Table of Contents
Membrane Excitability in Animal Cells
Animal cells differ in how strongly they can respond electrically to stimuli. A small group of cell types is excitable in the strict sense: their membrane can generate rapid, all‑or‑none action potentials (e.g. neurons, skeletal and cardiac muscle cells, some endocrine cells). Many other animal cells are only weakly excitable and respond with small, graded potential changes.
In this chapter, the focus is on what makes animal cells excitable, and how this differs between main excitable cell types.
Excitable vs. Non‑Excitable Animal Cells
All animal cells have a resting membrane potential, but:
- Non‑excitable cells (e.g. many epithelial cells, fibroblasts):
- Show small, slow changes in membrane potential.
- Do not generate self‑propagating action potentials.
- Mainly use electrical properties to drive transport (e.g. ion uptake) and cell volume regulation.
- Excitable cells (neurons, muscle fibers, some gland cells):
- Express high densities of voltage‑gated ion channels.
- Can amplify a local stimulus into a large, rapid action potential.
- Use electrical signals for information transmission (neurons), contraction (muscle), or secretion (endocrine cells).
The key difference, therefore, is not the existence of a membrane potential, but the equipment with specific gated ion channels and their organization.
Ion Channels as the Basis of Excitability
Excitability depends on specialized membrane proteins that selectively conduct ions and change their state in response to signals.
Types of Ion Channels in Animal Cells
Three major functional classes are central for excitability:
- Leak channels
- Always (or mostly) open.
- Set and stabilize the resting membrane potential, often with strong selectivity for $K^+$.
- Present in virtually all cells.
- Gated ion channels
- Open or close in response to specific signals:
- Voltage‑gated (respond to changes in membrane potential).
- Ligand‑gated (opened by binding of neurotransmitters or intracellular messengers).
- Mechanically gated (opened by stretch, pressure, vibration).
- Densely expressed in excitable cells.
- Their rapid, regulated opening creates steep, transient ion currents.
- Ion pumps and exchangers
- Use metabolic energy (often ATP) to maintain ion gradients.
- Do not directly generate fast excitatory events, but are essential to maintain the ionic conditions that make excitability possible.
Voltage‑Gated Channels and Action Potentials
The core of membrane excitability is the presence of voltage‑gated $Na^+$ and $K^+$ channels (and in some cells, $Ca^{2+}$ channels):
- Voltage‑gated $Na^+$ channels
- Open rapidly when the membrane depolarizes above a threshold.
- Allow a large inward $Na^+$ current that further depolarizes the membrane.
- Inactivate automatically after a few milliseconds.
- Voltage‑gated $K^+$ channels
- Open more slowly during depolarization.
- Allow outward $K^+$ current, repolarizing (and often hyperpolarizing) the membrane.
- Voltage‑gated $Ca^{2+}$ channels
- Present in many excitable cells.
- Often contribute to slower or plateau‑type depolarizations.
- Couple electrical activity to secretion or contraction (e.g. at synaptic terminals, in smooth and cardiac muscle).
The specific combination and kinetics of these channels shape the form of the action potential in different cell types.
Excitability and Threshold
A defining feature of excitable animal cells is the existence of a threshold:
- Subthreshold stimuli:
- Produce small, graded depolarizations.
- Are insufficient to open enough voltage‑gated $Na^+$ (or $Ca^{2+}$) channels to trigger a self‑sustaining response.
- Threshold (or suprathreshold) stimuli:
- Open sufficient voltage‑gated channels so that positive feedback occurs:
- Depolarization → more channels open → more depolarization.
- Result in an all‑or‑none action potential.
This threshold behavior is a hallmark of excitable animal cells and is critical for reliable signaling: weak noise is ignored, proper stimuli trigger full‑size responses.
Refractory Periods in Animal Cells
Excitable membranes show time‑dependent limitations on how frequently they can fire:
- Absolute refractory period
- Immediately after an action potential.
- Voltage‑gated $Na^+$ channels are inactivated and cannot reopen.
- No new action potential can be triggered, regardless of stimulus strength.
- Relative refractory period
- Follows the absolute refractory period.
- Some channels have recovered, but $K^+$ conductance is still elevated and the membrane is hyperpolarized.
- A stronger‑than‑normal stimulus is needed to reach threshold.
Refractory periods:
- Limit the maximum firing frequency.
- Enforce unidirectional propagation along axons.
- Influence patterns of muscle contraction (e.g. no tetanus in normal cardiac muscle).
Ion Channels and Conduction Velocity
The speed at which excitation travels along an excitable cell depends on:
- Membrane properties
- Higher membrane resistance and lower capacitance favor faster spread.
