The twitching or “dancing” of a frog’s severed leg, often triggered by salt, is a phenomenon rooted entirely in biology. This movement is not a sign of life but a physiological reflex known as post-mortem excitability. The underlying cause is the delayed shutdown of the nervous and muscular systems, which retain the cellular machinery needed to respond to a stimulus for a brief time after the central nervous system has ceased to function.
Residual Nerve Activity
The initial impulse for movement lies in the residual electrical potential stored within the nervous system. Even after the brain is dead, the peripheral nerves and the spinal cord’s reflex arcs can remain viable. Simple reflex actions are organized at the spinal cord level and bypass the brain entirely.
The local electrical signals within these peripheral pathways do not immediately dissipate. This allows nerve fibers to propagate an electrical impulse when externally stimulated. Since nerves and muscles remain connected, a locally generated signal travels down the axon to the muscle fiber, triggering contraction.
The Cellular Mechanism of Contraction
Movement requires an electrochemical process within the muscle cells. Contraction occurs through the sliding filament theory, involving the interaction of actin and myosin proteins. The muscle cell membrane (sarcolemma) maintains an electrical gradient by controlling the concentration of ions like sodium (\(Na^+\)) and potassium (\(K^+\)).
An electrical impulse (action potential) causes a sudden influx of sodium ions, depolarizing the muscle cell membrane. This triggers the release of stored calcium ions (\(Ca^{2+}\)) from the sarcoplasmic reticulum. The calcium ions then bind to regulatory proteins on the actin filaments, allowing the myosin heads to attach.
Once exposed, the myosin heads form cross-bridges with the actin filaments, pulling them inward and causing the muscle fiber to shorten (contraction). This process relies on the availability of necessary ions and the structural integrity of the muscle proteins. This local chemical activity can continue without a signal from the brain, provided the cellular components are functional.
Why External Stimuli Cause Movement
Post-mortem movement occurs when an external factor, such as a probe or table salt (sodium chloride), is applied to exposed muscle or nerve tissue. These stimuli disrupt the ionic balance of the cell membrane chemically or electrically. Salt, dissolved by tissue moisture, releases a high concentration of sodium ions directly onto the cells.
This sudden influx of sodium ions overwhelms the cell’s resting potential, forcing a depolarization that mimics a natural nerve impulse. The resulting action potential travels to the muscle fiber, causing rapid contraction. Similarly, a small electrical current instantly triggers the same depolarization. The movement is a forced response to an unnatural stimulus that bypasses the need for a functioning central nervous system.
When the Movement Stops
The period of post-mortem excitability ends when cells exhaust the required resources. The primary limitation is the depletion of adenosine triphosphate (ATP), the cell’s energy currency. ATP fuels the power stroke of the myosin heads during contraction and actively pumps calcium ions back into storage, which is necessary for muscle relaxation.
When ATP reserves are consumed, the myosin heads remain locked onto the actin filaments because there is no energy to detach the cross-bridges. This sustained state of contraction is known as rigor mortis. As cell membranes and internal structures break down, the ability to maintain ion gradients is lost, meaning the tissue can no longer generate an electrical impulse, and movement ceases.