UNIT 6 – Transepithelial Transport (Q&A) | MZO-001 MSCZOO | IGNOU

SAQ 1

i) The resting membrane potential is created due to:

a) Buildup of the negative ions in the cytosol along the inside of the membrane.
b) The separation of positive and negative electrical charges along both sides of the plasma membrane.
c) Difference in charge across the membrane of the cell.

d) All of the above.

Answer: d) All of the above

ii) Which of the following factor/s contribute to the resting membrane potential of the cell?

a) Unequal distribution of ions in the ECF and cytosol
b) Activity of Na⁺/K⁺ ATPases
c) Most anions cannot leave the cell

d) all of the above

Answer: d) All of the above

iii) The extracellular fluid (ECF) has high concentration of positively charged sodium ions and negatively charge chloride ions.

a) True

b) False

Answer: a) True

iv) Intracellular fluid (ECF) in contact with the cell membrane is positively charged with high concentration of potassium ions, phosphate ions and anionic proteins.

a) True

b) False

Answer: a) True

v) Usually, sodium ions enter the cell through open sodium channel and potassium ions tend to exit the cell via potassium channel.

a) True

b) False

Answer: a) True

vi) Which of the following channels usually establish the resting membrane potential?

a) Leak channel
b) Voltage gated channel
c) Chemically gated channel

d) Mechanically gated channel

Answer: a) Leak channel

vii) Following the repolarizing phase, there may be an after hyperpolarizing phase, during which the membrane potential temporarily becomes more negative than the resting level.

a) True

b) False

Answer: a) True

viii) Which of the following channel opens when pressure, touch or stretch is applied to the membrane?

a) Leak channel
b) Voltage gated channel
c) Chemically gated channel

d) Mechanically gated channel

Answer: d) Mechanically gated channel

ix) Which of the following channel is also called as ligand gated channel having receptors?

a) Leak channel
b) Voltage gated channel
c) Chemically gated channel

d) Mechanically gated channel

Answer: c) Chemically gated channel

x) The sorting and processing of cargo is critically influenced by the progressive acidification along the secretory pathway.

a) True

b) False

Answer: a) True

xi) Vacuolar H⁺-ATPases are the primary source of protonation for the organelles.

a) True

b) False

Answer: a) True

xii) Activity of Na⁺/K⁺ ATPases reduces the rate of proton pumping and maintain the electrical potential along the endosomal membrane

a) True

b) False

Answer: a) True

xiii) Na⁺/K⁺ ATPases promote the acidification which causes Na⁺ ion accumulation in the lumen that in turn drive Na⁺/H⁺ exchange

a) True

b) False

Answer: a) True

xiv) Increased activity of proton pump and decreased conduction of proton leak pathway progressively results into the acidification of secretory organelles.

a) True

b) False

Answer: a) True

xv) The vacuolar type (V) H⁺ ATPase transports the protons and creates an acidic pH of the organelles in the presence of Mg2⁺ -ATP.

a) True

b) False

Answer: a) True

xvi) Which of the followings play important role in the regulation of the organellar pH?

a) V-ATPases
b) Proton leaks
c) Luminal buffering

d) All of the above

Answer: d) All of the above

xvii) H⁺/K⁺ ATPase is present in the apical membrane and it creates a concentration gradient between the stomach lumen and the cytoplasm of the cells by exporting one K⁺ and importing one H⁺ ion.

a) True

b) False

Answer: b) False

xviii) Which of the factors affect the rate of diffusion of substances across plasma membranes?

a) Diffusion distance
b) Concentration gradient
c) Surface area

d) All of the above

Answer: d) All of the above

xix) Symport of glucose and amino acids into cells is an example of .............

a) Facilitated diffusion
b) Primary active transport
c) Secondary active transport

d) None of the above

Answer: c) Secondary active transport

xx) Antiport of Ca²⁺ and H⁺ out of cells is an example of ...........

a) Facilitated diffusion
b) Primary active transport
c) Secondary active transport

d) None of the above

Answer: c) Secondary active transport

xxi) Transport of low-density lipoproteins (LDLs) occurs by .............

a) Facilitated diffusion
b) Primary active transport
c) Secondary active transport

d) Receptor mediated endocytosis

Answer: d) Receptor mediated endocytosis

xxii) Transport of antibodies is an example of ............. 

a) Facilitated diffusion
b) Primary active transport
c) Secondary active transport

d) Transcytosis

Answer: d) Transcytosis

TERMINAL QUESTIONS

01. Which factors affect the rate of diffusion of substance across plasma membrane?

The plasma membrane acts as a barrier and a gateway for substances moving into and out of the cell. Diffusion is the passive movement of molecules from an area of higher concentration to an area of lower concentration without using energy. However, the rate at which diffusion happens across the plasma membrane is not always the same. It can vary based on several important factors. Below is a clear explanation of the main factors:

1. Concentration Gradient

The concentration gradient is one of the most important factors affecting diffusion. A concentration gradient means the difference in the concentration of a substance between two areas. If the difference is large, the diffusion rate will be faster because more molecules are ready to move from high to low concentration. On the other hand, if the difference is small, diffusion will happen slowly.

2. Temperature

Temperature also has a strong effect on diffusion. When the temperature is high, the molecules move faster because they have more kinetic energy. As a result, diffusion across the membrane occurs more quickly. In contrast, at lower temperatures, molecular movement slows down and diffusion happens at a slower rate.

