Chapter 2 Cell

1. Please describe the transport processes of substances through cell membranes?


Simple Diffusion

Facilitated Diffusion

→Facilitated Diffusion through channel.

→Facilitated Diffusion through carrier.

(2) Active Transport

Primary active transport

Secondary Active Transport

2. What is the characteristic of simple diffusion?

(1)Diffuse down its electrochemical gradient.

(2)Through the interstices of the lipid bilayer and through watery channels

(3)Passive transport (no ATP)

(4)Most are lipid soluble substances: O2, CO2, alcohol or small lipid insoluble and water soluble particles: urea and water from protein pore channels.

3. Please describe the characteristics of facilitated diffusion through ion channels?

(1)Diffuse down its electrochemical gradient.

(2)Interaction with protein channel

(3)Passive transport (no ATP)

(4)For ions: Na+ K+ Ca2+ H+ Cl-

4. Please describe the characteristics of facilitated diffusion through carriers?

(1)Diffuse down its electrochemical gradient.

(2)Interaction with carrier protein

(3)Passive transport (no ATP)

(4)For glucose, amino acid

(5)Diffuse Vmax


5. Please describe the primary active transport and the secondary active transport?

Active transport is divided into two types according to the source of the energy used to facilitate the transport: primary active transport and secondary active transport.

(1) Primary active transport: The energy is derived directly from breakdown of adenosine triphosphate (ATP) or some other high-energy phosphate compound.

(2) Secondary active transport: The energy is derived secondarily from energy that has been stored in the form of ionic concentration differences of secondary molecular or ionic substances between the two sides of a cell membrane, created originally by primary active transport.

The transport in both active transport types, depends on carrier proteins. These carrier proteins are capable of imparting energy to the transported substance to move it against the electrochemical gradient.

6. What is sodium-potassium pump and how does it work?

Na+-K+ pump is a complex of two separate globular proteins—a larger one called the α subunit, and a smaller one called the β subunit. The function of the smaller protein fix the protein complex in the lipid membrane, the larger protein has three specific features that are important for the functioning of the pump: It has three binding sites for sodium ions on the portion of the protein that protrudes to the inside of the cell.It has two binding sites for potassium ions on the outside.The inside portion of this protein near the sodium binding sites has adenosine triphosphatase (ATPase) activity.

When two potassium ions bind on the outside of the carrier protein and three sodium ions bind on the inside, the ATPase function of the protein becomes activated. Activation of the ATPase function leads to cleavage of one molecule of ATP, splitting it to adenosine diphosphate (ADP) and liberating a high-energy phosphate bond of energy. This liberated energy is then believed to cause a chemical and conformational change in the protein carrier molecule, extruding the three sodium ions to the outside and the two potassium ions to the inside.

Physiological significance of the Na+-K+ pump: Control cell volume and osmotic pressure, Develop and maintain Na+ and K+ concentration gradients across the membrane, Electrogenic action influences membrane potential, Maintain high intracellular K+ concentration gradients across the membrane. K+ is necessary for many metabolic reactions in the cytoplasm, Provides energy for secondary active transport.

7. Please describe the functions of calcium pump?

Calcium ions are normally maintained at an extremely low concentration in the intracellular cytosol of virtually all cells in the body. This level of maintenance is achieved mainly by two primary active transport calcium pumps. One, which is in the cell membrane, pumps calcium to the outside of the cell. The other pumps calcium ions into one or more of the intracellular vesicular organelles of the cell, such as the sarcoplasmic reticulum of muscle cells and the mitochondria in all cells. In each of these instances, the carrier protein penetrates the membrane and functions as an enzyme ATPase, with the capability to cleave ATP, and this protein has a highly specific binding site for calcium.

8. Please describe the functions of sodium-glucose co-transporters?

Glucose is transported into most cells against large concentration gradients; the mechanism of this action is entirely by co-transport. The transport carrier protein for sodium-glucose co-transporters has two binding sites on its exterior side, one for sodium and one for glucose. When they both become attached by sodium and glucose respectively, conformational change takes place, and the sodium and glucose are transported to the inside of the cell at the same time. The concentration of sodium ions is high on the outside and low inside, which provides energy for the transport. Sodium-glucose co-transporters are especially important mechanisms in transporting glucose across renal and intestinal epithelial cells.

9. What is the resting potential of neurons and how does it form?

Na+-K+ pump is an electrogenic pump, because more positive charges are pumped to the outside than to the inside for continuous pumping of three sodium ions to the outside occurs for each two potassium ions pumped to the inside of the membrane. The pumping of more sodium ions to the outside than the potassium ions being pumped to the inside causes continual loss of positive charges from inside the membrane, creating an additional degree of negativity (about 4 millivolts additional).

