Cell Surface Receptors: Types and Functions Indian Medical PG Practice Questions and MCQs
Practice Indian Medical PG questions for Cell Surface Receptors: Types and Functions. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Cell Surface Receptors: Types and Functions Indian Medical PG Question 1: Which of the following is a metabotropic receptor?
- A. GABA-A receptor
- B. Beta receptor for norepinephrine (Correct Answer)
- C. NMDA receptor
- D. Nicotinic acetylcholine receptor
Cell Surface Receptors: Types and Functions Explanation: ***Beta receptor for norepinephrine***
- **Beta-adrenergic receptors** (like those for norepinephrine) are **G protein-coupled receptors**, which are the hallmark of metabotropic receptors.
- Activation of these receptors leads to a cascade of **intracellular signaling events** through second messengers, rather than direct ion channel opening.
*GABA-A receptor*
- The **GABA-A receptor** is a **ligand-gated ion channel** (ionotropic receptor) that, when activated by GABA, allows chloride ions to flow into the neuron.
- This influx of **chloride ions** causes hyperpolarization, leading to an inhibitory effect.
*Nicotinic acetylcholine receptor*
- The **nicotinic acetylcholine receptor** is a **ligand-gated ion channel** (ionotropic receptor) that, upon binding acetylcholine, directly opens to allow the passage of sodium and potassium ions.
- This ion movement causes **depolarization** and excitation of the postsynaptic cell.
*NMDA receptor*
- The **NMDA receptor** is a type of **glutamate receptor** that functions as a **ligand-gated ion channel** (ionotropic receptor) and is permeable to Na+, K+, and Ca2+.
- Its activation requires both **glutamate binding** and depolarization to remove a magnesium block, directly leading to ion flow.
Cell Surface Receptors: Types and Functions Indian Medical PG Question 2: If there is a Gs alpha subunit gain-of-function mutation, this results in
- A. Increased cAMP (Correct Answer)
- B. Decreased cAMP
- C. Increased GTPase activity
- D. Decreased IP₃
Cell Surface Receptors: Types and Functions Explanation: ***Increased cAMP***
- A **gain-of-function mutation** in the **Gs alpha subunit** means it remains in its active, GTP-bound state for longer.
- The activated Gs alpha subunit stimulates **adenylyl cyclase**, leading to persistently high levels of **cAMP**.
*Decreased cAMP*
- This would result from a **loss-of-function** mutation in the Gs alpha subunit or a gain-of-function in an inhibitory G protein (Gi), not a Gs gain-of-function.
- A decrease in cAMP would inhibit downstream signaling pathways, which is the opposite of what occurs with Gs activation.
*Increased GTPase activity*
- **GTPase activity** is responsible for hydrolyzing GTP to GDP, which inactivates the G alpha subunit.
- A gain-of-function mutation often implies **reduced GTPase activity**, causing the G protein to stay active longer, not increased activity.
*Decreased IP*
- **IP3 (inositol trisphosphate)** is a secondary messenger produced via the activation of **phospholipase C**, typically by Gq proteins.
- Gs alpha subunit mutations primarily affect the **adenylyl cyclase/cAMP pathway**, not the inositol phosphate pathway.
