Nervous System Physiology

Overview

The Human Nervous System and Human Sensory Organs anatomy pages cover neuron and receptor structure; this page covers the electrochemical mechanism that makes that structure function — how a neuron generates and propagates an electrical signal, how it passes that signal to the next cell, and how a sensory receptor converts a physical stimulus into that same electrical language in the first place.

Key Concepts

The Resting Membrane Potential

Every neuron maintains a resting membrane potential (~-70 mV, inside negative relative to outside), generated by two structural features working together: the Na⁺/K⁺-ATPase pump (actively exports 3 Na⁺ for every 2 K⁺ imported, using ATP, establishing steep concentration gradients — high extracellular Na⁺, high intracellular K⁺) and a much higher density of K⁺ leak channels than Na⁺ leak channels in the resting membrane, making the membrane far more permeable to K⁺ than Na⁺ at rest. Because K⁺ can cross far more easily, the membrane potential sits much closer to K⁺’s own equilibrium potential (the voltage at which K⁺’s concentration gradient exactly balances the electrical gradient pulling it back in) than to Na⁺’s — this, not the pump’s charge asymmetry directly, is the primary reason the resting potential is negative and close to -70 to -90 mV rather than near zero.

Source: Biology LibreTexts

The Action Potential

A stimulus that depolarizes the membrane to threshold (~-55 mV) triggers a stereotyped, self-propagating, all-or-none electrical event via voltage-gated channels that open and close in a fixed sequence:

    graph LR;
    A["Depolarization to threshold"] --> B["Voltage-gated Na+ channels open (fast)"];
    B --> C["Rapid depolarization (Na+ influx), peak ~+30mV"];
    C --> D["Voltage-gated Na+ channels inactivate; Voltage-gated K+ channels open (slower)"];
    D --> E["Repolarization (K+ efflux)"];
    E --> F["Hyperpolarization (K+ channels slow to close)"];
    F --> G["Na+/K+ pump + leak channels restore resting potential"];
  

Source: Guyton and Hall, Textbook of Medical Physiology (Fig. 5-6)

Source: Guyton and Hall, Textbook of Medical Physiology (Fig. 5-7)

Source: Guyton and Hall, Textbook of Medical Physiology (Fig. 5-9)

Two refractory periods follow directly from this channel sequence, not from a separate mechanism: the absolute refractory period (a second action potential cannot be triggered no matter how strong the stimulus, because voltage-gated Na⁺ channels are inactivated, not merely closed, and cannot reopen until the membrane repolarizes) and the relative refractory period (a stronger-than-normal stimulus can trigger another action potential during the hyperpolarization phase, since the membrane is further from threshold than at rest). The absolute refractory period is also what enforces unidirectional propagation down an axon — the region just behind an advancing action potential is refractory, so the depolarization wave cannot reverse back on itself.

Because the action potential is all-or-none (a fixed amplitude, not graded), the nervous system encodes stimulus intensity as firing frequency (rate coding) rather than as the size of any individual signal — a strong stimulus produces a higher frequency of identical action potentials, not a larger one.

Propagation and Myelination

Action potentials propagate by local circuit currents: depolarization at one membrane patch passively spreads to (and threshold-depolarizes) the immediately adjacent patch, regenerating the full action potential there in turn. In myelinated axons (see Human Nervous System for oligodendrocyte/Schwann cell structure), the myelin sheath insulates the membrane between nodes of Ranvier, so voltage-gated channels are only present (and the action potential only actually regenerated) at these nodes — the depolarization jumps electrically from node to node (saltatory conduction, “saltatory” from the Latin for “leaping”), which is both faster (the passive electrotonic spread between nodes is faster than sequential channel-by-channel regeneration) and more energy-efficient (the Na⁺/K⁺ pump only has to restore ion gradients at the nodes, not along the entire membrane length) than continuous conduction in an unmyelinated axon.

Source: © 2012 Encyclopaedia Britannica, Inc. — explicit copyright notice visible in the image itself. This is a confirmed commercial copyright, not merely an unconfirmed license — must not go on the public site without a license or replacement.

Chemical Synaptic Transmission

At a chemical synapse, an arriving presynaptic action potential depolarizes the axon terminal, opening voltage-gated Ca²⁺ channels; Ca²⁺ influx triggers synaptic vesicles (pre-loaded with neurotransmitter) to fuse with the presynaptic membrane and release their contents by exocytosis into the synaptic cleft. Neurotransmitter diffuses across the cleft and binds postsynaptic receptors, which fall into two mechanistic classes exactly paralleling the two hormone-receptor classes on the Endocrine System Physiology page: ionotropic receptors (the receptor is itself a ligand-gated ion channel — binding directly opens the channel, fast, brief) and metabotropic receptors (G-protein-coupled, triggering a second-messenger cascade — slower, more prolonged, can modulate rather than directly gate an ion flow).

Source: Lumen Learning (courses.lumenlearning.com)

Binding produces either an excitatory postsynaptic potential (EPSP) (typically a channel admitting Na⁺, depolarizing the postsynaptic membrane toward threshold) or an inhibitory postsynaptic potential (IPSP) (typically a channel admitting Cl⁻ or releasing K⁺, hyperpolarizing the membrane away from threshold). A single EPSP is usually too small to reach threshold alone; postsynaptic summation — temporal (repeated EPSPs from one presynaptic neuron firing rapidly, overlapping before decaying) and spatial (simultaneous EPSPs from multiple different presynaptic neurons converging on the same postsynaptic cell) — combines many subthreshold inputs, with IPSPs subtracting from the same running total, so whether the postsynaptic neuron fires at all is a real-time net computation over all its synaptic inputs, not a response to any single one.