The Na+-K+ pump also causes large concentration gradients for sodium and potassium across the resting nerve membrane. There is a channel protein (sometimes called potassium channel, or potassium [K+] “leak” channel) in the nerve membrane through which potassium can leak even in a resting cell. These K+ leak channels may also leak sodium ions slightly but are far more permeable to potassium than to sodium. This differential in permeability is a key factor in determining the level of the normal resting membrane potential. Using the Goldman equation, value in the Goldman equation gives a potential inside the membrane of −86 millivolts.

Therefore, the net membrane potential when all these factors are operative at the same time is about −90 millivolts.

In summary, the diffusion potentials alone caused by potassium and sodium diffusion would give a membrane potential of about −86 millivolts, with almost all of this being determined by potassium diffusion. An additional −4 millivolts is then contributed to the membrane potential by the continuously acting electrogenic Na+-K+ pump, giving a net membrane potential of −90 millivolts.


10. Please describe the action potential of neurons and the mechanism underlying its formation?

When stimulate the nerve fiber with an appropriate stimulus, the nerve fiber membrane potential will suddenly change from the normal resting negative membrane potential to a positive potential and ends with an almost equally rapid change back to the negative potential. The rapid change in the membrane potential followed by a return to the resting membrane potential, called action potential.

The voltage-gated sodium channel is necessary actor in causing both depolarization and repolarization of the nerve membrane during the action potential. The voltage-gated potassium channel also plays an important role in increasing the rapidity of repolarization of the membrane.

1Voltage­Gated Sodium Channel has two gates (one near the outside of the channel called the activation gate, and another near the inside called the inactivation gate) and .three separate functional states. when the membrane potential is −90 millivolts, the inactivation gate is open and the activation gate is closed, which prevents any entry of sodium ions to the interior of the fiber through these sodium channels. When the membrane potential becomes less negative than during the resting state, rising from −90 millivolts toward zero, it finally reaches a voltage-usually somewhere between −70 and −50 millivolts—that causes a sudden conformational change in the activation gate, flipping it all the way to the open position. During this activated state, sodium ions can pour inward through the channel, increasing the sodium permeability of the membrane as much as 500- to 5000-fold. The same increase in voltage that opens the activation gate also closes the inactivation gate, however the conformational change that flips the inactivation gate to the closed state is a slower process than the conformational change that opens the activation gate. Therefore, after the sodium channel has remained open for a few 10,000ths of a second, the inactivation gate closes and sodium ions no longer can pour to the inside of the membrane. At this point, the membrane potential begins to return toward the resting membrane state, which is the repolarization process. Another important characteristic of the sodium channel inactivation process is that the inactivation gate will not reopen until the membrane potential returns to or near the original resting membrane potential level. Therefore, it is usually not possible for the sodium channels to open again without first repolarizing the nerve fiber.

2Voltage­Gated Potassium Channel has two functional states: during the resting state and toward the end of the action potential. During the resting state, the gate of the potassium channel is closed and potassium ions are prevented from passing through this channel to the exterior. When the membrane potential rises from −90 millivolts toward zero, this voltage change causes a conformational opening of the gate and allows increased potassium diffusion outward through the channel. However, because of the slight delay in opening of the potassium channels, for the most part, they open just at the same time that the sodium channels are beginning to close because of inactivation. Thus, the decrease in sodium entry to the cell and the simultaneous increase in potassium exit from the cell combine to speed the repolarization process, leading to full recovery of the resting membrane potential.

11. Please describe the absolute refractory period of nerve fiber?

After a cell is excited, its excitability appears a series of changes. At the time of the occurrence of the excitation and the initial period after the excitation, no matter how strong the stimulation is applied, the cells cannot be excited again, which is called absolute refractory period (ARP). During this period the excitability of the cell is zero. The reason is that shortly after the action potential is initiated, the sodium channels become inactivated and only when the membrane potential to return to or near the original resting membrane potential level, the inactivation gates can reopen, and then a new action potential can be initiated. The period during which a second action potential cannot be elicited, even with a strong stimulus.

12. Please describe the all­or­nothing principle of action potential propagation?

allmeans the action potential generated by the stimulus propagates on the nerve fibers with the same shape, amplitude and no attenuation. Nothing means there's no action potential, there's no spread of action potential. That is As long as the action potential is generated, the action potential will spread unattenuated on the nerve fibers, or it will not generate action potential at all, nor will it spread

13. What is the characteristic of local potential?

 (1) A graded potential: The magnitude is related to the intensity of the stimulus and does not have all or none characteristics. because the ion channels only partially open can not meet the ion balance electric potential, and therefore is not "all or nothing"

(2) Conducted with attenuation: Unlike an action potential spreading unattenuated along the cell membrane, the local potential can only be propagated a short distance along the membrane to the adjacent, and rapidly attenuate or even disappear with the increase of the spreading distance. This method is called electrotonic spreading.

