Cell Surface Receptors: Types and Functions — MCQs
Which of the following is a metabotropic receptor?
If there is a Gs alpha subunit gain-of-function mutation, this results in
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
Which of the following binds to intracellular receptors?
All the following hormones have receptors on the plasma membrane of target tissues except:
One of the ways that cells communicate with each other is by secretion of various molecules. The secreted molecule is known as
Which of the following stimulate adenylate cyclase with G-protein coupled action ?
Which of the following statements about G protein-coupled receptors (GPCRs) is correct?
Which intervention is best in patients operated for bilateral acoustic neuroma for hearing rehabilitation?
Which of the following statements best describes the mechanism of action of insulin on target cells?
Cell Surface Receptors: Types and Functions Indian Medical PG Practice Questions and MCQs
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
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.
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
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.
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)
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
Question 4: Which of the following binds to intracellular receptors?
- A. Growth hormone
- B. Vitamin E
- C. Estrogen (Correct Answer)
- D. Insulin
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.
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
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.
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)
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.
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
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.
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.
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.
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
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.
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)
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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