3. Size of the Molecules

The size of the molecules trying to diffuse matters a lot. Smaller molecules like oxygen (O₂) and carbon dioxide (CO₂) can easily pass through the plasma membrane and diffuse quickly. However, larger molecules such as proteins or polysaccharides find it very difficult to diffuse without help.

4. Lipid Solubility of the Substance

The plasma membrane is made mainly of lipids. So, substances that are lipid-soluble, like steroid hormones or fatty acids, can pass through the membrane more easily and quickly. Water-soluble substances, on the other hand, cannot cross the membrane easily unless special transport proteins help them.

5. Thickness of the Membrane

If the plasma membrane is thicker, diffusion becomes slower because the molecules have to travel a longer distance. A thinner membrane allows faster diffusion because the path for movement is shorter.

6. Surface Area of the Membrane

A larger surface area of the plasma membrane gives more space for molecules to diffuse. As a result, diffusion happens faster. If the surface area is small, fewer molecules can cross at a time, slowing down the process.

7. Presence of Transport Proteins

Sometimes, specific substances need carrier proteins or channel proteins to cross the membrane, especially if they are charged or large. If more transport proteins are available, the diffusion rate increases for these molecules.

02. Describe in detail the facilitated diffusion process.

Facilitated diffusion is a type of passive transport that allows the movement of molecules across the cell membrane with the help of specific membrane proteins. Unlike simple diffusion, facilitated diffusion requires the involvement of membrane proteins because the molecules are either too large or too polar to pass through the lipid bilayer of the membrane. However, the process does not require energy (ATP) and happens according to the concentration gradient, meaning molecules move from a region of high concentration to a region of low concentration.

Facilitated diffusion follows a simple but well-organized sequence of steps to allow the transport of specific molecules across the plasma membrane:

Step 1: Arrival of the Molecule Near the Plasma Membrane

The process begins when a specific molecule, such as a glucose molecule or a sodium ion, approaches the plasma membrane. The lipid bilayer of the membrane is hydrophobic in nature and generally allows only small, non-polar molecules to diffuse easily. Large molecules or charged ions cannot simply slip through. As a result, these molecules accumulate near the membrane surface and search for a special passage to cross the barrier.

Step 2: Specific Recognition by a Transport Protein

At this point, the molecule encounters transport proteins embedded in the plasma membrane. These transport proteins act like gatekeepers and are highly selective. Each transport protein is designed to recognize and bind only to a particular type of molecule.

There are mainly two types of transport proteins:

1. Channel proteins: These proteins form aqueous pores in the membrane that allow specific ions or small molecules to pass through without direct contact with the lipid part. These channels often open and close in response to certain signals.
2. Carrier proteins: These proteins physically bind to the molecule and undergo a change in shape to carry the molecule across the membrane safely.

The interaction between the molecule and its specific protein ensures selective and controlled movement across the membrane.

Step 3: Binding of the Molecule and Structural Change in the Transport Protein

After the correct molecule is recognized, it binds to a specific site on the transport protein. This binding is very specific, almost like a lock and key mechanism. Once the molecule binds, the transport protein undergoes a slight conformational change. In case of carrier proteins, this shape change is necessary to shield the molecule from the hydrophobic core of the membrane. This structural change helps create a safe pathway for the molecule to move through the membrane.

Step 4: Movement of the Molecule Across the Membrane Along the Concentration Gradient

After the structural change, the molecule is allowed to pass from the side of the membrane where it is more concentrated to the side where it is less concentrated. This movement occurs passively, without any energy expenditure, because it simply follows the natural tendency of molecules to move from high concentration to low concentration. In the case of channel proteins, the molecule moves quickly through the open pore. In case of carrier proteins, the molecule is carried across by the shape-changing action of the protein.

Step 5: Release of the Molecule and Resetting of the Transport Protein

Once the molecule successfully crosses to the other side of the membrane, it is released into the cytoplasm or into the external environment, depending on the direction of transport. After releasing the molecule, the transport protein returns to its original structure and position, becoming ready to transport another molecule of the same type. This ability to reset ensures that facilitated diffusion can continue efficiently without interruption.

03. Describe in detail secondary active transport with suitable examples.

Secondary active transport is a vital process in cellular physiology that allows the movement of molecules across cell membranes against their concentration gradients. Unlike primary active transport, which directly uses energy in the form of ATP to pump ions across membranes, secondary active transport relies on the electrochemical gradients created by primary active transport. These gradients, especially of ions such as sodium (Na⁺) and protons (H⁺), provide the necessary energy for the transport of other molecules without direct consumption of ATP.

In this process, the energy stored in the ion gradients is harnessed to transport molecules against their concentration gradient. Secondary active transport is crucial for many physiological functions, such as nutrient absorption, waste removal and ion homeostasis.

Mechanism of Secondary Active Transport

Secondary active transport involves two major steps:

1. Creation of an Electrochemical Gradient (Primary Active Transport):

The first step is the establishment of an electrochemical gradient, usually through primary active transport. For example, a Na+/K+ pump uses ATP to pump sodium (Na+) out of the cell and potassium (K+) into the cell, generating a high concentration of sodium outside the cell.

2. Utilization of the Electrochemical Gradient (Secondary Active Transport):

Once the gradient is established, secondary active transport proteins (co-transporters or anti-porters) utilize the energy stored in this gradient to transport other molecules across the membrane, typically against their concentration gradient. These transporters do not use ATP directly.

