Chapter 1 – The Neuron

Figure 1.1

This diagram shows the complete structure of a typical neuron with all major components labeled. Dendrites branch from the cell body in multiple directions, providing extensive surface area for receiving inputs from other neurons. The cell body contains the nucleus and is the metabolic center of the neuron. The axon hillock is labeled at the junction where the cell body transitions into the axon. The axon extends as a single long projection and is covered with myelin segments (shown in gray), with the final segment terminating in the presynaptic terminal. This comprehensive view illustrates how all neuronal components work together: dendrites receive information, the cell body integrates signals, the axon conducts electrical signals, and the presynaptic terminal releases neurotransmitters to communicate with other cells.

Figure 1.2

This diagram highlights the dendritic structure of a neuron, with dendrites shown in green branching from the cell body in a tree-like pattern. The dendrites are labeled and an inset box provides a magnified view of dendritic spines. The inset shows a section of dendrite with small protrusions extending from the dendritic shaft, labeled as “Dendritic Spines.” These spines appear as small knob-like or mushroom-shaped structures projecting from the dendrite surface. Dendritic spines are important sites of synaptic contact and help increase the surface area available for receiving synaptic inputs from other neurons. The main neuron structure shows the typical organization with the dendritic tree, cell body, and myelinated axon.

Figure 1.3

This diagram shows the internal structure of a neuronal cell body (soma) with detailed organelles. The cell body is highlighted in green with an inset box showing the major cellular organelles. The nucleus appears as a large blue oval structure containing the cell’s DNA. Surrounding the nucleus are various organelles including mitochondria (shown as red oval structures), rough endoplasmic reticulum (shown as layered membrane structures), smooth endoplasmic reticulum, and the Golgi apparatus (shown as stacked membrane structures). These organelles are responsible for essential cellular functions including protein synthesis, cellular respiration, and molecular packaging. The neuron also shows typical dendrites and a myelinated axon extending from the cell body.

Figure 1.4

This diagram illustrates the basic structure of a neuron with emphasis on the axon. The neuron shows dendrites extending from the cell body, and a long axon projecting from the axon hillock (labeled at the junction between cell body and axon). The axon extends to the right and is covered with myelin segments (shown in green). The axon hillock is specifically highlighted as the region where the cell body transitions into the axon, which is the site where action potentials are typically initiated. This figure demonstrates the fundamental organization of the axon as a single, long projection that begins at the axon hillock and can extend great distances to reach target cells.

Animation 1.1

An animation showing the propagation of an action potential down a neuron axon. The animation begins with a cross-sectional view of an axon at rest, displaying a membrane potential of -65 mV on a voltage indicator. The action potential initiates at the axon hillock (the junction between cell body and axon) as a wave of depolarization. As the wave progresses, the voltage indicator shows the membrane potential rapidly rising from -65 mV to approximately +40 mV (the peak), then quickly falling back below the resting potential to about -80 mV (undershoot), before returning to -65 mV. This electrical wave travels sequentially down the length of the axon, depicted as a moving zone of membrane potential change. The axon is shown with myelin sheaths (white insulating segments) and Nodes of Ranvier (gaps between myelin), where the action potential appears to “jump” from node to node in saltatory conduction. When the action potential reaches the presynaptic terminal at the end of the axon, small vesicles are shown releasing neurotransmitter molecules into the synaptic cleft.

Figure 1.5

This diagram shows the structure of a myelinated axon with detailed labeling of myelin and Nodes of Ranvier. The neuron displays typical morphology with dendrites, cell body, and a long axon extending to the right. The axon is covered with segments of myelin sheath (shown in green) with gaps between them labeled as “Nodes of Ranvier.” The myelin appears as discrete segments wrapped around portions of the axon, while the nodes are the uncovered regions of axonal membrane between myelin segments. This structure is essential for saltatory conduction, where action potentials jump from node to node, significantly increasing conduction speed compared to unmyelinated axons.

Figure 1.6

This anatomical diagram illustrates the dramatic variation in axon length using a human body outline. The figure shows a side view of a human silhouette with the brain and spinal cord highlighted. Two types of neurons are contrasted: a short axon interneuron within the spinal cord (shown in an inset box of the spinal cord cross-section) and a long axon that extends from the spinal cord down to the foot. The long axon represents sensory or motor neurons that must travel the entire length of the leg to reach peripheral targets like the toe, demonstrating how axon length is directly related to the distance the neuron must span to connect its input and output regions.

