Andrew Fielding Huxley discovered muscle contraction, nerve functions

Andrew Fielding Huxley – discoverer of nerve action potentials

Category : Personalities
Published by : Data Research Analyst, Worldofchemicals.com

Biography& Contributions

Andrew Fielding Huxley was a physiologist, biophysicist and Nobel Prize laureate born in Hampstead, London, on November 22, 1917 – died on May 30, 2012. Huxley won the 1963 Nobel Prize in Physiology or Medicine. His researches centred on nerve and muscle fibres and dealt particularly with the chemical phenomena involved in the transmission of nerve impulses.

Huxley and Hodgkin’s researches were concerned largely with studying the exchange of sodium and potassium ions that causes a brief reversal in a nerve cell’s electrical polarization; this phenomenon, known as an action potential, results in the transmission of an impulse along a nerve fibre. Huxley made contributions of fundamental importance to knowledge of the process of contraction by a muscle fibre.

The findings in nerve prompted a cascade of important discoveries whose implications range from the fundamentals of channel function, through their application to excitable tissues generally, to their translation to understanding the basic mechanisms of disease. Firstly, of those concerning sodium channel properties and function itself, the voltage dependence of the sodium conductance and its rate constants led Hodgkin and Huxley to predict that channel opening and closing would involve net transfers of intramembrane charge in response to alterations in the trans-membrane electric field.

In the 1950s Huxley began working on muscle contraction. Huxley and Hodgkin measured voltages and ion fluxes in and out of single nerve cells, and finally deduced the events by which a signal is propagated along a nerve. Huxley has also developed a microtome for electron microscope sections, and a micromanipulator.

Huxley’s final interest concerned the cross bridge interactions mediating the cross bridge sliding itself accompanied by ATP breakdown (Huxley, 1957b). Cytsolic Ca2+ elevation then initiates cyclic reactions between projections on the myosin filaments and active sites on the actin filaments in the form of cross bridge formation and configurational change that drives a filament sliding and ATP breakdown. Huxley’s 1974 model explained the resulting tension transients in terms of elastic and step-wise shortening elements driven by an actin-myosin binding through a sequence of attachment sites reflecting increasing strengths of interaction

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