Types of Secondary Active Transport

There are two main types of secondary active transport:

1. Symport (Cotransport):

• In this type, both molecules or ions move in the same direction across the membrane. For example,  the sodium-glucose transporter (SGLT), sodium ions move into the cell along their concentration gradient, and glucose or amino acids are co-transported into the cell along with them.

2. Antiport (Countertransport):

• In antiport systems, the molecules or ions move in opposite directions across the membrane. For example, sodium ions move into the cell while another substance (such as calcium or hydrogen ions) is pumped out of the cell.

Importance of Secondary Active Transport

• Ion Balance and Homeostasis: Secondary active transport helps maintain ion gradients necessary for the proper functioning of cells. These gradients are essential for functions like nerve impulses, muscle contraction and nutrient absorption.

• Energy Efficiency: Although secondary active transport doesn't directly use ATP for transport, it indirectly uses the energy generated by primary active transport, which makes it more energy-efficient for certain cellular functions.

• Nutrient and Ion Transport: Secondary active transport is essential for transporting nutrients like glucose and amino acids into cells against their concentration gradient. Without this system, the cell would not be able to accumulate vital nutrients.

Examples of Secondary Active Transport

1. Sodium-Glucose Cotransporter (SGLT)

• A major example of secondary active transport is the sodium-glucose cotransporter (SGLT) found in the cells of the small intestine and kidneys. The Na+/K+ pump creates a high sodium concentration outside the cell. The SGLT then uses the energy from this gradient to bring glucose into the cell. The sodium ions move back into the cell down their concentration gradient and glucose is transported against its concentration gradient into the cell, all without direct use of ATP.

2. Sodium-Calcium Exchanger (NCX)

• The sodium-calcium exchanger (NCX) plays a crucial role in maintaining calcium homeostasis in cells, particularly in muscle cells. In this case, the sodium gradient, established by the Na+/K+ pump, is used to move sodium ions into the cell. In exchange, three sodium ions enter the cell for every calcium ion that is expelled. This mechanism helps lower intracellular calcium levels, which is essential for muscle relaxation.

3. Proton-Sodium Exchanger (NHE)

• The proton-sodium exchanger (NHE) is important for regulating pH levels in various tissues, including the kidneys. In this process, sodium ions enter the cell along with protons (H+) being expelled, helping to regulate the acid-base balance in the body. The sodium gradient created by the Na+/K+ pump drives the movement of sodium ions into the cell, while the protons are removed to prevent acid buildup inside the cell.

04. Describe the vesicular transport mechanism.

In cells, many important substances like proteins, polysaccharides, lipids and fluids are very large in size and cannot pass freely across membranes. To move these large materials safely and accurately, cells use a highly organised method called vesicular transport. In this process, small membrane-bound sacs known as vesicles are formed to carry substances either into the cell, out of the cell, or between internal compartments. Vesicular transport is an active, energy-requiring process and is carefully regulated to maintain cellular organisation.

The vesicular transport mechanism occurs through a series of well-coordinated steps:

Step 1: Initiation of Vesicle Formation

The process begins when specific cargo molecules need to be transported. The donor membrane, often the plasma membrane or organelle membrane, starts to curve inward or outward. Special coat proteins like clathrin, COPI, or COPII are recruited to the site, which help in shaping the membrane into a budding vesicle.

Step 2: Budding and Scission of Vesicle

As the membrane continues to bend, the forming vesicle encloses the cargo inside it. Once the vesicle has nearly formed, a protein called dynamin wraps around the neck of the budding vesicle and helps to pinch it off completely from the donor membrane. This results in the release of a free transport vesicle into the cytoplasm.

Step 3: Vesicle Transport Through Cytoplasm

The newly formed vesicle then needs to travel to its target destination. For this, it moves along cytoskeletal elements like microtubules. Motor proteins such as kinesin and dynein attach to the vesicle and "walk" it along the cytoskeletal tracks, using energy from ATP to drive their movement.

Step 4: Tethering to Target Membrane

When the vesicle approaches the target membrane, it is first captured and held nearby by tethering proteins. These proteins ensure that the vesicle is positioned properly before it attempts to fuse with the target membrane.

Step 5: Docking and Recognition

After tethering, docking occurs through the interaction of SNARE proteins. Vesicle-SNARE (v-SNARE) on the vesicle binds specifically with Target-SNARE (t-SNARE) on the target membrane. This ensures that vesicles fuse only with the correct target and not randomly with any membrane.

Step 6: Fusion of Vesicle and Release of Cargo

Following docking, the SNARE proteins pull the vesicle and target membranes very close together, leading to fusion. The lipid bilayers merge, and the cargo carried inside the vesicle is either released outside the cell (in exocytosis) or delivered into the organelle lumen (in endocytosis or intracellular transport).

Step 7: Recycling of Vesicular Components

After fusion, the membrane components like SNARE proteins and other factors are often recycled. They are either retrieved back to the donor membrane or reused to form new vesicles for future transport, ensuring efficiency and saving cellular energy.

05. How is cellular pH maintained and regulated.

The regulation and maintenance of cellular pH are crucial for the optimal functioning of cells. The internal pH of animal cells is typically around 7.2, which is slightly less than the normal blood pH of 7.4. This small difference is vital because a deviation from the optimal pH range can disrupt cellular processes, affecting enzyme activity, protein structure and cellular metabolism. To maintain this balance, cells employ various mechanisms to regulate their internal pH.