Figure 1.7

This diagram demonstrates the relationship between axon diameter, myelination, and action potential propagation speed. The main neuron shows a typical structure with dendrites, cell body, and axon. An inset box in the upper right displays four cross-sectional views of axons arranged from fastest to slowest conduction speed. The fastest axon (leftmost) shows a large diameter with thick myelin wrapping (multiple concentric circles around a green center). Moving rightward, the axons become progressively smaller in diameter with thinner myelin sheaths, and the rightmost axon shows a very small diameter with no myelin. This illustrates how larger diameter axons with thicker myelin sheaths conduct action potentials faster than smaller, unmyelinated axons.

Figure 1.8

This simplified diagram shows the basic synaptic contact between two neurons. A presynaptic cell is shown on the left making synaptic contact with a postsynaptic cell on the right. The postsynaptic neuron displays typical neuronal features including dendrites, cell body, and a myelinated axon with gray myelin segments. The synapse is highlighted with green coloring at the contact point, emphasizing where the presynaptic terminal forms synaptic connections with the postsynaptic cell membrane. This illustrates the fundamental principle of neuronal communication through synaptic contacts.

Figure 1.9

This diagram illustrates the synaptic relationship between neurons, showing a presynaptic cell and postsynaptic cell. The presynaptic neuron is shown on the left with its axon terminal (highlighted in green) making synaptic contact with the dendrites and cell body of the postsynaptic neuron on the right. The presynaptic terminal contains small green structures representing synaptic vesicles or neurotransmitter release sites. The postsynaptic neuron shows typical neuronal morphology with branching dendrites and a myelinated axon (shown with gray myelin segments). This illustrates the directional nature of synaptic transmission, where the presynaptic cell releases neurotransmitters that act upon the postsynaptic cell.

Figure 1.10

This diagram shows different types of neuron structures illustrating the variability in neuronal morphology. The top row displays two examples: on the left, a multipolar neuron with extensive dendritic branching (shown in brown/orange) extending from a central cell body (black circle), and a single axon (blue) projecting downward with terminal branches. On the right is a bipolar neuron with dendrites extending upward and a single axon extending downward. The bottom row shows additional examples including a neuron with highly elaborate dendritic arborization resembling a tree-like structure on the left, and a simpler unipolar neuron structure on the right. All neurons demonstrate the common structural components of dendrites, cell body, and axon, but with dramatically different branching patterns and overall morphology depending on their location and function in the nervous system.

Chapter 2 – Ion Movement

Figure 2.1.

This diagram illustrates the molecular structure of the neuronal membrane’s phospholipid bilayer. The membrane is composed of two layers of phospholipid molecules arranged with their hydrophilic heads (shown as circular structures) facing outward toward both the extracellular and intracellular solutions, and their hydrophobic tails (shown as straight lines) pointing inward toward the center of the membrane. The top layer shows phospholipid molecules with their hydrophilic heads oriented toward the extracellular solution, while the bottom layer has hydrophilic heads facing the intracellular solution. The hydrophobic tails of both layers meet in the middle, creating a barrier that prevents water and water-soluble molecules like ions from freely crossing the membrane. This arrangement is fundamental to the membrane’s selective permeability properties.

Figure 2.2

This diagram shows the phospholipid bilayer with embedded ion channels that allow specific ions to cross the membrane. The membrane structure shows the same phospholipid arrangement as the previous figure, but now includes various types of ion channels spanning the width of the membrane. Blue dotted channels represent sodium channels, green striped channels represent potassium channels, and yellow solid channels represent chloride channels. These protein channels provide pathways for ions to move across the membrane when open, bypassing the impermeable phospholipid bilayer. The channels are shown as large protein structures that completely span from the extracellular solution to the intracellular solution, creating selective pores for ion movement.

Animation 2.1

An animation demonstrating the selective permeability of ion channels in a neuronal membrane. The animation begins with a cross-section of the cell membrane showing three types of ion channels in their closed conformations: dotted blue sodium channels, striped green potassium channels, and solid yellow chloride channels. Various ions are present on both sides of the membrane – sodium ions (blue spheres with + charge), potassium ions (green spheres with + charge), and chloride ions (yellow spheres with – charge). Initially, with all channels closed, the ions remain stationary on their respective sides of the membrane. The animation then shows individual channels opening and closing in sequence. When a sodium channel opens, only sodium ions move through it, flowing down their electrochemical gradient. When a potassium channel opens, only potassium ions pass through. When a chloride channel opens, only chloride ions move through that specific channel. The animation emphasizes the selectivity principle – each channel type allows only its specific ion to pass, demonstrating the lock-and-key relationship between channels and ions.

Animation 2.2

An animation illustrating how concentration and electrical gradients drive ion movement across a neuronal membrane. The scene begins with a cross-section of the membrane showing open ion channels. On one side of the membrane, there is a high concentration of ions (depicted as colored spheres), while the other side has fewer. As the animation progresses, ions move through the channels from the region of high concentration to the region of low concentration, demonstrating diffusion. At the same time, positively charged ions are shown being pulled toward negatively charged regions and repelled from positive ones, illustrating electrical forces. The animation highlights how these two forces combine to form the electrochemical gradient, which determines the overall direction of ion movement.

