Neurons are the fundamental communicators within the nervous system, transmitting vital information via electrical signals. When a neuron receives input, it generates an electrical response, known as a nerve impulse. Understanding how these impulses are generated and how their characteristics change with varying stimulus strengths is central to comprehending nervous system function. This process involves electrical charges and specialized protein channels within the neuron’s axon, the long projection that carries signals away from the cell body.
The Axon’s Resting State and Initial Reactions
An axon, when not actively transmitting a signal, maintains a baseline electrical state known as its resting membrane potential. This state is characterized by a negative charge inside the axon compared to the outside, typically around -70 millivolts (mV). This charge difference is established by an uneven distribution of ions, with a higher concentration of sodium ions outside the cell and potassium ions inside. This is maintained by the sodium-potassium pump and selective ion channels. More potassium “leak” channels are open at rest than sodium channels, allowing potassium to diffuse out more readily, contributing to the internal negativity.
When a weak stimulus reaches the axon, it causes small, localized electrical changes called graded potentials. These responses are proportional to the stimulus strength; a stronger stimulus produces a larger graded potential. However, these potentials are temporary and dissipate quickly from their point of origin.
Reaching the Firing Point: The Threshold
For a nerve impulse to be generated, the electrical change caused by a stimulus must reach a specific critical level called the threshold potential. This threshold, typically around -55 mV to -50 mV, is a notable depolarization from the resting state. This voltage level is most readily achieved at the axon hillock, where the axon originates.
Once the membrane potential at the axon hillock reaches this threshold, it triggers a rapid opening of voltage-gated sodium channels. This influx of positively charged sodium ions causes a swift reversal of the membrane potential, marking the beginning of a full nerve impulse. Graded potentials can summate to reach this critical threshold, pushing the axon to its firing point.
The Unchanging Signal: All-or-None Response
Once the threshold potential is reached, the axon generates an electrical signal known as an action potential, which operates on an “all-or-none” principle. This means if the stimulus reaches threshold, a full-strength action potential is produced; if it falls short, no action potential occurs.
Initially, voltage-gated sodium channels open, allowing a swift influx of sodium ions that causes the membrane potential to rapidly depolarize and become positive, reaching a peak around +30 mV. Following this rapid depolarization, the sodium channels inactivate, and voltage-gated potassium channels open more slowly, allowing potassium ions to flow out of the axon. This outward movement of positive charge repolarizes the membrane, bringing its potential back towards the resting state.
The potassium channels often remain open for a brief period longer than necessary, causing a slight overshoot where the membrane potential becomes even more negative than the resting potential, a phase known as hyperpolarization, before returning to rest. The amplitude of an individual action potential is consistent for a given axon, regardless of how much the stimulus strength exceeds the threshold.
Communicating Intensity: Frequency Modulation
Since individual action potentials are all of the same amplitude, the nervous system conveys stimulus intensity through frequency modulation. Stronger stimuli are encoded by an increase in the frequency, or rate, at which action potentials are generated by the axon. For example, a light touch might trigger a few action potentials, while firm pressure would elicit a rapid burst of many action potentials.
The ability of an axon to fire repeatedly is influenced by periods known as refractory periods. Immediately after an action potential, there is an absolute refractory period during which the axon cannot generate another action potential, because voltage-gated sodium channels are temporarily inactivated.
Following this, during the relative refractory period, a stronger-than-normal stimulus is required to trigger another action potential because the membrane is often hyperpolarized. These refractory periods limit the maximum firing rate of an axon, regulating how much intensity information can be conveyed.