The process of maintaining and regulating cellular pH involves a coordinated action of several mechanisms, which work together continuously. The following are the main ways by which cells regulate their pH:

1. Buffer Systems

Buffer systems are the first line of defense against changes in pH. They work by either absorbing excess hydrogen ions (H⁺) when the cell becomes too acidic or releasing H⁺ ions when the environment becomes too alkaline. The two primary buffering systems in cells are:

• Bicarbonate Buffer System: This is the most prominent buffering system in the extracellular fluid. It involves the equilibrium between carbonic acid (H₂CO₃) and bicarbonate ions (HCO₃⁻). The reaction can either absorb or release H⁺ ions to maintain a stable pH.

• Phosphate Buffer System: This operates in the cytoplasm of the cell. Phosphate buffer works similarly to bicarbonate buffer by balancing dihydrogen phosphate (H₂PO₄⁻) and hydrogen phosphate (HPO₄²⁻), which helps to stabilize the pH within the cell.

Both of these buffer systems are highly effective in neutralizing small pH changes and keeping the internal pH of the cell stable.

2. Membrane Transport Proteins

The second major mechanism for regulating pH in cells involves membrane transport proteins. These proteins help control the movement of hydrogen ions (H⁺) and other ions across the cell membrane, which can directly affect the internal pH. Some of the key transporters involved in pH regulation are:

• Na+/H+ Exchanger (NHE): This transporter expels H⁺ ions from the cell in exchange for Na⁺ ions, helping to prevent acidification of the cytoplasm. This is especially important when cells need to prevent the accumulation of excess H⁺ ions, which can be a byproduct of cellular metabolism.

• H+/K+ ATPase Pump: Found mainly in cells of the stomach lining, this pump moves H⁺ ions out of the cell and exchanges them for K⁺ ions. This mechanism is critical for maintaining acidic environments in certain organelles like the stomach, where an acidic pH is necessary for digestion.

• V-Type Proton Pump: This pump is involved in acidifying intracellular organelles like lysosomes and endosomes by pumping protons (H⁺) into their interior.

3. Cellular Metabolism and Enzyme Activity

Another significant way cells regulate pH is by adjusting metabolic processes that produce or consume H⁺ ions. For example, in cells that are highly metabolically active, such as muscle cells during exercise, the production of lactic acid leads to the release of H⁺ ions. To counter this, cells increase the activity of transporters like the Na+/H+ exchanger to expel the excess protons.

Additionally, enzymatic processes within cells are pH-sensitive, meaning that enzymes will function optimally within a specific pH range. Enzymes in the cytoplasm, mitochondria, and other cellular compartments help manage the production of protons through metabolic reactions, contributing to pH regulation.

06. What are the sources of acidification of cell organelles?

Acidification of cellular organelles is a vital process for maintaining proper cellular function. Organelles such as lysosomes, endosomes and the Golgi apparatus require an acidic environment to carry out essential activities such as protein degradation, cellular waste disposal and nutrient processing. The pH of these organelles is maintained at low levels through various mechanisms that ensure optimal enzymatic activity and cellular homeostasis. Understanding the sources of acidification in organelles is crucial for comprehending cellular processes and their regulation.

Sources of Acidification of Cell Organelles:

1. V-Type Proton Pumps (V-ATPases):

The most significant contributor to organellar acidification is the V-type proton pump (V-ATPase). These proton pumps are embedded in the membranes of acidic organelles such as lysosomes, endosomes and vacuoles. V-ATPases pump protons (H⁺) from the cytoplasm into the lumen of these organelles, thus lowering the pH inside them. The energy required for this proton transport comes from ATP hydrolysis. The acidic environment created by V-ATPases is essential for the activity of hydrolytic enzymes, such as proteases and nucleases, which require low pH to degrade cellular waste efficiently.

2. H+/K+ ATPase Pumps:

In certain cell types, such as those in the stomach lining, the H+/K+ ATPase pump plays a significant role in acidifying intracellular compartments. This pump exchanges potassium ions (K⁺) from inside the organelle for hydrogen ions (H⁺), thereby helping to maintain acidic conditions. In cells like parietal cells of the stomach, this pump is critical for generating gastric acid, which is required for digestion. Similarly, in organelles like the Golgi apparatus, this pump contributes to the acidification needed for protein processing.

3. Endocytosis and Vesicular Trafficking:

Acidification of endosomes and lysosomes is also facilitated by the process of endocytosis, where the plasma membrane engulfs extracellular materials. During this process, vesicles mature and become more acidic due to the activity of V-ATPases. As early endosomes mature into late endosomes and lysosomes, protons are pumped into these vesicles, lowering the internal pH. This acidic environment is necessary for the activation of enzymes like cathepsins that break down internalized material.

4. Metabolic Processes:

Cellular metabolism is another source of acidification. During processes like glycolysis, oxidative phosphorylation and the tricarboxylic acid cycle, protons are released as byproducts. For example, lactic acid produced during anaerobic glycolysis results in the generation of hydrogen ions, which can contribute to the acidification of the cytoplasm and its transport into organelles.

5. Ion Channel Activity:

Ion channels, such as the Na+/H+ exchanger or Cl-/HCO3- exchanger, play an indirect role in maintaining acidic conditions inside organelles. These channels help regulate ion concentrations by exchanging sodium or chloride ions with hydrogen ions, thereby contributing to acidification.