Animation 2.3

An animation demonstrating ion equilibrium across a neuronal membrane. The animation begins with equal numbers of positive ions (seven on each side) positioned on both sides of the membrane. Ion channels embedded in the membrane are open, and individual ions continuously move back and forth across the channels. Despite this constant bidirectional flow, the total number of ions on each side remains unchanged throughout the animation. This emphasizes the concept of equilibrium: when concentration and electrical gradients are equal in strength but opposite in direction, there is no net ion movement even though ions are still crossing the membrane.

Chapter 3 – Membrane Potential

Figure 3.1

This diagram illustrates the experimental setup for measuring membrane potential in a neuron. A neuron is shown with typical morphology including dendrites, cell body, and myelinated axon. Two electrodes are positioned to measure the voltage difference across the membrane: a reference electrode placed in the extracellular solution (labeled and shown penetrating from above) and a recording electrode inserted directly into the cell body (also labeled). The wavy line above represents the extracellular solution. The membrane potential is calculated as the voltage difference between these two electrode locations, with the recording electrode measuring the intracellular voltage and the reference electrode providing the extracellular baseline.

Figure 3.2

This figure shows two graphs illustrating changes in membrane potential over time. The left graph demonstrates depolarization (decrease in membrane potential), where the membrane potential starts at -65 mV and increases toward 0 mV, shown as an upward curve. The right graph shows hyperpolarization (increase in membrane potential), where the membrane potential starts at -65 mV and becomes more negative, shown as a downward curve. Both graphs have time in milliseconds on the x-axis and membrane potential in millivolts on the y-axis. The terminology clarifies that depolarization represents a decrease in membrane potential (movement toward 0) while hyperpolarization represents an increase in membrane potential (movement away from 0).

Figure 3.3

This diagram shows the charge distribution across a neuronal membrane at rest. The neuron displays typical morphology with dendrites and cell body. Two electrodes (reference and recording) are positioned as in the membrane potential measurement setup. Around the cell body, small circles with positive (+) and negative (-) symbols illustrate the charge distribution. The positive charges (shown in orange/red circles) are concentrated outside the cell, while negative charges (shown in blue circles) are concentrated inside the cell. This uneven charge distribution creates the negative resting membrane potential, with the inside of the neuron being more negatively charged relative to the outside.

Figure 3.4

This diagram shows the distribution of specific ions across the neuronal membrane at rest. The phospholipid bilayer is shown with embedded ion channels (blue dotted for sodium, green striped for potassium, yellow solid for chloride). In the extracellular solution, there are high concentrations of sodium ions (Na+, blue circles), calcium ions (Ca2+, purple circles), and chloride ions (Cl-, yellow circles). In the intracellular solution, there are high concentrations of potassium ions (K+, green circles) and anions (A-, gray circles representing negatively charged proteins and organic molecules). This uneven distribution of ions across the membrane is fundamental to establishing the electrochemical gradients that drive ion movement and maintain the resting membrane potential.

Figure 3.5

This diagram illustrates the electrochemical gradients acting on sodium and potassium ions at rest. The membrane setup is similar to previous figures, showing the phospholipid bilayer with ion channels and the characteristic ion distribution. On the right side, arrows indicate the direction of electrochemical gradients: a blue downward arrow labeled “Sodium” shows that sodium’s electrochemical gradient drives it into the cell, while a green upward arrow labeled “Potassium” shows that potassium’s electrochemical gradient drives it out of the cell. These opposing gradients reflect the combination of concentration and electrical forces acting on each ion type when the membrane is permeable to them.

Animation 3.1

An animation showing sodium ion movement across a neuronal membrane and how it relates to membrane potential changes. The scene begins with sodium ions (blue spheres with + charges) concentrated outside the cell and fewer sodium ions inside. Sodium channels (dotted blue) open in the membrane, allowing sodium to flow inward. Both the concentration gradient (high to low sodium) and the electrical gradient (positive ions moving toward the negatively charged inside) drive sodium entry. As sodium enters, the cell’s membrane potential becomes less negative, shown by a shifting voltage scale. When the potential approaches 0 mV and becomes positive, the electrical gradient reverses: now, the inside is positive, so the electrical force pushes sodium outward while the concentration gradient still pulls sodium inward. Eventually, these two forces balance. At this equilibrium point, sodium continues moving in and out, but net flow is zero. This equilibrium potential for sodium is approximately +60 mV.