Cell Surface Receptors: Types and Functions Indian Medical PG Question 3: Sequence the events in neuromuscular action potential conduction:
1. Sodium channels open in the end plate
2. Calcium enters at the nerve terminal
3. Release of acetylcholine
- A. $1 \rightarrow 2 \rightarrow 3$
- B. $1 \rightarrow 3 \rightarrow 2$
- C. $3 \rightarrow 2 \rightarrow 1$
- D. $2 \rightarrow 3 \rightarrow 1$ (Correct Answer)
Cell Surface Receptors: Types and Functions Explanation: ***Correct: $2 \rightarrow 3 \rightarrow 1$***
- **Calcium entry at the nerve terminal** is the initial trigger - when an action potential reaches the presynaptic nerve terminal, voltage-gated calcium channels open, allowing Ca²⁺ influx
- **Acetylcholine release** follows - the increased intracellular calcium causes synaptic vesicles containing acetylcholine to fuse with the presynaptic membrane and release the neurotransmitter into the synaptic cleft
- **Sodium channels open in the end plate** last - acetylcholine binds to nicotinic receptors on the motor end plate, opening ligand-gated sodium channels, which depolarizes the muscle membrane and triggers muscle contraction
*Incorrect: $1 \rightarrow 2 \rightarrow 3$*
- Places sodium channel opening first, which is physiologically impossible
- Sodium channels at the motor end plate only open in response to acetylcholine binding
- Cannot occur before acetylcholine is released from the nerve terminal
*Incorrect: $1 \rightarrow 3 \rightarrow 2$*
- Incorrectly sequences sodium channel opening before calcium entry
- Violates the fundamental principle that calcium influx is required for neurotransmitter release
- Acetylcholine cannot be released without prior calcium entry
*Incorrect: $3 \rightarrow 2 \rightarrow 1$*
- Places acetylcholine release before calcium entry, which is impossible
- Calcium-triggered exocytosis is an absolute requirement for neurotransmitter release
- Without calcium influx, vesicles cannot fuse with the presynaptic membrane
Cell Surface Receptors: Types and Functions Indian Medical PG Question 4: Which of the following binds to intracellular receptors?
- A. Growth hormone
- B. Vitamin E
- C. Estrogen (Correct Answer)
- D. Insulin
Cell Surface Receptors: Types and Functions Explanation: ***Estrogen***
- **Estrogen** is a **steroid hormone** that, due to its **lipophilic nature**, can easily pass through the cell membrane to bind to **intracellular receptors** in the cytoplasm or nucleus.
- This binding leads to the formation of a **hormone-receptor complex** that acts as a transcription factor, regulating **gene expression**.
*Growth hormone*
- **Growth hormone** is a **peptide hormone** and therefore **hydrophilic**, meaning it cannot freely cross the cell membrane.
- It binds to **transmembrane receptors** on the cell surface, initiating intracellular signaling cascades through pathways like the **JAK/STAT pathway**.
*Vitamin E*
- **Vitamin E** is a **lipid-soluble vitamin** and an important **antioxidant**, but it does not function as a signaling molecule that binds to intracellular receptors to regulate gene expression in the same manner as steroid hormones.
- While it diffuses across membranes due to its lipophilicity, its primary role is to protect cell membranes from **oxidative damage**.
*Insulin*
- **Insulin** is a **protein hormone** that is **hydrophilic** and cannot pass through the cell membrane.
- It binds to **tyrosine kinase receptors** on the cell surface, triggering a cascade of intracellular events like the **PI3K/Akt pathway** to regulate glucose metabolism.
Cell Surface Receptors: Types and Functions Indian Medical PG Question 5: All the following hormones have receptors on the plasma membrane of target tissues except:
- A. Epinephrine
- B. Glucagon
- C. Estradiol (Correct Answer)
- D. Thyrotropin
Cell Surface Receptors: Types and Functions Explanation: ***Estradiol***
- **Estradiol** is a **steroid hormone** derived from cholesterol, making it **lipid-soluble**.
- Due to its lipid solubility, estradiol can readily pass through the **plasma membrane** and bind to **intracellular receptors** in the cytoplasm or nucleus.
*Epinephrine*
- **Epinephrine** is a **catecholamine hormone** and is **water-soluble**.
- Water-soluble hormones cannot cross the lipid bilayer of the plasma membrane and thus bind to **receptors located on the cell surface**.
*Glucagon*
- **Glucagon** is a **peptide hormone** and is **water-soluble**.
- Like other peptide hormones, it binds to **specific receptors embedded in the plasma membrane** to elicit its cellular effects via second messenger systems.
*Thyrotropin*
- **Thyrotropin**, also known as **Thyroid-Stimulating Hormone (TSH)**, is a **glycoprotein hormone** and is **water-soluble**.
- TSH exerts its action by binding to **receptors on the plasma membrane** of thyroid follicular cells.
Cell Surface Receptors: Types and Functions Indian Medical PG Question 6: One of the ways that cells communicate with each other is by secretion of various molecules. The secreted molecule is known as
- A. A receptor molecule
- B. An integrin
- C. A spectrin tetramer
- D. A signaling molecule (Correct Answer)
Cell Surface Receptors: Types and Functions Explanation: ***A signaling molecule***
- Cells communicate by releasing **signaling molecules** that travel to other cells and bind to specific receptors.
