Central Nervous System Pharmacology Practice Questions

Q: Buprenorphine is a partial agonist at which opioid receptor?

Mu. ***Mu*** - Buprenorphine primarily acts as a **partial agonist** at the **mu opioid receptor**, providing analgesic effects with a ceiling effect on respiratory depression. - Its partial agonism at the mu receptor contributes to its lower potential for respiratory depression and overdose compared to full mu agonists. *Kappa* - While buprenorphine has some antagonist activity at the kappa receptor, its primary therapeutic action is not at this receptor. - **Kappa receptor agonists** like pentazocine can produce dysphoria and psychotomimetic effects. *Delta* - The delta opioid receptor is involved in analgesia and emotional responses, but buprenorphine has very low affinity and activity at this receptor. - **Delta receptor agonists** are not widely used clinically due to limited efficacy and side effects. *ORL-1* - The ORL-1 (Opioid Receptor-like 1) receptor, also known as the nociceptin receptor, is distinct from classical opioid receptors. - Buprenorphine has **no significant activity** at the ORL-1 receptor, which primarily mediates pain, anxiety, and learning.

Q: Where is the benzodiazepine binding site located on GABA receptors?

γ-subunit. ***γ-subunit*** - The **benzodiazepine binding site** is located at the interface between the **α and γ subunits** of the GABA-A receptor, with the **γ-subunit (especially γ2) being essential** for benzodiazepine sensitivity. - The presence of the **γ2 subunit** is **mandatory** for benzodiazepine binding - receptors lacking this subunit are **insensitive to benzodiazepines**. - Benzodiazepines bind to this site and act as **positive allosteric modulators**, increasing the frequency of **chloride channel opening** in response to GABA. - This is the **standard answer** for NEET-PG and medical PG examinations in India. *α-subunit* - The **α-subunit** contributes to forming the benzodiazepine binding pocket at the α-γ interface. - Different **α-subunit isoforms** (α1, α2, α3, α5) determine the pharmacological profile and tissue distribution of benzodiazepine effects. - However, the **α-subunit alone** cannot bind benzodiazepines without the γ-subunit. *β-subunit* - The **β-subunit** contains the primary binding site for **GABA** itself. - It does not participate in benzodiazepine binding but is crucial for the receptor's overall function and GABAergic signaling. *δ-subunit* - The **δ-subunit** replaces the γ-subunit in certain GABA-A receptor subtypes that mediate **tonic inhibition**. - Receptors containing **δ-subunits** are **insensitive to benzodiazepines** but sensitive to neurosteroids and certain general anesthetics. - This is a key distinguishing feature between phasic (γ-containing) and tonic (δ-containing) GABA-A receptors.

Q: All are symptoms of morphine withdrawal except?

Fall in BP. ***Fall in BP*** - **Hypotension (fall in BP)** is **not** typically a symptom of opioid withdrawal; rather, **hypertension** can occur due to sympathetic overdrive. - Opioid withdrawal symptoms are primarily characterized by **hyperactivity** and increased sympathetic nervous system activity. *Mydriasis* - **Mydriasis (dilated pupils)** is a classic symptom of opioid withdrawal, resulting from reduced parasympathetic tone and increased sympathetic activity. - In contrast, opioid intoxication causes **miosis (pinpoint pupils)**. *Yawning* - **Yawning** is a very common and early symptom of opioid withdrawal, often accompanied by feelings of fatigue and restlessness. - It reflects generalized **autonomic dysregulation** during withdrawal. *Lacrimation* - **Lacrimation (tearing)** is another prominent autonomic symptom of opioid withdrawal. - This, along with rhinorrhea, contributes to the **"flu-like" symptoms** experienced during withdrawal.

Q: Botulinum toxin type B is used in which disease?

Cervical dystonia. ***Cervical dystonia*** * **Botulinum toxin type B (Myobloc/NeuroBloc)** is specifically approved for the treatment of **cervical dystonia**, which involves involuntary contractions of neck muscles. * It works by blocking the release of **acetylcholine** at the neuromuscular junction, leading to muscle relaxation. *Strabismus* * **Botulinum toxin type A (Botox, Dysport, Xeomin)** is the preferred and most commonly used form for treating **strabismus** by temporarily weakening specific extraocular muscles. * Type B is generally not indicated for strabismus due to differences in potency and duration of action. *Blepharospasm* * **Botulinum toxin type A** (e.g., Botox) is the primary treatment for **blepharospasm**, an involuntary forceful closure of the eyelids. * While both types inhibit acetylcholine release, type A has a more established and concentrated use in treating localized muscle spasms like blepharospasm. *Glabellar lines* * **Botulinum toxin type A** is widely used for cosmetic applications such as reducing **glabellar lines** (frown lines between the eyebrows). * Its efficacy and safety for cosmetic indications are well-established, making type A the standard choice over type B.