Figure 3.6

This figure consists of two panels (A and B) showing ion movement relative to equilibrium potentials. Panel A shows a membrane at -70 mV with sodium channels open. Sodium ions flow into the cell (shown by downward arrows) because the cell’s membrane potential is more negative than sodium’s equilibrium potential of +60 mV. A graph shows the membrane potential moving upward (toward +60 mV) as indicated by a red line. Panel B shows the same membrane at -70 mV but with chloride channels open. Chloride ions flow out of the cell (shown by upward arrows) because the cell’s membrane potential is more negative than chloride’s equilibrium potential of -65 mV. The graph shows membrane potential moving upward toward -65 mV. Both panels demonstrate how ions move in directions that drive the membrane potential toward their respective equilibrium potentials.

Chapter 4 – The Membrane at Rest

Figure 4.1

This diagram illustrates a neuronal membrane at rest showing the uneven distribution of ions across the phospholipid bilayer. The extracellular solution (top) contains higher concentrations of sodium ions (Na+, shown in blue circles), calcium ions (Ca2+, shown in purple circles), and chloride ions (Cl-, shown in yellow circles). The intracellular solution (bottom) contains higher concentrations of potassium ions (K+, shown in green circles) and anions (A-, shown in gray circles). Embedded in the membrane are various leak ion channels: sodium leak channels (blue dotted channels), potassium leak channels (green striped channels), and chloride leak channels (yellow solid channels). The diagram shows that significantly more potassium leak channels are open compared to sodium leak channels, which explains why the membrane at rest is most permeable to potassium. This differential permeability, combined with the concentration gradients, contributes to the negative resting membrane potential of approximately -65 mV.

Figure 4.2

This diagram shows the same neuronal membrane setup as the previous image but with fewer leak channels illustrated to emphasize the key concept of differential permeability. The extracellular solution (top) shows sodium ions (Na+, blue circles), calcium ions (Ca2+, purple circles), and chloride ions (Cl-, yellow circles), while the intracellular solution (bottom) contains potassium ions (K+, green circles) and anions (A-, gray circles). The membrane contains the same types of leak channels: sodium leak channels (blue dotted), potassium leak channels (green striped), and chloride leak channels (yellow solid). This simplified view clearly demonstrates that at rest, there are more open potassium leak channels than sodium leak channels, which is the primary reason why the membrane has higher permeability to potassium. This differential permeability drives potassium efflux, making the inside of the cell more negative relative to the outside.

Animation 4.1

An animation showing potassium ion movement across a neuronal membrane at rest. Potassium ions (green spheres with + charge) are concentrated inside the cell, while fewer are outside. Non-gated potassium channels (striped green) are open in the membrane, allowing potassium to diffuse outward. As potassium leaves, it carries positive charge out of the cell, making the inside more negative. This movement drives the membrane potential closer to potassium’s equilibrium potential of –80 mV. Sodium channels (dotted blue) and chloride channels (solid yellow) are shown but remain closed.

Animation 4.2

An animation illustrating how multiple ions contribute to the resting membrane potential. Potassium ions (green, +) flow outward through open potassium leak channels (striped green). At the same time, some sodium ions (blue, +) enter through sodium leak channels (dotted blue), and chloride ions (yellow, –) enter through chloride leak channels (solid yellow). Because more potassium channels are open, potassium movement dominates, pulling the potential negative. However, sodium and chloride fluxes offset this, keeping the resting membrane potential slightly more positive than potassium’s equilibrium potential alone.

Animation 4.3

An animation of the sodium-potassium pump cycling through ion transport. The pump protein is embedded in the cell membrane. Inside the neuron, three sodium ions (blue, +) bind to the pump. ATP attaches, and the protein changes shape, closing to the inside and opening outward. The sodium ions are released outside the cell. Then, two extracellular potassium ions (green, +) bind to the pump. The phosphate from ATP detaches, causing the protein to flip back to its inward-facing conformation. The potassium ions are released into the cell. The cycle repeats, showing continuous export of sodium and import of potassium, maintaining the concentration gradients needed for the resting membrane potential.

Chapter 5 – Postsynaptic Potentials

Animation 5.1

An animation showing a postsynaptic neuron’s dendritic membrane with sodium (dotted blue), potassium (striped green), and chloride (solid yellow) channels. A stimulus opens these channels, allowing ions to briefly flow across the membrane. Sodium ions (blue, +) move inward, potassium ions (green, +) move outward, and chloride ions (yellow, –) move inward depending on the channel type. This demonstrates how different ion channels mediate postsynaptic potentials.

Animation 5.2

The animation begins with sodium channels (dotted blue) opening in response to a stimulus. Sodium ions (blue, +) rush into the cell, driven by concentration and electrical gradients. As sodium enters, the membrane potential moves upward toward 0 mV, creating a depolarization called an excitatory postsynaptic potential (EPSP). The trace of membrane potential shows a brief positive shift. Once the stimulus ends, sodium channels close, and the membrane potential returns to rest.