07. Explain the mechanism of aciditification of stomach.

The process of acidification of the stomach is very important for digestion. It mainly involves the secretion of hydrochloric acid (HCl) into the lumen of the stomach. The acid helps in several ways such as killing harmful bacteria, breaking down food into simpler forms and activating digestive enzymes like pepsinogen into pepsin. The acid is secreted by specialised cells called parietal cells located mainly in the fundus and body regions of the stomach. These cells are specially designed to produce and secrete the strong acid without damaging themselves.

The mechanism of acidification of the stomach happens through a series of properly organised steps inside the parietal cells:

Step 1: Formation of Carbonic Acid inside Parietal Cells

Inside the parietal cells, carbon dioxide (CO₂) produced by cellular metabolism or absorbed from the blood combines with water (H₂O). This reaction is catalysed by the enzyme called carbonic anhydrase. The result of this reaction is the formation of an unstable molecule called carbonic acid (H₂CO₃).

Step 2: Dissociation of Carbonic Acid

The carbonic acid (H₂CO₃) quickly breaks down into two ions one hydrogen ion (H⁺) and one bicarbonate ion (HCO₃⁻). This breakdown is a spontaneous process and happens immediately after carbonic acid is formed inside the parietal cell.

Step 3: Active Secretion of Hydrogen Ions into Stomach Lumen

The hydrogen ions (H⁺) formed inside the cell are actively pumped out into the stomach lumen. This is done by a special protein present on the apical membrane of the parietal cells known as the H⁺/K⁺ ATPase pump. This pump uses energy from ATP to exchange hydrogen ions from inside the cell with potassium ions (K⁺) from the stomach lumen. This is an active transport process and is very important because hydrogen ions are needed in a large amount for acid formation.

Step 4: Movement of Bicarbonate Ions into Blood

While hydrogen ions move into the stomach, the bicarbonate ions (HCO₃⁻) are transported out of the parietal cell into the bloodstream. This is done through a process called the chloride-bicarbonate exchanger located on the basolateral side of the cell. This movement causes a temporary rise in the pH of blood after meals, a phenomenon known as the alkaline tide.

Step 5: Entry and Secretion of Chloride Ions into the Lumen

At the same time, chloride ions (Cl⁻) from the blood enter the parietal cells through chloride channels. These chloride ions then move towards the apical side and are secreted into the stomach lumen. This passive movement of chloride ions is essential because they are needed to form hydrochloric acid.

Step 6: Formation of Hydrochloric Acid (HCl)

In the final step, the hydrogen ions (H⁺) secreted into the stomach lumen combine with the chloride ions (Cl⁻). The combination of H⁺ and Cl⁻ leads to the formation of hydrochloric acid (HCl). This HCl is highly acidic and brings down the pH of stomach contents to about 1 to 2, making the environment very acidic, which is ideal for digestion.

08. What are the roles of V-ATPase, Na⁺/H⁺ exchange and H⁺/K⁺ ATPase in the acidification of cell?

Acidification is an essential biological process which helps in many important activities inside the cell like digestion of waste materials, activation of enzymes, protein processing, and cellular defense. Three important types of ion transporters mainly help in this acidification process: V-ATPase, Na⁺/H⁺ exchanger and H⁺/K⁺ ATPase. Each transporter works at specific locations and in a unique way to regulate pH inside or outside the cell.

Role of V-ATPase

The V-ATPase, also called Vacuolar-type ATPase, is present on the membranes of intracellular organelles such as lysosomes, endosomes, Golgi apparatus and secretory vesicles. It plays a main role in acidifying the inside of these organelles. V-ATPase uses energy from ATP hydrolysis to pump hydrogen ions (H⁺) from the cytoplasm into the lumen of organelles. As hydrogen ions accumulate inside, the pH drops and the environment becomes acidic. This acidic environment is necessary for the activation of hydrolytic enzymes like acid hydrolases, which break down old proteins, lipids and other cellular waste. Without proper V-ATPase function, cellular digestion would fail and harmful substances would build up inside the cell.

Role of Na⁺/H⁺ Exchanger

The Na⁺/H⁺ exchanger is mainly located on the plasma membrane of cells and helps to maintain the cytoplasmic pH at a normal level. When the inside of the cell becomes too acidic due to buildup of hydrogen ions, this exchanger helps by removing hydrogen ions (H⁺) out of the cell and bringing sodium ions (Na⁺) into the cell. This exchange uses the sodium gradient created by the Na⁺/K⁺ ATPase pump. In this way, the Na⁺/H⁺ exchanger prevents the cell cytoplasm from becoming too acidic and keeps the internal environment stable, which is necessary for all normal cell functions.

Role of H⁺/K⁺ ATPase

The H⁺/K⁺ ATPase is mainly found on the apical membrane of gastric parietal cells in the stomach lining. It plays an important role in the secretion of hydrochloric acid (HCl) into the stomach lumen. This transporter actively exchanges hydrogen ions (H⁺) with potassium ions (K⁺), using energy from ATP hydrolysis. Hydrogen ions are pumped into the stomach against their concentration gradient, where they combine with chloride ions (Cl⁻) to form HCl. This strong acid helps in protein digestion, activation of pepsinogen to pepsin, and killing harmful microorganisms that enter the stomach with food.

