In Aplysia, long-term sensitisation differs from short-term sensitisation primarily because it:

Question

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The question asks about how long-term sensitisation in Aplysia differs from short-term sensitisation. We'll evaluate each option in turn and explain why it does or does not fit the known biology.
Option 1: 'Involves only transient increases in presynaptic calcium influx without structural changes.' This describes short-term sensitisation, where transient Ca2+ influx leads to increased neurotransmitter release but without lasting structural modifications. It does not account for gene transcription or new synaptic growth, so it is not the mechanism of long-term sensitisation.
Option 2: 'Results from decreased activity of presynaptic phosphatases, causing temporary facilitation only.' Decreased phosphatase activity could enhance phosphorylation and transmission, but as written this implies a temporary, not lasting, effect and focuses on a specific enzymatic change without addressing gene transcription or structural changes. It fails to capture the enduring changes characteristic of long-term sensitisation.
Option 3: 'Requires repeated stimulation, leading to new gene transcription, protein synthesis, and growth of additional presynaptic terminals, thereby producing lasting enhancement of neurotransmitter release.' This option describes the core mechanism of long-term sensitisation: persistent changes requiring gene transcription and protein synthesis, culminating in structural changes at the presynaptic terminal and sustained heightened transmitter release. This aligns with established findings in Aplysia research.
Option 4: 'Depends solely on postsynaptic AMPA receptor insertion, independent of presynaptic changes.' Long-term sensitisation in Aplysia involves presynaptic changes (increased transmitter release and growth of presynaptic terminals) and gene expression; attributing the enduring effect solely to postsynaptic AMPA receptor insertion ignores the presynaptic structural plasticity that characterizes long-term forms. This makes the statement inaccurate for long-term sensitisation.
In summary, the third option uniquely matches the distinctive feature of long-term sensitisation—repeated stimulation driving gene transcription, protein synthesis, and structural presynaptic changes that produce lasting enhancement of neurotransmitter release—whereas the other options describe mechanisms more consistent with short-term or mischaracterized plasticity.

NEUR20001_2025_SM2 Assessment for Workshop 9 - neural plasticity and glia

In Aplysia, long-term sensitisation differs from short-term sensitisation primarily because it:

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NEUR20001_2025_SM2 Assessment for Workshop 9 - neural plasticity and glia

In Aplysia, long-term sensitisation differs from short-term sensitisation primarily because it:

View Explanation

Log in for full answers

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