Animation 5.3

The animation shows chloride channels (solid yellow) opening at a resting potential of –60 mV. Chloride ions (yellow, –) move into the cell, attracted by both concentration and electrical gradients. Their entry makes the inside more negative, causing hyperpolarization called an inhibitory postsynaptic potential (IPSP). The voltage trace briefly dips downward before returning to rest as channels close.

Animation 5.4

At a resting potential of –65 mV, equal to chloride’s equilibrium potential, chloride channels (solid yellow) open. Chloride ions move in both directions through the open channels, but the flows are balanced, resulting in no net ion movement. The membrane potential trace remains flat, showing no change. This demonstrates that chloride conductance can be inhibitory even without a shift in potential, because it stabilizes the membrane near equilibrium.

Animation 5.5

The animation begins with the cell at –70 mV, more negative than chloride’s equilibrium potential (–65 mV). When chloride channels (solid yellow) open, chloride ions (yellow, –) exit the cell. This outward movement removes negative charge, producing a slight depolarization of the membrane potential. However, the effect is still inhibitory, since chloride conductance works to hold the cell near –65 mV, opposing further depolarization. The trace shows a small upward shift but stabilizes short of threshold.

Animation 5.6

The animation shows repeated excitatory stimuli opening sodium channels (dotted blue) in rapid succession. Each stimulus allows sodium influx (blue, +), producing a depolarization. With repeated inputs, depolarizations add together, summating into a larger excitatory postsynaptic potential. The voltage trace shows progressively larger upward deflections, demonstrating how summation increases the chance of reaching threshold for action potential initiation.

Figure 5.1

This figure illustrates different types of excitatory postsynaptic potential (EPSP) summation. On the left is a diagram of a postsynaptic neuron with four myelinated axon inputs (Input 1-4) making synaptic contact with the dendrites and cell body. Three panels on the right show different stimulation patterns and their effects on membrane potential. The first panel “EPSP Alone” shows Input 1 providing a single excitatory stimulus (blue vertical line), resulting in a small depolarization from -65 mV. The second panel “Temporal Summation” shows Input 1 providing multiple rapid stimuli in succession (three blue vertical lines), resulting in progressively larger depolarizations that build upon each other. The third panel “Spatial Summation” shows all four inputs (1-4) providing simultaneous excitatory stimuli, resulting in a large depolarization that is the sum of all individual EPSPs.

Figure 5.2

This figure demonstrates the interaction between excitatory and inhibitory postsynaptic potentials. On the left is a diagram of a postsynaptic neuron receiving input from three myelinated axons (Input 1-3). Two panels on the right compare different stimulation scenarios. The left panel “EPSP Alone” shows Input 1 providing an excitatory stimulus (blue vertical line), resulting in a depolarization from -65 mV toward -50 mV. The right panel “EPSP & IPSP Summation” shows simultaneous stimulation with Input 1 providing an excitatory stimulus (blue line) and Input 3 providing an inhibitory stimulus (red vertical line). The resulting membrane potential change is much smaller (red trace), demonstrating how inhibitory inputs can counteract or reduce the effects of excitatory inputs when they occur simultaneously.

Animation 5.7

The animation shows simultaneous opening of sodium channels (dotted blue) and chloride channels (solid yellow). Sodium ions (blue, +) flow inward, driving depolarization toward sodium’s equilibrium potential (+60 mV). Chloride ions (yellow, –) also flow inward, pulling the potential toward chloride’s equilibrium (–65 mV). The combined ion flows produce a weaker depolarization than sodium alone. The voltage trace shows a reduced upward deflection compared to a single EPSP.

Chapter 6 – Action Potentials

Figure 6.1

This graph shows the characteristic shape of an action potential plotted as membrane potential (in mV) versus time. The trace begins at the resting membrane potential (indicated by a dotted horizontal line at approximately -65 mV). The membrane potential shows small initial fluctuations representing EPSPs that summate to reach threshold. Once threshold is reached, there is a rapid depolarization (rising phase) that shoots up to approximately +30 mV, followed by an equally rapid repolarization (falling phase) that returns toward rest. The trace then dips below the resting potential (undershoot) before finally returning to the resting membrane potential. The entire event occurs over just a few milliseconds, demonstrating the brief but dramatic nature of the action potential.