- These molecules transmit information, initiating a **response** in the target cell.
*A receptor molecule*
- A **receptor molecule** is located on the target cell's surface or inside the cell and binds to the signaling molecule, rather than being the secreted molecule itself.
- Its role is to **receive** the signal, not to transmit it from the secreting cell.
*An integrin*
- **Integrins** are transmembrane proteins that link the cell's cytoskeleton to the extracellular matrix, facilitating cell adhesion and migration.
- They are primarily involved in **cell-matrix interactions** and less directly in general cell-to-cell signaling via secretion.
*A spectrin tetramer*
- A **spectrin tetramer** is a component of the cytoskeleton, particularly important in maintaining the shape and structural integrity of red blood cells.
- It functions as an **intracellular structural protein** and is not a secreted molecule involved in cell-to-cell communication.
Cell Surface Receptors: Types and Functions Indian Medical PG Question 7: Which of the following stimulate adenylate cyclase with G-protein coupled action ?
- A. Shiga toxin
- B. Cholera toxin (Correct Answer)
- C. Diphtheria toxin
- D. Pseudomonas toxin
Cell Surface Receptors: Types and Functions Explanation: ***Cholera toxin***
- Cholera toxin is a **G-protein-activating toxin** that irreversibly activates **adenylate cyclase**.
- This leads to increased intracellular levels of **cAMP**, causing excessive fluid secretion into the intestinal lumen and severe diarrhea.
*Shiga toxin*
- Shiga toxin acts by inactivating the **60S ribosomal subunit**, thereby inhibiting protein synthesis in eukaryotic cells.
- Its primary effect is **cytotoxicity**, not direct stimulation of adenylate cyclase.
*Diphtheria toxin*
- Diphtheria toxin inhibits **protein synthesis** by inactivating **elongation factor-2 (EF-2)** through ADP-ribosylation.
- This toxin specifically targets host cells, leading to cellular death and tissue damage.
*Pseudomonas toxin*
- **Exotoxin A** produced by *Pseudomonas aeruginosa* also inhibits **protein synthesis** by ADP-ribosylating and inactivating **EF-2**, similar to diphtheria toxin.
- It does not directly affect adenylate cyclase activity.
Cell Surface Receptors: Types and Functions Indian Medical PG Question 8: Which of the following statements about G protein-coupled receptors (GPCRs) is correct?
- A. The alpha subunit of G proteins determines whether they are stimulatory or inhibitory. (Correct Answer)
- B. G proteins bind hormones directly before transmitting signals to receptors.
- C. G proteins are active when bound to GDP and inactive when bound to GTP.
- D. G proteins require the beta and gamma subunits to remain bound to the alpha subunit to transmit signals.
Cell Surface Receptors: Types and Functions Explanation: ***The alpha subunit of G proteins determines whether they are stimulatory or inhibitory.***
- The **alpha subunit** of a G protein determines its specific function, such as activating or inhibiting downstream enzymes like adenylyl cyclase, thereby classifying the G protein as Gs (stimulatory), Gi (inhibitory), or Gq.
- This specificity arises from the **alpha subunit's unique binding sites** for downstream effectors and its intrinsic GTPase activity, which regulates its activation state.
*G proteins require the beta and gamma subunits to remain bound to the alpha subunit to transmit signals.*
- This is **incorrect**. Upon activation, the **alpha subunit dissociates from the beta-gamma dimer**, and both components function **independently** to modulate downstream effectors.
- The **alpha subunit** regulates enzymes like adenylyl cyclase or phospholipase C, while the **beta-gamma complex** can independently modulate ion channels and other effector proteins.
*G proteins bind hormones directly before transmitting signals to receptors.*
- **G protein-coupled receptors (GPCRs)** are responsible for binding hormones (ligands) directly, which then causes a **conformational change in the receptor**.
- This conformational change is what then activates the associated G protein, which subsequently transmits the signal to intracellular effectors.
