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Basic Neurosciences · Paper A

Synaptic plasticity (long-term potentiation)

The idea

Synaptic plasticity matters because it is the physical process that turns experience into memory. It works by changing how strongly neurons connect to each other. Long-term potentiation (LTP) is a lasting strengthening of the connection, or synapseThe tiny gap between two nerve cells where a chemical signal passes from one to the other.Read more →, between two neurons after they fire together repeatedly. For example, imagine two neurons that fire together every time a phone number is rehearsed: the synapse between them grows stronger. In practice, LTP is the leading cellular explanation for how memories form and persist in the hippocampusA brain structure central to forming new memories.Read more → (a brain structure central to memory).

How it works

LTP is triggered when NMDA (N-methyl-D-aspartate) receptors, a type of glutamate receptor, let calcium flow into the receiving neuron once it is sufficiently activated. This calcium influx sets off changes that make the synapseThe tiny gap between two nerve cells where a chemical signal passes from one to the other.Read more → respond more strongly to future signals. The process is described as Hebbian, from the principle 'cells that fire together, wire together': simultaneous activity in two connected neurons drives the strengthening. LTP is concentrated in the hippocampusA brain structure central to forming new memories.Read more →, matching that structure's central role in forming new memories. Take a rat that keeps finding food at the same maze location: the synapses encoding that memory strengthen with each successful trial. In practice, drugs or lesions that block NMDA receptorsA glutamate receptor in the brain involved in learning and memory, and a target of drugs like ketamine and memantine.Read more → impair LTP and produce measurable deficits in new memory formation.

How to spot it

  • Prolonged low-frequency stimulation of a hippocampal pathway produces a lasting weakening rather than strengthening of synaptic responses. What is this process called?
  • Early strengthening of a synapseThe tiny gap between two nerve cells where a chemical signal passes from one to the other.Read more → lasts only an hour or two, but a later enduring phase requires an additional cellular step. Which step does the later phase require?
  • Once the coincidence-detecting glutamate receptor opens, one ion entering the postsynaptic cell acts as the trigger for the downstream strengthening cascade. Which ion is this?
  • A researcher applies a drug that blocks the coincidence-detecting glutamate receptor before delivering high-frequency stimulation. What is the expected effect on synaptic strengthening?

Tell it apart

  • Long-term potentiation, a lasting synaptic strengthening from repeated co-activity, unlike short-term facilitation which fades within minutes.
  • NMDA receptor, required to trigger LTP via calcium influx, whereas AMPA receptors mediate the everyday fast synaptic response.
  • Hippocampus, the structure most associated with LTP and new memory formation, unlike the amygdala'sA brain structure central to processing fear and emotional reactions.Read more → role in emotional memory.
  • Hebbian plasticity, strengthening driven by simultaneous firing, rather than a fixed, unchanging synaptic connection.

Watch for

  • That developmental process removes whole synapsesThe tiny gap between two nerve cells where a chemical signal passes from one to the other.Read more → rather than weakening them.
  • That process increases rather than reduces transmitter release.
  • That process is the strengthening being contrasted here.
  • That process is a brief enhancement lasting only minutes.
  • The synapseThe tiny gap between two nerve cells where a chemical signal passes from one to the other.Read more → remains chemical throughout this process.

Use it again

  • Localise the clue to the relevant anatomical level, cell type, pathway or molecular process.
  • Map that structure or process to its normal function.
  • Predict the deficit or clinical sign produced when it is disrupted.
  • Reject options that belong to a neighbouring structure, pathway or level of explanation.

Try a question from this area

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