Q: Botulinum toxin acts on

Synapse. ***Synapse*** - **Botulinum toxin** acts by inhibiting the release of **acetylcholine** at the **neuromuscular junction**, which is a type of synapse. - This blockade of neurotransmitter release at the **presynaptic terminal** prevents muscle contraction, leading to paralysis. *Smooth muscle of intestine* - While botulinum toxin can affect smooth muscle indirectly by paralyzing the motor nerves innervating them, its primary site of action is the **synapse** itself, not directly on the muscle fibers. - The toxin primarily targets the nerve endings, rather than the mechanical contractility of the muscle cell. *Central nervous system* - **Botulinum toxin** does not readily cross the **blood-brain barrier**, meaning its primary effects are peripheral. - Its therapeutic and toxic effects are localized to the **peripheral nervous system** and neuromuscular junctions. *Sensory nerves* - **Botulinum toxin** specifically targets **motor nerve endings** to inhibit acetylcholine release, leading to muscle paralysis. - It does not directly affect the function of **sensory nerve transmission** or pain perception in the same way.

Q: Which of the following is a benzylisoquinoline muscle relaxant?

Doxacurium. ***Doxacurium*** - **Doxacurium** is a long-acting, non-depolarizing neuromuscular blocker classified as a **benzylisoquinoline** compound [1]. - These agents are known for their minimal cardiovascular effects and lack of histamine release in therapeutic doses [1]. *Vecuronium* - **Vecuronium** is an **aminosteroid** non-depolarizing neuromuscular blocker [2]. - It is known for its intermediate duration of action and minimal cardiovascular effects [1]. *Rocuronium* - **Rocuronium** is also an **aminosteroid** non-depolarizing neuromuscular blocker [2]. - It has a rapid onset of action, making it suitable for rapid sequence intubation, and can be reversed by **sugammadex**. *Pancuronium* - **Pancuronium** is an **aminosteroid** non-depolarizing neuromuscular blocker with a long duration of action [1]. - It is associated with a vagolytic effect that can cause an increase in **heart rate** and **blood pressure** [1].

Q: Which is a GABA transaminase inhibitor?

Valproate. ***Valproate*** - Valproate is known to inhibit **GABA transaminase**, an enzyme responsible for the breakdown of **gamma-aminobutyric acid (GABA)**. - By inhibiting this enzyme, valproate increases the concentration of **GABA** in the brain, enhancing its inhibitory effects and contributing to its anticonvulsant properties. *TCA* - **Tricyclic antidepressants (TCAs)** primarily work by inhibiting the reuptake of **norepinephrine** and **serotonin** in the brain. - They do not directly inhibit GABA transaminase but rather modulate monoamine neurotransmission. *Sertraline* - **Sertraline** is a **selective serotonin reuptake inhibitor (SSRI)** that works by blocking the reabsorption of **serotonin** into presynaptic neurons. - Its primary mechanism of action is focused on serotonin pathways, not on GABA metabolism. *Gabapentin* - **Gabapentin** is an anticonvulsant that is thought to exert its effects by modulating **calcium channels** and increasing **GABA synthesis**, but it is not a direct inhibitor of GABA transaminase. - Its mechanism of action is distinct from directly preventing GABA breakdown.

Q: Which anxiolytic acts through 5-HT1A receptor partial agonism without exhibiting significant anticonvulsant or muscle relaxant properties?