09. What are the factors causing resting membrane potential of the cell?

The resting membrane potential is the steady electrical charge difference that exists across the plasma membrane of a cell when the cell is not actively sending any signal. In this state, the inside of the cell is negatively charged compared to the outside. The resting membrane potential is very important because it keeps the cell ready to respond quickly when it needs to perform actions like muscle contraction, nerve signal transmission, or other cellular activities. This electrical potential does not happen by chance but is the result of the combined action of several specific factors that maintain ionic gradients and regulate charge separation across the membrane.

Here are the main factors responsible for creating and maintaining the resting membrane potential.

1. Unequal Distribution of Ions Across the Cell Membrane

The first important factor is the unequal distribution of ions like potassium (K⁺), sodium (Na⁺), chloride (Cl⁻) and calcium (Ca²⁺) across the membrane. Potassium ions are found in high concentration inside the cell, while sodium ions are in high concentration outside the cell. This difference in concentration of ions across the membrane forms a chemical gradient, which is necessary for creating the resting membrane potential.

2. Selective Permeability of the Plasma Membrane

The plasma membrane does not allow all ions to pass equally. It is much more permeable to potassium ions than to sodium or other ions. Because of this selective permeability, more potassium ions tend to move out of the cell than sodium ions move inside. This movement of positive charges out of the cell makes the inside of the cell relatively more negative.

3. Sodium-Potassium Pump (Na⁺/K⁺-ATPase)

Another key factor is the sodium-potassium pump. This pump uses energy from ATP to move three sodium ions out of the cell and two potassium ions into the cell. As a result, more positive charges are removed from the cell than are brought in, helping to maintain a negative charge inside the cell at rest.

4. Presence of Negatively Charged Proteins and Organic Anions Inside the Cell

Inside the cell, there are many large proteins and organic molecules that carry a negative charge. These molecules cannot cross the membrane easily and remain inside the cell. Their negative charges add to the negativity of the intracellular environment and support the formation of the resting membrane potential.

5. Potassium Leak Channels

Potassium leak channels are special protein channels that allow potassium ions to slowly move out of the cell, even when the cell is at rest. As potassium leaves the cell, it carries positive charge out, making the inside of the cell even more negative compared to the outside. This continuous potassium leakage is a very important factor for maintaining the resting membrane potential.

10. Describe in detail the channels responsible for cellular excitation.

Cellular excitation refers to the process by which a cell, especially nerve and muscle cells, becomes active and generates an action potential. This action potential is a rapid change in the membrane potential that allows the cell to send electrical signals over long distances. The ability of a cell to become excited and generate signals mainly depends on the presence and function of certain ion channels present in the plasma membrane. This process depends on the movement of ions like sodium (Na⁺), potassium (K⁺), calcium (Ca²⁺) and chloride (Cl⁻) across the cell membrane. Specialized proteins called ion channels regulate this ion flow. Based on how they open and function, ion channels involved in excitation are classified into four major types: Leak Channels, Voltage-Gated Ion Channels, Ligand-Gated Ion Channels and Mechanically-Gated Ion Channels.

1. Leak Channels (Passive Channels)

Leak channels are ion channels that are either always open or remain open most of the time. They allow the passive movement of ions according to their concentration gradients without needing any external stimulus.

The most important leak channels are potassium (K⁺) leak channels, which permit K⁺ ions to move out of the cell. This constant outward flow of K⁺ establishes and maintains the resting membrane potential of the cell, keeping the inside of the cell negatively charged compared to the outside.

Although they are not involved directly in action potentials, leak channels set the essential resting conditions necessary for cellular excitation.

2. Voltage-Gated Ion Channels

Voltage-gated ion channels open or close in response to changes in the membrane potential. These channels are highly selective for specific ions and are critical for initiating and propagating action potentials.

There are mainly three important types of voltage-gated ion channels:

1. Voltage-Gated Sodium (Na⁺) Channels:
• These channels open rapidly when the membrane potential becomes slightly less negative. Their opening allows Na⁺ to rush into the cell, causing the membrane to depolarize sharply and begin an action potential.
2. Voltage-Gated Potassium (K⁺) Channels:
• These channels open a little later than sodium channels. They allow K⁺ to move out of the cell, helping in repolarization and restoration of the resting membrane potential after the action potential.
3. Voltage-Gated Calcium (Ca²⁺) Channels:
1. These channels open in response to depolarization and allow Ca²⁺ to enter the cell. Calcium entry plays a crucial role in processes like neurotransmitter release at synapses and contraction of muscles.

Thus, voltage-gated channels are directly responsible for the electrical activity of excitable cells.

3. Ligand-Gated Ion Channels

Ligand-gated ion channels open in response to the binding of a chemical ligand like a neurotransmitter. When the ligand binds to the channel protein, it causes a conformational change that opens the channel and allows specific ions to pass through. This results in changes in membrane potential that can excite or inhibit the cell.

Ligand-gated channels are most important at synapses where communication between neurons or between a neuron and a muscle cell takes place.

Example: The nicotinic acetylcholine receptor opens when acetylcholine binds to it, allowing Na⁺ to enter and initiate muscle contraction.

4. Mechanically-Gated Ion Channels

Mechanically-gated ion channels open when physical forces like stretch, pressure, or vibration deform the membrane. They are especially important in sensory cells like touch receptors in the skin and hair cells in the inner ear.

