postsynaptic spike by a few–tens of milliseconds, the synapse undergoes LTP via large NMDA-receptor–dependent Ca²⁺ influx and kinase activation; if the order is reversed (post before pre) within a similar window, the synapse undergoes LTD via smaller Ca²⁺ signals and phosphatase activation. This matches well-established experimental data: presynaptic-before-postsynaptic timing leads to LTP through substantial Ca²⁺ entry through NMDA receptors and activation of calcium/calmodulin-dependent kinases, while the opposite order yields LTD through more modest Ca²⁺ signals activating phosphatases.
Option 4 states that any two spikes within ~100 ms always produce potentiation, regardless of order, because temporal proximity alone strengthens synapses. This is incorrect because STDP is highly sensitive to the order of spikes; identical short intervals with reversed order do not necessarily produce potentiation and can produce LTD instead. The claim of order-insensitive potentiation ignores the core timing dependence that defines STDP.
In summary, evaluating the claims against STDP biology shows that Option 3 best aligns with the established mechanism, while Options 1, 2, and 4 misstate timing dependence, intracellular signaling, or both. The accuracy hinges on recognizing that the direction and magnitude of plasticity in STDP depend on the precise pre-before-post versus post-before-pre sequence within a restricted time window, with NMDA receptor–mediated Ca²⁺ signaling and kinase/phosphatase pathways driving LTP and LTD, respectively.

NEUR20001_2025_SM2 Assessment for Workshop 9 - neural plasticity and glia

Which statement best describes spike-timing–dependent plasticity (STDP) and its primary cellular mechanism?

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NEUR20001_2025_SM2 Assessment for Workshop 9 - neural plasticity and glia

Which statement best describes spike-timing–dependent plasticity (STDP) and its primary cellular mechanism?

View Explanation

Log in for full answers

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