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💊 Peripheral Nerve Sodium Channel Pain Signaling Simulator

This simulation models the pain signaling pathway through sodium channels of nociceptors for peripheral pain, offering a detailed understanding of the mechanisms involved.

Novel Non-Opioid Analgesics2DModerate60 FPS
peripheral-nerve-sodium-channel-signaling-simulator ↗ Open standalone

Tissue Stimulus Activates the Nociceptor Ending

Free nerve endings in skin sense damage-signaling stimuli.

  • Free: Nociceptor endings (unmyelinated terminal branches)
  • 3: Stimulus modalities (mechanical, thermal, chemical)
  • ~200/cm²: Skin nociceptor density (in human skin)
  • Noxious: Activation threshold (only strong stimuli trigger)

What a nociceptor is

A bare sensory ending that detects tissue-damaging stimuli.

Three stimulus types

Pressure, heat or cold, and irritant chemicals all qualify.

Why endings stay bare

No myelin at the tip keeps receptor proteins exposed.

Stimulus-Gated Channels Build a Generator Potential

Ion channels convert stimulus energy into an electrical signal.

  • TRPV1: Key channels (heat and capsaicin sensor)
  • Piezo2: Mechano channel (pressure-gated pore)
  • Graded: Potential type (not all-or-none)
  • Na⁺ / Ca²⁺: Ion carrying current (cation influx)

Transduction channels

TRPV1 senses heat; Piezo2 senses stretch and pressure.

Graded depolarization

Channel opening scales smoothly with stimulus strength.

Local, not propagating

The generator potential decays with distance from the source.

Summation matters

Repeated or stronger stimuli sum toward threshold.

Depolarization Crosses Threshold at the First Node

Voltage-gated sodium channels wait near the spike-initiation zone.

  • ≈ -55 mV: Threshold voltage (typical axon threshold)
  • ≈ -70 mV: Resting potential (before stimulus)
  • Nav1.7: Key channel (sets nociceptor excitability)
  • No spike: Below-threshold outcome (signal simply fades)

All-or-none decision

Below threshold nothing propagates; above it, a spike fires.

Nav1.7 and Nav1.8

These channel subtypes set nociceptor firing threshold.

Clinical relevance

Nav1.7 mutations cause rare pain-insensitivity syndromes.

Sodium Influx Fires the Action Potential

Voltage-gated sodium channels snap open in a self-reinforcing cascade.

  • ≈ +30 mV: Peak voltage (depolarization overshoot)
  • <1 ms: Channel kinetics (activation then inactivation)
  • K⁺ efflux: Repolarization (restores resting state)
  • All-or-none: Signal type (fixed amplitude spike)

Regenerative sodium influx

Open channels depolarize the membrane, opening more channels.

Fast inactivation

Sodium channels close automatically within a millisecond.

Potassium repolarizes

Delayed potassium efflux resets the membrane voltage.

The Signal Travels the Axon to the Spinal Cord

Fiber type sets how fast the pain message reaches the cord.

  • 5-30 m/s: A-delta speed (myelinated, sharp fast pain)
  • 0.5-2 m/s: C-fiber speed (unmyelinated, dull slow pain)
  • Saltatory: A-delta conduction (jumps between nodes)
  • Continuous: C-fiber conduction (wave creeps along membrane)

Saltatory conduction

Myelin forces current to jump node to node, speeding transit.

Unmyelinated conduction

C-fibers regenerate the spike continuously along the membrane.

Two pain sensations

Fast A-delta signals sharp pain; slow C-fibers signal dull ache.

Arrival at the cord

The spike reaches synapses in the spinal dorsal horn.

⚙ Under the hood

This simulation models the pain signaling pathway through sodium channels of nociceptors for peripheral pain, offering a detailed understanding of the mechanisms involved.

CanvasBiomedicine

2D · HTML5 Canvas 2D · 60 FPS target · runs fully client-side, no install

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