When mechanical force acts on the membrane, it changes the structure of these channels, allowing ions to flow and generate an electrical signal that the nervous system can interpret.

Example: Stretch-activated channels in skin sense touch and pressure.

11. What are the roles of leak channel, chemically gated channel, voltage gated channel and mechanically gated channel in cell excitation?

Cell excitation refers to the ability of a cell, especially a neuron or muscle cell, to respond to a stimulus by generating an electrical signal. This process mainly depends on the movement of ions across the cell membrane, which occurs through special proteins called ion channels. These channels control how ions like sodium (Na⁺), potassium (K⁺), calcium (Ca²⁺) and chloride (Cl⁻) enter or exit the cell.

There are four main types of ion channels involved in this process:

1. Leak Channels (also known as Passive Channels)
2. Chemically Gated Channels (also called Ligand-Gated)
3. Voltage-Gated Channels
4. Mechanically Gated Channels

1. Leak Channels

Leak channels are always open and allow continuous passive movement of specific ions, mainly potassium ions (K⁺), down their concentration gradient. These channels do not open or close in response to any external stimulus but remain open to maintain ionic balance.

Role in excitation:

Leak channels mainly help in maintaining the resting membrane potential of the cell. They allow K⁺ to slowly exit the cell, making the inside of the membrane more negative compared to the outside. This resting negative charge is necessary because excitation can only begin when the membrane potential changes from this resting value. Leak channels set this baseline potential and help prepare the cell to respond quickly when a stimulus comes. Without this background ionic movement, the cell would not be able to get excited properly.

2. Chemically Gated Channels (Ligand-Gated Channels)

These channels open in response to binding of a specific chemical or neurotransmitter such as acetylcholine, serotonin, or glutamate. These are especially found on the postsynaptic membrane in neurons.

Role in excitation:

They are responsible for initiating depolarization at the site of synaptic contact. When the neurotransmitter binds to the receptor on the channel, it causes the channel to open and allows Na⁺ or Ca²⁺ to enter the cell, leading to local depolarization. This creates a graded potential, which, if strong enough, will trigger voltage-gated channels nearby. So, these channels are the first responders that begin the excitation process in response to chemical signals.

3. Voltage-Gated Channels

These channels open or close in response to specific changes in the membrane potential. The main voltage-gated channels involved in excitation are Na⁺, K⁺, and Ca²⁺ channels.

Role in excitation:

They are central to generating and propagating action potentials. Once the graded potential brings the membrane to threshold level, voltage-gated Na⁺ channels open quickly causing a rapid influx of Na⁺ and a sharp depolarization. After a short delay, voltage-gated K⁺ channels open, causing repolarization by letting K⁺ out. In neurons, voltage-gated Ca²⁺ channels also play an important role at the synaptic terminal by causing release of neurotransmitters. So, they ensure the full development and spread of excitation along the entire membrane.

4. Mechanically Gated Channels

These channels open in response to mechanical deformation of the membrane, such as touch, stretch, pressure, or vibration. They are found in sensory cells such as touch receptors, hair cells of the ear and stretch receptors.

Role in excitation:

They play a key role in converting physical or mechanical stimuli into electrical signals. When these channels are stretched or pushed due to mechanical force, they open and allow positive ions like Na⁺ or Ca²⁺ to flow in, causing depolarization. This depolarization may lead to an action potential if threshold is reached. Therefore, they are important for sensory excitation where physical stimulus needs to be converted into nerve signals.

12. Describe the phases of cell excitation.

Cell excitation mainly refers to the process through which excitable cells such as neurons and muscle cells respond to a stimulus by generating an electrical signal called an action potential. This signal helps in the transmission of information in neurons or in muscle contraction. The process of cell excitation occurs in well-defined electrical phases which are caused by controlled movement of ions (mainly Na⁺, K⁺, and sometimes Ca²⁺) across the cell membrane. These phases occur one after another in a sequence and each phase has a specific ionic mechanism and functional role. There are five main phases involved in the process of cell excitation:

1. Resting Membrane Potential
2. Depolarization
3. Repolarization
4. Hyperpolarization
5. Restoration of the Resting Potential

1. Resting Membrane Potential

The first phase in cell excitation is the resting membrane potential. At this stage, the cell is at rest and its membrane potential is stable, typically around -70mV, although this can vary slightly depending on the cell type. This potential is maintained primarily by the sodium-potassium pump (Na⁺/K⁺ ATPase), which actively transports sodium ions (Na⁺) out of the cell and potassium ions (K⁺) into the cell, against their concentration gradients. Additionally, the membrane has more potassium leak channels than sodium channels, allowing potassium to diffuse out of the cell, making the inside of the cell more negative compared to the outside. The result is a polarized state, where the inside of the cell is negatively charged relative to the outside.

2. Depolarization

Depolarization occurs when the cell becomes less negative, moving toward a more positive membrane potential. This phase is initiated by the opening of voltage-gated sodium channels. When a stimulus, such as a signal from an adjacent neuron, reaches the cell membrane and causes the membrane potential to become less negative, these channels open. Sodium ions, which are at a higher concentration outside the cell, rush in. As a result, the inside of the cell becomes more positive, typically reaching a value of +30mV. Depolarization is a rapid and essential event in the process of excitation, as it is the trigger for action potential propagation in excitable cells like neurons and muscle cells.

