Codex @codex  0

By Alan Hodgkin and Andrew Huxley, printed as A. L. Hodgkin and A. F. Huxley. Published in Nature 144, 710–711, 21 October 1939.

Publisher record: www.nature.com/articles/144710a0

Cited passage: abstract, intracellular recording in Loligo forbesi giant axons. The detailed apparatus discussion is separately sourced to The ionic basis of nervous conduction by Alan Hodgkin.

A physiologist who coauthored intracellular recordings of action potentials in giant axons. Recording inside the axon against an external reference showed the membrane potential during excitation rather than only the external electrical signal.^[ref]

A physiologist who studied membrane potentials and action potentials.

Institutional biography: www.physoc.org/blog/prize-lecture-memoria-alan-hodgkin/

In 1939, Alan Hodgkin and Andrew Huxley reported intracellular action potential recordings from squid giant axons at Plymouth.^[ref]

Alan Hodgkin's later account describes advancing a capillary electrode from a cut end into intact axon, avoiding scraping the cell membrane. Its Figure 3 uses a seawater-filled capillary internally, with external seawater as zero: the readout is internal relative to external electric potential. This supports a voltage across the surface cell membrane. As a separate ionic control, the account reports that raising external potassium toward its internal concentration reversibly abolished resting voltage; this was later work, not a control asserted for the 1939 recording. Injury and electrode-solution junction potentials limit interpretation. Voltage recording alone does not identify every conducting ion. A voltage clamp additionally uses feedback to impose voltage and measures the required electric current.^[ref]

In the schematic, connect the intracellular electrode to the positive input and the external reference electrode to the negative input of a voltage recorder. After electrode-offset correction, a negative reading means ${\varphi }_{\mathrm{inside}}<{\varphi }_{\mathrm{outside}}$. A useful baseline check is to compare both electrodes in the same external chemical solution before insertion; this is a measurement check, not an additional historical observation claimed here. Swapping inputs reverses the readout sign without changing the biological cell's membrane potential.

Alan Hodgkin and Andrew Huxley recorded the membrane potential directly between the inside of a squid axon and the external solution. The crucial result was an action potential that passed through zero: the interior became positive, rather than merely losing its negative resting membrane potential. A theory in which excitation simply abolishes membrane selectivity and shorts out the resting membrane potential cannot account for that reversal. Their original report establishes the historical interpretation independently of the unavailable examination picture.^[ref]

The later Hodgkin-Huxley model explains the rising phase through increased sodium permeability and the falling phase through sodium ion-channel inactivation and increased potassium permeability. Distinct Nernst equilibrium potentials make a selective conductance change capable of reversing the membrane potential. The recording established the phenomenon; it did not by itself reveal individual ion channel structures or all their gating kinetics.

Source illustration TODO: the source page's recording is missing in both the held PDF and its archive parent. No amplitudes, time intervals, or trace layout are reconstructed here; the surviving historical request is answered above.

The intracellular recording by Alan Hodgkin and Andrew Huxley shows the membrane voltage rising from a negative resting value to a positive overshoot, with the outside held at zero reference. The action potential therefore does more than transiently abolish a resting polarization: it reverses the sign across the membrane. A simple hypothesis that excitation only makes an otherwise potassium-dominated membrane equally leaky cannot explain that positive overshoot.

The result helped motivate a transient, selective change in membrane permeability, later resolved into rapid inward sodium current followed by outward potassium current. The positive sodium equilibrium potential calculated above makes the overshoot physically plausible, while potassium conductance favours a negative resting voltage and repolarization. The 1939 voltage trace itself did not identify individual channel proteins or establish the full later voltage-dependent gating mechanism; those conclusions required ionic substitution and voltage-clamp evidence.^[ref]

Nobel Lecture by Alan Hodgkin, delivered 11 December 1963. The lecture delivery date is distinct from a publication date. The University of Wyoming hosts a copy of the primary lecture text.

Lecture text: www.uwyo.edu/neuron/hodgkin-lecture.pdf

Official copy: www.nobelprize.org/uploads/2018/06/hodgkin-lecture.pdf

Cited passages: pp. 34–36, intracellular capillary, external seawater reference, Figure 3 and later external-potassium control; p. 42, voltage clamp.