*G proteins are active when bound to GDP and inactive when bound to GTP.*
- **G proteins are generally active when bound to GTP** and inactive when bound to GDP.
- Upon activation, the G protein exchanges GDP for GTP, which leads to its conformational change and dissociation into active alpha and beta-gamma subunits.
Cell Surface Receptors: Types and Functions Indian Medical PG Question 9: Which intervention is best in patients operated for bilateral acoustic neuroma for hearing rehabilitation?
- A. Bilateral cochlear implant
- B. Auditory brainstem implant (ABI) (Correct Answer)
- C. Unilateral cochlear implant
- D. High power hearing aid
Cell Surface Receptors: Types and Functions Explanation: ***Auditory brainstem implant (ABI)***
- Patients with bilateral acoustic neuromas often suffer damage to both **auditory nerves** during surgery, rendering cochlear implants ineffective.
- The **ABI** bypasses the damaged auditory nerves and directly stimulates the **cochlear nucleus** in the brainstem, allowing for sound perception.
*Bilateral cochlear implant*
- This intervention is suitable when the **auditory nerve** remains intact and functional, which is typically not the case after bilateral acoustic neuroma surgery.
- Cochlear implants depend on the integrity of the auditory nerve to transmit electrical signals to the brain.
*Unilateral cochlear implant*
- Similar to bilateral cochlear implants, a unilateral implant relies on a functional **auditory nerve** on the implanted side.
- In bilateral acoustic neuroma, both auditory nerves are usually compromised or sacrificed, making a unilateral implant unsuitable for binaural hearing rehabilitation.
*High power hearing aid*
- Hearing aids only amplify sound and are effective for **sensorineural hearing loss** where the cochlea and auditory nerve are still functional.
- They would not be beneficial in cases where the auditory nerve is damaged or absent, as occurs after bilateral acoustic neuroma removal.
Cell Surface Receptors: Types and Functions Indian Medical PG Question 10: Which of the following statements best describes the mechanism of action of insulin on target cells?
- A. Insulin binds to a receptor on the outer surface of the plasma membrane, activating adenylate cyclase through the Gs protein.
- B. Insulin binds to a cytoplasmic receptor and is transferred as a hormone receptor complex to the nucleus to modulate gene expression.
- C. Insulin enters the cell and causes the release of calcium ions from intracellular stores.
- D. Insulin binds to a transmembrane receptor on the outer surface of the plasma membrane, activating the tyrosine kinase in the cytosolic domain of the receptor. (Correct Answer)
Cell Surface Receptors: Types and Functions Explanation: ***Insulin binds to a transmembrane receptor on the outer surface of the plasma membrane, activating the tyrosine kinase in the cytosolic domain of the receptor.***
- **Insulin** is a **peptide hormone** and cannot freely pass through the lipid bilayer, thus it binds to a **transmembrane receptor** on the cell surface.
- This binding leads to the activation of the receptor's intrinsic **tyrosine kinase activity** in the intracellular domain, initiating a signaling cascade.
*Insulin binds to a cytoplasmic receptor and is transferred as a hormone receptor complex to the nucleus to modulate gene expression.*
- This mechanism describes the action of **steroid hormones**, which are lipid-soluble and can cross the cell membrane, binding to **intracellular receptors**.
- **Insulin** acts via a **cell surface receptor** and its downstream effects are mediated through signal transduction pathways, not direct nuclear translocation.
*Insulin binds to a receptor on the outer surface of the plasma membrane, activating adenylate cyclase through the Gs protein.*
- This mechanism is characteristic of **G-protein coupled receptors (GPCRs)**, which activate or inhibit enzymes like adenylate cyclase via G-proteins to produce second messengers like cyclic AMP.
- The **insulin receptor** is a **receptor tyrosine kinase**, not a GPCR, and does not directly activate adenylate cyclase via Gs protein.
*Insulin enters the cell and causes the release of calcium ions from intracellular stores.*
- While some hormones and neurotransmitters can trigger the release of intracellular **calcium ions**, this is typically mediated by specific pathways (e.g., GPCRs linked to phospholipase C).
- **Insulin** does not directly enter target cells to cause calcium release; its actions are primarily mediated through receptor tyrosine kinase signaling pathways.
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