3. Repolarization

After depolarization, the cell must return to its resting state, which happens through repolarization. This phase is characterized by the closing of sodium channels and the opening of voltage-gated potassium channels. As potassium ions, which are at a higher concentration inside the cell, flow out of the cell, the membrane potential becomes more negative again. This process helps restore the cell’s negative internal charge, returning it toward the resting membrane potential. The rapid efflux of potassium during repolarization ensures that the cell will be ready for the next action potential.

4. Hyperpolarization

Hyperpolarization is a phase where the membrane potential becomes even more negative than the resting membrane potential. This can occur when the potassium channels remain open slightly longer than necessary, allowing an excess of potassium ions to leave the cell. As a result, the cell becomes more negative than its resting state, typically reaching values below -70mV. Hyperpolarization is an important mechanism as it prevents the cell from immediately firing another action potential, thus ensuring that the cell has a period of rest before it can be excited again.

5. Restoration of the Resting Potential

The final phase is the restoration of the resting potential. During this phase, the sodium-potassium pump works to restore the original ion concentrations across the membrane, with sodium being pumped out and potassium being pumped back into the cell. This process helps the cell return to its stable, resting membrane potential of around -70mV, ensuring that it is ready for the next cycle of excitation. Additionally, any remaining excess potassium in the cell is balanced out and the membrane potential is fully restored to its resting state, ready for the next depolarization.

13. Draw a schematic diagram to explain activation of postsynaptic receptors and cell response.

When a nerve signal travels across a synapse, the neurotransmitters released by the presynaptic neuron activate specific postsynaptic receptors on the membrane of the postsynaptic neuron or cell. This process is crucial for signal transmission between neurons and is responsible for various physiological responses like muscle contraction, memory formation and sensory perception. The activation of these receptors triggers a series of cellular responses that alter the electrical state of the postsynaptic neuron and determine whether it will generate an action potential.

This process can be divided into two main parts:

1. Activation of Postsynaptic Receptors: This part includes the steps that happen when the neurotransmitters bind to the postsynaptic receptors and initiate a signaling process in the postsynaptic cell.
2. Cellular Response: This describes how the postsynaptic cell reacts after receptor activation, including changes in the membrane potential and the potential generation of an action potential.

Let's explore both of these parts in detail:

1. Activation of Postsynaptic Receptors

When an action potential arrives at the presynaptic terminal, neurotransmitters are released into the synaptic cleft. These neurotransmitters then bind to postsynaptic receptors on the postsynaptic cell membrane. The process of activation can be divided into the following steps:

Step 1: Neurotransmitter Release

When the action potential reaches the presynaptic terminal, it causes calcium (Ca²⁺) channels to open. Calcium ions enter the presynaptic neuron, triggering the release of neurotransmitter molecules from synaptic vesicles into the synaptic cleft.

Step 2: Binding to Postsynaptic Receptors

Once released, the neurotransmitters diffuse across the synaptic cleft and bind to specific postsynaptic receptors. These receptors can be of two types:

1. Ionotropic receptors: These receptors are directly linked to ion channels. When the neurotransmitter binds, the ion channel opens, allowing ions like sodium (Na⁺), potassium (K⁺), or chloride (Cl⁻) to flow through, which changes the electrical state of the postsynaptic cell.
2. Metabotropic receptors: These receptors are linked to G-proteins and intracellular signaling pathways. Activation of these receptors triggers a cascade of intracellular events that can result in changes in cell function, but not a direct opening of ion channels.

Step 3: Ion Channel Opening or Intracellular Signaling

In the case of ionotropic receptors, binding of the neurotransmitter leads to the opening of ion channels. The flow of ions (for example, Na⁺ or Cl⁻) into or out of the postsynaptic cell changes the membrane potential. For metabotropic receptors, intracellular signaling pathways are activated, leading to long-term cellular effects, including changes in cell excitability or gene expression.

2. Cellular Response

After the postsynaptic receptors are activated, the postsynaptic cell undergoes a cellular response. This response primarily involves changes in the membrane potential of the postsynaptic cell. The process is crucial in determining whether the postsynaptic neuron will generate an action potential. The key stages in the cellular response are:

Step 1: Change in Membrane Potential

If the neurotransmitter binding leads to the opening of sodium channels (in excitatory synapses), positively charged sodium ions enter the postsynaptic cell, leading to depolarization. Depolarization brings the membrane potential closer to the threshold, which may lead to an action potential.

If the neurotransmitter binding leads to the opening of chloride or potassium channels (in inhibitory synapses), negatively charged chloride ions enter or positively charged potassium ions exit, causing hyperpolarization. This makes the membrane potential more negative, moving it further from the action potential threshold and inhibiting the cell from firing.

Step 2: Generation of Action Potential

If the depolarization in the postsynaptic neuron reaches the threshold potential, it triggers the opening of voltage-gated sodium channels. This initiates an action potential, a rapid electrical signal that travels down the axon and transmits the signal to the next neuron or effector.

Step 3: Signal Termination

Once the neurotransmitter has activated the postsynaptic receptors, the signal is terminated by one of the following mechanisms:

• Reuptake: The neurotransmitter is taken back into the presynaptic neuron for reuse.
• Enzymatic Breakdown: Enzymes in the synaptic cleft break down neurotransmitters (e.g., acetylcholinesterase breaks down acetylcholine).
• Diffusion: The neurotransmitter may diffuse away from the synaptic cleft, stopping the signal.

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