Animation 6.1

An animation showing the propagation of an action potential down a neuron axon. The animation begins with a cross-sectional view of an axon at rest, displaying a membrane potential of -65 mV on a voltage indicator. The action potential initiates at the axon hillock (the junction between cell body and axon) as a wave of depolarization. As the wave progresses, the voltage indicator shows the membrane potential rapidly rising from -65 mV to approximately +40 mV (the peak), then quickly falling back below the resting potential to about -80 mV (undershoot), before returning to -65 mV. This electrical wave travels sequentially down the length of the axon, depicted as a moving zone of membrane potential change. The axon is shown with myelin sheaths (white insulating segments) and Nodes of Ranvier (gaps between myelin), where the action potential appears to “jump” from node to node in saltatory conduction. When the action potential reaches the presynaptic terminal at the end of the axon, small vesicles are shown releasing neurotransmitter molecules into the synaptic cleft.

Figure 6.2

This diagram illustrates the locations of voltage-gated ion channels along a neuron. The neuron displays typical morphology with dendrites, cell body, axon hillock (labeled), myelinated axon segments, and presynaptic terminal (labeled). Red arrows point to specific locations where voltage-gated ion channels are concentrated: at the axon hillock, at several points along the myelinated axon (likely at Nodes of Ranvier), and at the presynaptic terminal. These locations are critical for action potential initiation, propagation, and neurotransmitter release. The diagram emphasizes that voltage-gated channels are not uniformly distributed throughout the neuron but are strategically located at key sites necessary for electrical signaling.

Animation 6.2

This animation shows a segment of neuronal membrane containing different types of voltage-gated ion channels. As excitatory postsynaptic potentials summate, the membrane potential reaches threshold. Voltage-gated sodium channels (blue, dotted) open first, allowing sodium ions to flow rapidly into the neuron. A moment later, voltage-gated potassium channels (green, striped) open, and potassium exits the neuron. Chloride channels (yellow, solid) are present but remain closed. The ion movement is driven by electrochemical gradients, not energy. The sequence illustrates how voltage-gated channels open and close in response to voltage changes and are responsible for generating the action potential.

Figure 6.3

This detailed graph shows the labeled phases of an action potential. The trace starts with small depolarizations (EPSPs) that reach threshold (marked by a dotted horizontal line). The rising phase is labeled as the rapid depolarization from threshold to the peak. The overshoot is labeled at the peak where the membrane potential becomes positive (approximately +30 mV). The falling phase is labeled as the rapid repolarization back toward rest. The undershoot (or afterhyperpolarization) is labeled where the membrane potential becomes more negative than the resting potential before finally returning to rest. This comprehensive labeling helps identify each distinct phase of the action potential and its relationship to the resting membrane potential and threshold.

Animation 6.3

Animation focuses on the rising phase of the action potential. When the membrane potential reaches threshold, voltage-gated sodium channels (dotted blue) open immediately. Sodium ions rush into the neuron, driven by the sodium electrochemical gradient. This inward flow depolarizes the membrane, rapidly moving the membrane potential to a positive value. Potassium (striped green) and chloride (solid yellow) channels remain closed during this phase. This fast depolarization marks the steep upward slope seen in an action potential graph.

Animation 6.4

Depicts the falling phase of the action potential. Voltage-gated sodium channels (dotted blue) are now inactivated—shown with a block over the channel—preventing further sodium entry. At the same time, voltage-gated potassium channels (striped green) open after a short delay and allow potassium to leave the cell, driven by its concentration and electrical gradients. This efflux of positively charged potassium repolarizes the membrane, moving it back toward a negative value. Chloride channels (solid yellow) remain closed. This phase shows how delayed potassium channel opening and sodium channel inactivation cause the action potential to fall back toward resting potential.

Animation 6.5

Animation continues from the falling phase, showing the undershoot of the action potential. Sodium channels (dotted blue) are now de-inactivated, returning to their closed but ready-to-open state. Potassium channels (striped green) remain open briefly, allowing continued potassium efflux. As a result, the membrane potential becomes more negative than the resting potential (hyperpolarized). This undershoot phase reflects the membrane moving closer to the potassium equilibrium potential (~ -80 mV). Chloride channels (solid yellow) are not active in this phase. The animation emphasizes how lingering potassium channel activity shapes the tail end of the action potential.

Animation 6.6

This animation illustrates the neuron’s return to resting membrane potential after an action potential. Both sodium (dotted blue) and potassium (striped green) voltage-gated channels are now closed. The sodium-potassium pump is active (shown cycling ions), moving 3 sodium ions out and 2 potassium ions in, using ATP. Additionally, leak channels maintain resting ion permeability. This coordinated activity restores the original intracellular and extracellular ion concentrations and stabilizes the resting potential, preparing the neuron for another action potential.

Animation 6.7

This animation illustrates the directional propagation of the action potential. Starting at the axon hillock, voltage-gated sodium channels (dotted blue) open, causing a local depolarization and triggering adjacent segments of axon to also reach threshold. The action potential moves forward as each new segment depolarizes. Previously active sodium channels enter the inactivated state, shown as blocked, which prevents the action potential from moving backward. Potassium channels (striped green) follow behind to repolarize the membrane. The animation clearly shows how the refractory period ensures unidirectional movement of the action potential toward the synaptic terminal.