- Myelin (in vertebrate axons) alters these properties, but its structural details belong elsewhere.
- Axon or fiber diameter
- Larger diameter → lower internal resistance → faster conduction.
- Many invertebrates use giant axons to increase conduction speed.
- Distribution of voltage‑gated channels
- Dense clustering at specific membrane regions (e.g. at nodes in myelinated axons, at neuromuscular junctions) enhances efficient conduction and responsiveness.
Although conduction mechanisms are treated in detail in a separate chapter, all these features depend on the underlying excitability of the membrane.
Excitability in Different Animal Cell Types
Neurons
Neurons are the primary information‑processing cells:
- High density of voltage‑gated $Na^+$ and $K^+$ channels along axons.
- Integrate synaptic (chemical or electrical) inputs at dendrites and soma.
- Generate action potentials typically at a specialized region (e.g. axon hillock in vertebrates).
- Frequency and pattern of action potentials encode information.
Special features:
- Many neurons express voltage‑gated $Ca^{2+}$ channels at terminals, coupling electrical signals to neurotransmitter release.
- Some neurons are intrinsically pacemaking: their ion channel composition causes rhythmic spontaneous firing without external stimuli.
Skeletal Muscle Fibers
Skeletal muscle cells convert electrical excitation into mechanical contraction:
- Receive excitation via neuromuscular junctions.
- Depolarization triggers an action potential that propagates along the sarcolemma and into T‑tubules.
- Excitability is tuned for:
- Reliable activation by motor neurons.
- Rapid activation and relaxation of contraction.
Compared to neurons, skeletal muscle:
- Has a larger cell diameter.
- Uses action potentials primarily to control intracellular calcium release from specialized stores, not to transmit information over long distances.
Cardiac Muscle Cells
Cardiomyocytes have specialized excitability properties:
- Express distinct sets of voltage‑gated $Na^+$, $Ca^{2+}$, and $K^+$ channels.
- Many ventricular muscle cells show a prolonged plateau phase of the action potential, mainly due to sustained $Ca^{2+}$ influx.
- Have a long refractory period, preventing rapid re‑excitation and tetanic contraction.
Some cardiac cells (e.g. in the sinoatrial node):
- Are pacemaker cells.
- Exhibit spontaneous, rhythmic depolarizations due to special ion currents, setting the heart rhythm.
Smooth Muscle Cells
Smooth muscle shows diverse excitability patterns:
- Often rely more on $Ca^{2+}$‑based action potentials or graded potentials than on classic $Na^+$ spikes.
- Can be:
- Single‑unit (visceral): electrically coupled via gap junctions, contracting as a coordinated sheet.
- Multi‑unit: each fiber more independently controlled by nerves.
Stimuli for excitation include:
- Autonomic nerve input.
- Hormones and local mediators.
- Mechanical stretch.
Excitability here is closely linked to tonic or phasic contractile behavior, adapted to organ function (e.g. blood vessels vs. intestine).
Endocrine and Other Secretory Cells
Some gland cells use excitability to control secretory output:
- Action potentials or large depolarizations open voltage‑gated $Ca^{2+}$ channels.
- Elevated intracellular $Ca^{2+}$ triggers exocytosis of hormones or other products.
- Patterns of excitability (bursts, oscillations) regulate the amount and timing of secretion.
Examples include pancreatic beta cells and certain hypothalamic neurons with endocrine function.
Modulation of Excitability
Excitability is not fixed; it is highly modifiable:
- Chemical modulators (neurotransmitters, hormones, local mediators) can:
- Change the probability of ion channel opening.
- Alter threshold, firing frequency, or refractory periods.
- Ionic composition of extracellular fluid (e.g. $K^+$, $Ca^{2+}$ concentrations) strongly influences:
- Resting potential.
- Distance to threshold.
- Drugs and toxins may:
- Block channels (e.g. some anesthetics, tetrodotoxin blocking $Na^+$ channels).
- Keep channels open or inactive, severely altering excitability.
These modulatory influences underlie many physiological regulation mechanisms and many pathological states (e.g. arrhythmias, seizures, muscle weakness).
Functional Significance in Animals
In animal organisms, excitability enables:
- Rapid long‑distance communication (neurons, nerve nets, CNS).
- Coordinated movement and posture (skeletal, cardiac, smooth muscle).
- Precise control of secretion (endocrine and exocrine cells).
- Integration of sensory information and motor responses, forming the basis of behavior.
Thus, the particular combination and regulation of ion channels in animal cells make possible the complex and adaptable electrical signaling that characterizes animal life.