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neurons-1 · content 1 · setup format 1
What supports the explanation?
Human evidence that PIEZO2 contributes to touch and body-position sensing
Two participants with loss-of-function variants; sensory effects differed by test. Context for sensory signaling, not validation of the squid-membrane simulation.
Exact modern-convention rate and current equations
Pinned hh.mod revision 8202fe7. Our original solver uses direct rate functions, specified reversal potentials and RK4; it does not copy the optional voltage lookup table or use NEURON as a runtime.
Vesicle release, receptor binding and transmitter clearance
Institutional explanation of chemical communication. Receiver effects depend on the receiving cell; a released vesicle does not itself travel intact across the gap.
The illustrative cleft dimension has a preparation-specific comparison
Electron tomography study of adult-rat cortical/hippocampal axospinous synapses, synaptic-cleft section. Reported 20–30 nm range; 25 nm here is an illustrative choice.
PDB 2R9R biological assembly 1, A4B4, entry revision 1.2. Original structure by Long et al., Nature 2007, DOI 10.1038/nature06265. The 2.4 Å value is experimental resolution.
Deposited coordinate data may be reused with their provenance
PDB archive data are CC0. Local processed protein envelopes preserve chain/entity identities, coordinate transform and checksums; credit Long et al. and the archive.
The HH bench is one deterministic uniform squid membrane patch at 6.3°C. It cannot calculate human conduction velocity, thoughts, diagnoses, learning or disease.
The whole-cell geometry and propagation highlight are original teaching illustrations. Displayed axon length and playback speed are not measured physiological values.
The model fixes ion gradients, temperature and channel parameters. It omits stochastic channel openings, pumps, axonal cable currents, synaptic kinetics and changing concentrations.
Chemical-synapse events and the calcium-closure comparison are qualitative. They do not calculate release probability, diffusion constants, postsynaptic spike timing or a drug effect.
The 2R9R asset is a smoothed protein-coordinate envelope from biological assembly 1. Lipids, ions and small ligands are omitted. Mesh smoothing is not experimental resolution or a measured gating motion.
The paper activity has authored discrete recovery rules. Its rounds do not measure the refractory period of the HH model or a person.
A specified historical membrane experiment: The Hodgkin–Huxley bench represents one uniform squid giant-axon membrane compartment at 6.3°C. It uses the modern NEURON voltage convention, not the original paper’s resting-relative sign convention. Capacitance is 1 μF/cm²; maximum Na/K/leak conductances are 120/36/0.3 mS/cm² and reversal potentials are +50/−77/−54.3 mV.
The voltage equation: C dV/dt = Iapp − INa − IK − IL. INa = 120 m³h(V − 50), IK = 36 n⁴(V + 77), and IL = 0.3(V + 54.3). Positive ionic current is outward; positive applied current depolarizes. m is sodium activation, h is sodium availability against inactivation, and n is potassium activation. Gating variables are continuous model states, not literal moving door counts.
Equilibrium and numerical time: The exact zero-current equilibrium for these parameters is about −64.97405 mV, with gates initialized at their steady values. All four differential equations use RK4 with steps no larger than 0.005 ms, split at stimulus boundaries. Rendering speed does not change this integration. Reference traces, pulse counts, removable rate singularities and convergence are checked separately.
Counting is not triggering: A spike is counted at an upward 0 mV crossing, with its time interpolated between adjacent samples. This is a detection convention for these experiments, not the voltage at which the biological feedback begins. The solver does not change its equations at that crossing. Stronger input does not impose a proportionally taller spike.
Voltage clamp asks another question: In the optional fixed −20 mV demonstration, voltage is held constant while gates relax analytically from the resting values. Sodium conductance rises then falls; potassium conductance increases more slowly. That is a voltage-clamp response, not a freely evolving action potential. At 1 ms the computed gNa/gK are about 17.404/2.241 mS/cm²; at 5 ms they are about 1.484/13.026.
Ion channels and pumps have different roles: Fast spikes depend on channel currents and capacitance. Na/K pumps help maintain the concentration gradients, exchanging three Na outward for two K inward per cycle; they are not an instantaneous reset after every spike. This HH model holds reversal potentials fixed and has no explicit pump, changing ion concentration or spatial propagation state.
From nanometers to a whole cell: The 2R9R reference preserves a static biological assembly of four engineered Kv1.2–Kv2.1 channel subunits with four beta subunits. It is a rat-derived molecular example, not the molecular identity of the squid model’s potassium current. The synapse uses an illustrative 25 nm cleft, within the 20–30 nm range reported for the cited adult-rat synapses. The cell illustration and membrane icons use separate, unmeasured display scales.
What has been checked
Analytical reference cases, conservation or transition invariants, finite drawing commands, bounded setup parsing, discovery and route integrity are checked automatically. These checks do not establish anatomical fidelity, learner outcomes or browser/device compatibility. Independent subject review, learner trials, comprehensive accessibility review and browser video encoding checks remain pending.
Each source supports the associated claim. Sources do not certify this implementation or its visuals.
About the cover illustration
Original offline rendering of the lesson’s illustrative neuron geometry. Cell shape, scale and teaching colors are authored representations. The independently sourced potassium-channel structure and electrical model have separate provenance; the cover is not a microscopy image.