Figure 6.4

A comparative diagram showing three different types of axons with varying diameters and myelination. The largest axon (top) has a wide diameter and thick myelin sheaths with regular Nodes of Ranvier, labeled as having fast action potential conduction speed. The middle axon has moderate diameter with thinner myelin sheaths, labeled as having intermediate conduction speed. The smallest axon (bottom) has a narrow diameter with no myelin sheath present (unmyelinated), labeled as having slow conduction speed. Each axon is drawn to scale to emphasize the size differences. The myelin sheaths are shown as white or light-colored wrappings around the axons, with their thickness proportional to axon diameter. Voltage-gated channels may be indicated at the nodes of the myelinated axons and distributed along the entire length of the unmyelinated axon. The diagram illustrates the positive correlation between axon diameter, degree of myelination, and conduction velocity.

Animation 6.8

Comparison of action potential propagation in unmyelinated vs. myelinated axons. On the left, an unmyelinated axon shows a wave-like movement of the action potential, with sequential activation of voltage-gated sodium and potassium channels along the entire length of the axon. On the right, a myelinated axon shows the action potential jumping between Nodes of Ranvier, where the voltage-gated channels are concentrated. This saltatory conduction allows the signal to move more quickly by skipping over myelinated segments. The animation highlights both mechanisms side by side to show the speed advantage conferred by myelin.

Figure 6.5

This diagram shows the molecular mechanism underlying unidirectional action potential propagation along a myelinated axon. Three panels represent different states during propagation: “At Rest,” “Falling Phase,” and “Rising Phase.” Each panel shows a segment of axon with myelin and insets depicting the status of voltage-gated sodium (blue dotted) and potassium (green striped) channels. At rest, channels are closed. During the falling phase, sodium channels are inactivated (shown in purple) while potassium channels are open. During the rising phase, sodium channels are open and active. The diagram shows how the refractory state of sodium channels in the “falling phase” region prevents the action potential from propagating backward, while the “rising phase” region continues forward propagation.

Figure 6.6

This figure demonstrates how neurons encode stimulus strength through action potential frequency. Panel A shows a weak stimulus (depicted as a black bar) that generates only two action potentials during the stimulus period. Panel B shows a strong stimulus (same duration but presumably higher intensity) that generates six action potentials in rapid succession during the stimulus period. Both panels show identical action potential shapes and amplitudes, emphasizing that individual action potentials do not change in magnitude. Instead, stronger stimuli are encoded by higher frequencies of action potential firing. The resting membrane potential is marked by dotted lines in both traces.

Figure 6.7

This figure illustrates the absolute and relative refractory periods during action potentials. Panel A shows the absolute refractory period (highlighted in blue) spanning the rising and falling phases when voltage-gated sodium channels are either open or inactivated. During this time, no additional action potentials can be generated regardless of stimulus strength. The membrane diagram shows sodium channels in their inactivated state (purple). Panel B shows the relative refractory period (highlighted in green) during the undershoot phase when sodium channels have recovered but potassium channels remain open. During this time, action potentials can be generated but require stronger-than-normal stimuli to overcome the hyperpolarization caused by open potassium channels.

Figure 6.8

This figure compares action potentials under normal and altered extracellular conditions using two panels. Panel A labeled “Control” shows three normal action potentials with typical characteristics: rapid rising phases reaching approximately +30 mV, sharp peaks, fast falling phases, and brief undershoots before returning to the resting membrane potential (marked by a dotted line). Panel B labeled “Low Extracellular Sodium” shows the effect of reduced external sodium concentration on action potential shape. These action potentials have noticeably slower rising phases, reduced peak amplitudes (reaching only about -10 mV instead of +30 mV), and overall smaller magnitude changes. The timing between action potentials appears similar, but the individual action potentials are dramatically altered in both speed and amplitude due to the weakened sodium electrochemical gradient.

Chapter 7 – Voltage Clamp

Figure 7.1

This diagram shows the initial preparation for a voltage clamp experiment in two panels. Panel A displays a complete neuron with dendrites, cell body, and myelinated axon. A rectangular box highlights a segment of the axon that will be removed for experimentation. Panel B shows the isolated axon segment placed in an experimental chamber containing physiological extracellular solution (represented by the wavy line above the axon). The isolated axon maintains its cylindrical structure and contains all the voltage-gated ion channels necessary for studying action potential mechanisms. This preparation allows researchers to study ion channel function in a controlled environment where the axon segment retains the same ion concentrations and electrochemical gradients as in the intact neuron.