Sensory Transduction

Every sensory receptor performs the same fundamental task regardless of stimulus type — converting a physical or chemical stimulus into a graded change in membrane potential (a receptor potential) — via a modality-specific transduction mechanism:

• Photoreceptors (rods/cones) — in darkness, rod photoreceptors are held in a partially depolarized state by cGMP-gated Na⁺ channels held open by cGMP, causing continuous neurotransmitter release onto the bipolar cell. Light striking the visual pigment rhodopsin (opsin + the light-absorbing chromophore retinal) isomerizes retinal, activating a G-protein cascade (transducin) that ultimately lowers cGMP, closing the Na⁺ channels, hyperpolarizing the cell, and reducing neurotransmitter release — photoreceptors are unusual in being inhibited, not excited, by their adequate stimulus.

Source: Dee Unglaub Silverthorn, Human Physiology: An Integrated Approach (Fig. 10.32)

• Mechanoreceptors (cochlear hair cells) — sound-induced fluid displacement in the cochlea (see Human Sensory Organs for structure) bends the hair cell’s stereocilia, mechanically stretching tip-link protein filaments that directly pull open mechanically-gated cation channels, depolarizing the cell — a direct mechanical-to-electrical transduction with no second-messenger step, among the fastest of all sensory transduction mechanisms.

Source: Dee Unglaub Silverthorn, Human Physiology: An Integrated Approach (Fig. 10.19)

• Chemoreceptors (olfactory/taste) — an odorant or tastant molecule binds a surface G-protein-coupled receptor, triggering a second-messenger cascade (paralleling metabotropic synaptic receptors above) that opens cation channels and depolarizes the receptor cell — mechanistically closer to hormone/metabotropic signaling than to the direct mechanical gating of hair cells.

The Reflex Arc

A reflex arc is the minimal circuit producing a rapid, stereotyped, involuntary motor response to a stimulus, bypassing (though not necessarily excluding) conscious cortical processing: receptor → sensory (afferent) neuron → integration in the CNS (in a simple spinal reflex, often a single synapse directly onto a motor neuron — a monosynaptic reflex, e.g. the patellar/knee-jerk reflex — or via one or more interneurons in a polysynaptic reflex) → motor (efferent) neuron → effector (muscle or gland). The speed advantage of a monosynaptic reflex over any voluntary response is structural: fewer synapses means less cumulative synaptic delay (each chemical synapse imposes a delay on the order of 1 ms for vesicle release and diffusion) before the effector is reached.

Source: Dee Unglaub Silverthorn, Human Physiology: An Integrated Approach (Fig. 13.5)

Source: Dee Unglaub Silverthorn, Human Physiology: An Integrated Approach (Fig. 13.6)

Comparative Structures

Common Exam Questions

• “Explain why the resting membrane potential is closer to the K⁺ equilibrium potential than the Na⁺ equilibrium potential, referencing relative channel permeability rather than the Na⁺/K⁺ pump alone.”
• “Explain the ionic basis of the absolute refractory period and why it enforces unidirectional action potential propagation.”
• “Explain why saltatory conduction is faster and more energy-efficient than continuous conduction, referencing the distribution of voltage-gated channels along a myelinated axon.”
• “Distinguish temporal from spatial summation, and explain how EPSPs and IPSPs interact at a postsynaptic neuron receiving both simultaneously.”
• “Explain why light causes photoreceptor hyperpolarization rather than depolarization, tracing the full transduction cascade.”
• “Explain, in terms of synaptic delay, why a monosynaptic reflex is faster than a voluntary motor response to the same stimulus.”

Visual Reference

Interactive

• Action potential voltage-clamp simulator (Plotly) — a graph of membrane voltage vs. time with individually toggleable Na⁺ and K⁺ conductance traces plotted alongside; scrubbing a time marker shows exactly which channels are open/closed/inactivated at each phase, directly tying the voltage trace to the underlying channel states rather than requiring students to memorize the phases as a list.

• Synaptic summation sandbox (SVG/JS) — a postsynaptic neuron receiving adjustable EPSP/IPSP inputs (number, timing, and excitatory/inhibitory identity all adjustable via sliders/toggles), with a live running membrane-potential trace showing whether the combined input crosses threshold — makes summation a manipulable, testable idea rather than a static diagram.

Static (placed inline in Key Concepts above, next to the concept each one illustrates, rather than collected here)

Practice Problems

1. Explain why an action potential cannot be triggered during the absolute refractory period even by a very strong stimulus.
2. A neuron receives five subthreshold EPSPs in rapid succession from the same presynaptic terminal. Name this phenomenon and explain why it can bring the postsynaptic membrane to threshold when no single EPSP could.
3. Explain why myelin loss (as in demyelinating disease) slows nerve conduction, referencing the distribution of voltage-gated channels.
4. Trace the phototransduction cascade from a photon striking rhodopsin to a change in neurotransmitter release, explaining why the net effect is a decrease rather than increase in release.
5. Diagram a monosynaptic reflex arc for the patellar reflex, labeling each of the five components and explaining why this arc is faster than an equivalent voluntary movement.