(3) Local potential has no refractory period. Local potential can be sum up. Although a subliminal stimuli only can cause a partial response, can not trigger action potential, but multiple stimuli are given continuously at the same place, multiple local potential caused by these multiple continuous stimuli add up in time, are likely to lead the membrane depolarization to threshold potential, and trigger action potentials, we called temporal summation effects. If multiple stimuli are given at the same time in the adjacent area, multiple local potential caused by it add up in space, are likely to lead membrane depolarization to threshold potential, and trigger action potentials, we called spatial summation effects

14. Please describe the “Walk-Along” Theory of muscle contraction

Before contraction begins, the heads of the cross-bridges bind with ATP. The ATPase activity of the myosin head immediately cleaves the ATP but leaves the cleavage products, ADP plus phosphate ion, bound to the head. In this state, the conformation of the head is such that it extends perpendicularly toward the actin filament but is not yet attached to the actin. When the troponin-tropomyosin complex binds with calcium ions, active sites on the actin filament are uncovered and the myosin heads then bind with these sites.

The bond between the head of the cross-bridge and the active site of the actin filament causes a conformational change in the head, causes profound changes in the intramolecular forces between the head and arm of its cross-bridge. The new alignment of forces causes the head to tilt toward the arm and to drag the actin filament along with it. This tilt of the head is called the power stroke. The energy that activates the power stroke is the energy already stored, like a “cocked” spring, by the conformational change that occurred in the head when the ATP molecule was cleaved earlier.

Once the head of the cross-bridge tilts, release of the ADP and phosphate ion that were previously attached to the head is allowed. At the site of release of the ADP, a new molecule of ATP binds. This binding of new ATP causes detachment of the head from the actin and the head returns to its extended direction.

After the head has detached from the actin, the new molecule of ATP is cleaved to begin the next cycle, leading to a new power stroke. That is, the energy again “cocks” the head back to its perpendicular condition, ready to begin the new power stroke cycle, the head combines with a new active site farther down along the actin filament and the actin filament moves another step. Thus, the heads of the cross-bridges bend back and forth and step by step walk along the actin filament, pulling the ends of two successive actin filaments toward the center of the myosin filament.This process is called “Walk-Along” Theory of Contraction. Thus, the process proceeds again and again, until the actin filaments pull the Z membrane up against the ends of the myosin filaments or until the load on the muscle becomes too great for further pulling to occur. Each one of the cross-bridges is believed to operate independently of all others, each attaching and pulling in a continuous repeated cycle. Therefore, the greater the number of cross-bridges in contact with the actin filament at any given time, the greater the force of contraction.

15. Please describe the isometric contraction and isotonic contraction?

Muscle contraction is said to be isometric when the muscle does not shorten during contraction and isotonic when it does shorten but the tension on the muscle remains constant throughout the contraction.

16. What is motor unit?

The ending of each moto neuron that leaves the spinal cord are divided into branches, each branch of the nerve endings innervate a muscle fiber, so a moto neuron innervates multiple muscle fibers. All the muscle fibers innervated by a single nerve fiber are called a motor unit.

17. What is tetanization of muscle contraction? Please outline the mechanism underlying its formation?

When the frequency reaches a critical level, the successive contractions eventually become so rapid that they fuse together and the whole muscle contraction appears to be completely smooth and continuous. This process is called tetanization.

Tetany occurs because enough calcium ions are maintained in the muscle sarcoplasm, even between action potentials, so that full contractile state is sustained without allowing any relaxation between the action potentials. Another reason is that during a contraction, the action potential duration (equivalent to the absolute refractory period) is only 2 to 4ms, and the contraction may take decades or even hundreds of milliseconds, making it possible for skeletal muscles to receive new stimuli and undergo new excitations and contractions during mechanical contraction. The new contraction process may sum up with the last contraction process which has not yet ended.

18. Please describe the process of excitation-contraction coupling?

The T tubule action potentials cause release of calcium ions inside the muscle fiber in the immediate vicinity of the myofibrils, and these calcium ions then cause contraction. This overall process is called excitation-contraction coupling.

when an action potential spreads over a muscle fiber membrane, a potential change also spreads along the T tubules to the deep interior of the muscle fiber. As the action potential reaches the T tubule, the voltage change is sensed by receptors that are linked to calcium release channels, in the adjacent sarcoplasmic reticular cisternae. Activation of receptors triggers the opening of the calcium release channels in the cisternae, as well as in their attached longitudinal tubules. These channels remain open for a few milliseconds, releasing calcium ions into the sarcoplasm surrounding the myofibrils. When the troponin-tropomyosin complex binds with calcium ions, active sites on the actin filament are uncovered and the myosin heads then bind with these sites. The bond between the head of the cross-bridge and the active site of the actin filament causes a conformational change in the head, causes profound changes in the intramolecular forces between the head and arm of its cross-bridge. The new alignment of forces causes the head to tilt toward the arm and to drag the actin filament along with it, cause contraction.


Chapter 1 Introduction of Physiology-Review Questions with Reference Answers by Dr. Shuwei Jia
Chapter 3 Blood-Review Questions with Reference Answers by Dr. Shuwei Jia



Chapter 2 Cell-Review Questions with Reference Answers by Dr. Shuwei Jia

For 2017 International Medical Students