Figure 7.2

This diagram illustrates the electrode configuration for measuring membrane potential in the isolated axon preparation. The cylindrical axon segment is surrounded by extracellular solution (wavy line). Two electrodes are positioned for measurement: a reference electrode placed in the extracellular solution and a recording electrode inserted into the axon interior. These electrodes are connected to measuring equipment that calculates the voltage difference between the intracellular and extracellular compartments. This setup represents the initial step in voltage clamp methodology, establishing baseline membrane potential measurements before experimental manipulation begins.

Figure 7.3

This diagram outlines the four sequential steps of the voltage clamp control system using three electrodes. The isolated axon is equipped with a reference electrode in the extracellular solution, a recording electrode inside the axon, and a current-passing electrode also inserted into the axon. The process flows as follows: first, measure the membrane potential using the recording and reference electrodes; second, set the desired membrane potential value; third, compare the measured potential with the desired potential; and fourth, make the measured membrane potential equal to the desired potential by injecting current through the current-passing electrode. This system enables researchers to maintain constant membrane potential while studying ion channel behavior.

Figure 7.4

This diagram emphasizes the continuous, cyclical nature of voltage clamp control by showing the same three-electrode setup surrounded by directional arrows forming a closed loop. The process flows clockwise through the four steps: measure membrane potential → set desired membrane potential → compare measured with desired → inject corrective current → return to measure membrane potential. The arrows indicate that this cycle repeats continuously throughout the experiment, ensuring that any changes in membrane potential due to ion channel activity are immediately detected and corrected by appropriate current injection, thereby maintaining a constant voltage across the membrane despite ongoing ionic currents.

Figure 7.5

This diagram shows the initial state of a voltage clamp experiment, displaying the isolated axon with reference and recording electrodes in position. Red text indicates “Cell at rest at -65 mV,” showing the axon’s resting membrane potential measurement before any experimental manipulation. This represents the baseline condition where the axon exhibits its natural resting potential due to the normal distribution of ions and leak channel activity. The setup shows only the measurement electrodes since no current injection is required at this stage—the system is simply recording the inherent electrical state of the axon membrane.

Figure 7.6

This diagram shows the experimental setup after researchers have established the target membrane potential for the voltage clamp experiment. The axon shows “Cell at rest at -65 mV” in red text, indicating the current measured potential, while “Desired potential: 0 mV” appears above in red, showing the experimental target voltage. The reference and recording electrodes continue measuring the membrane potential, while the system prepares to begin current injection that will bring the membrane potential from its resting value of -65 mV to the desired experimental value of 0 mV. This step represents the transition from passive measurement to active voltage control.

Figure 7.7

This diagram illustrates the comparison phase where the voltage clamp system evaluates the difference between actual and desired membrane potentials. The setup shows “Cell at rest at -65 mV” and “Desired potential: 0 mV” with red text stating “Actual potential too low; must depolarize.” This represents the system’s assessment that the current membrane potential is more negative than the target value, requiring depolarization to reach the desired potential. The comparison determines what type of corrective action (current injection) will be needed to achieve the experimental membrane potential, setting the stage for active voltage control.

Figure 7.8

This final diagram demonstrates the voltage clamp system actively maintaining the desired membrane potential through current injection. The current-passing electrode is shown injecting positive current into the axon (indicated by “Inject positive current into the cell”). A voltage trace graph on the right shows the membrane potential recording, with “Current turned on” marking when the potential rapidly jumps from -65 mV to 0 mV and remains there. This illustrates successful voltage clamping, where the equipment maintains membrane potential at the desired value through continuous current injection that compensates for any ion flow through voltage-gated channels activated by the depolarization.

Animation 7.1

The animation shows a section of axon membrane clamped at 0 mV. Voltage-gated sodium channels in the membrane open immediately because the membrane potential is above threshold. Sodium ions, represented as small positively charged particles, rush into the axon through the blue sodium channels. Normally this influx would depolarize the membrane further, but the voltage clamp setup detects the ion flow and instantly injects an equal amount of negative current into the axon. This injected current offsets the sodium influx and keeps the membrane potential fixed at 0 mV. The animation emphasizes that sodium channels function normally, but the clamp prevents any change in the overall membrane potential by balancing sodium’s inward current with an equal and opposite injected current.

Animation 7.2

The animation begins with sodium channels inactivated and potassium channels (shown as green channels) opening after a short delay, as they would in an action potential. Potassium ions flow outward from the axon, leaving behind negative charge. Normally this efflux would repolarize the membrane, but in the voltage clamp experiment, the equipment responds immediately. The clamp injects an equal amount of positive current into the axon, exactly counteracting the potassium outflow. The membrane potential is held steady at 0 mV throughout. The animation illustrates how the clamp can prevent voltage change while still allowing normal activation and function of the potassium channels.