Neuroplasticity Simulator: Synaptic Potentiation, STDP & Learning

simulator intermediate ~10 min
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w = 1.14 — LTP: synapse potentiated 128%

With pre-before-post timing (+10ms) and 50 repetitions at learning rate 0.1, the synapse strengthens from 0.5 to 1.14 — a 128% increase characteristic of long-term potentiation.

Formula

Δw = η × A₊ × exp(-Δt/τ₊) if Δt > 0 (LTP)
Δw = -η × A₋ × exp(Δt/τ₋) if Δt < 0 (LTD)
w(n) = w₀ + Σᵢ₌₁ⁿ Δwᵢ × (1 - w/w_max)

Wiring the Brain Through Experience

The brain is not a fixed circuit — it rewires itself continuously in response to experience. Every time you learn a new skill, form a memory, or recover from injury, synaptic connections are being created, strengthened, weakened, or eliminated. This experience-dependent neuroplasticity, operating from molecular to systems levels, is the biological foundation of learning. This simulator focuses on spike-timing-dependent plasticity (STDP), the millisecond-precision learning rule that governs synaptic change.

The STDP Window

Spike-timing-dependent plasticity depends on the precise temporal order of pre- and postsynaptic firing. When the presynaptic neuron fires 1-20ms before the postsynaptic neuron (positive Δt), the synapse is strengthened — long-term potentiation (LTP). When the order is reversed (negative Δt), the synapse is weakened — long-term depression (LTD). This asymmetric time window implements a causal learning rule: connections that predict postsynaptic firing are reinforced.

Repetition and Consolidation

A single paired spike produces only a small synaptic change. Robust plasticity requires repeated pairings — the repetitions parameter n captures this. In the brain, repetitive practice strengthens motor skills through LTP in motor cortex and cerebellum. During sleep, hippocampal memory traces are replayed and consolidated into neocortical long-term storage through another round of synaptic modification.

Stability vs Plasticity

The brain faces a fundamental dilemma: too much plasticity causes catastrophic forgetting of old memories, while too little prevents new learning. Metaplasticity — the plasticity of plasticity itself — helps resolve this by adjusting learning thresholds based on recent synaptic history. The BCM (Bienenstock-Cooper-Munro) theory formalizes this as a sliding threshold that prevents runaway potentiation or depression.

FAQ

What is neuroplasticity?

Neuroplasticity is the brain's ability to reorganize its structure and function in response to experience. At the synaptic level, connections between neurons can be strengthened (long-term potentiation, LTP) or weakened (long-term depression, LTD) based on patterns of activity. This underlies learning, memory, and recovery from brain injury.

What is spike-timing-dependent plasticity (STDP)?

STDP is a biological learning rule where the relative timing of pre- and postsynaptic spikes determines synaptic change. If the presynaptic neuron fires just before the postsynaptic neuron (positive Δt), the synapse is strengthened (LTP). Reverse timing (negative Δt) weakens it (LTD). This implements a causal learning rule.

What is Hebb's rule?

Donald Hebb (1949) proposed that when neuron A repeatedly contributes to firing neuron B, the connection between them is strengthened — often paraphrased as 'neurons that fire together wire together.' STDP is the modern, temporally precise version of this principle.

Can neuroplasticity be enhanced?

Environmental enrichment, physical exercise, spaced repetition, and sleep all enhance neuroplasticity. At the molecular level, BDNF (brain-derived neurotrophic factor) promotes synaptic growth. Transcranial magnetic stimulation (TMS) can also modulate plasticity by inducing LTP-like or LTD-like changes in cortical circuits.

Sources

Embed

<iframe src="https://homo-deus.com/lab/cognitive-neuroscience/neuroplasticity/embed" width="100%" height="400" frameborder="0"></iframe>
View source on GitHub