Buspirone. ***Buspirone*** - **Buspirone** is a unique anxiolytic that primarily acts as a **partial agonist at 5-HT1A receptors**. - Unlike benzodiazepines, it lacks significant **anticonvulsant**, **muscle relaxant**, or **sedative-hypnotic properties** and does not lead to physical dependence or withdrawal. *Diazepam* - **Diazepam** is a **benzodiazepine** that acts by enhancing the effect of **GABA** at GABA-A receptors, leading to significant anxiolytic, sedative, muscle relaxant, and anticonvulsant effects. - It does not primarily act via **5-HT1A receptor partial agonism**. *Zolpidem* - **Zolpidem** is a **non-benzodiazepine hypnotic** that selectively binds to the **GABA-A receptor** subunit, primarily mediating sedative effects. - While it's used for insomnia, it doesn't primarily act as a **5-HT1A partial agonist** and is not typically used for its anxiolytic properties in the same way as buspirone. *Phenobarbitone* - **Phenobarbitone** is a **barbiturate** that acts by prolonging the opening of **chloride channels** associated with GABA-A receptors, leading to strong sedative, hypnotic, and anticonvulsant effects. - Its mechanism of action is distinct from **5-HT1A receptor partial agonism**, and it carries a high risk of dependence and overdose.

Q: Which dopamine receptor is known for its inhibitory action in the central nervous system?

Dopamine Receptor D2. ***Dopamine Receptor D2*** - The **D2 receptor** is a member of the D2-like family (D2, D3, D4), which are **G-protein coupled receptors** that inhibit adenylyl cyclase activity. - Its activation typically leads to a **decrease in neuronal excitability** and neurotransmitter release, providing an inhibitory effect in the CNS. *Dopamine Receptor D5* - The **D5 receptor** belongs to the D1-like family (D1, D5), which are **G-protein coupled receptors** that stimulate adenylyl cyclase activity. - Activation of D5 receptors typically leads to **excitatory effects** rather than inhibitory ones in the CNS. *No inhibitory dopamine receptor present* - This statement is incorrect as specific dopamine receptor subtypes, particularly the **D2-like family**, are well-established to exert inhibitory actions in the CNS. - These inhibitory effects are crucial for various physiological processes, including motor control and reward pathways. *Dopamine Receptor D1* - The **D1 receptor** is part of the D1-like family (D1, D5) and is known for its **excitatory effects** in the CNS. - Activation of D1 receptors leads to an **increase in intracellular cAMP** and generally enhances neuronal activity.

Q: Which of the following drugs is used for Smoking Cessation?

Bupropion. ***Bupropion*** - **Bupropion** is an antidepressant that is also approved as a smoking cessation aid. It works by inhibiting the reuptake of **dopamine** and **norepinephrine**, which can help reduce nicotine cravings and withdrawal symptoms. - It is often prescribed as a first-line pharmacotherapy for smoking cessation, with a typical treatment duration of 7-12 weeks. *Buprenorphine* - **Buprenorphine** is a partial opioid agonist primarily used to treat opioid addiction. It is not indicated for smoking cessation. - While it can help manage withdrawal symptoms from opioids, it has no direct mechanism of action that would reduce nicotine dependence or cravings. *Methadone* - **Methadone** is a full opioid agonist primarily used for the treatment of opioid use disorder (OUD) and chronic pain management. It is not used for smoking cessation. - Its mechanism involves binding to opioid receptors to prevent withdrawal symptoms and reduce cravings for other opioids. *Naltrexone* - **Naltrexone** is an opioid antagonist used primarily for the treatment of alcohol dependence and opioid use disorder. It is not indicated for smoking cessation. - It blocks the effects of opioids and reduces alcohol cravings, but does not affect nicotine pathways or dependence.

Question 1

Buprenorphine is a partial agonist at which opioid receptor?

Accepted Answer

Mu

Answer

Kappa

Answer

Delta

Answer

ORL-1

Question 2

Where is the benzodiazepine binding site located on GABA receptors?

Accepted Answer

γ-subunit

Answer

β-subunit

Answer

δ-subunit

Answer

α-subunit

Question 3

All are symptoms of morphine withdrawal except?

Accepted Answer

Fall in BP

Answer

Yawning

Answer

Lacrimation

Answer

Mydriasis

Question 4

Botulinum toxin type B is used in which disease?

Accepted Answer

Cervical dystonia

Answer

Blepharospasm

Answer

Strabismus

Answer

Glabellar lines

Question 5

Botulinum toxin acts on

Accepted Answer

Synapse

Answer

Smooth muscle of intestine

Answer

Central nervous system

Answer

Sensory nerves

Question 6

Which of the following is a benzylisoquinoline muscle relaxant?

Accepted Answer

Doxacurium

Answer

Rocuronium

Answer

Pancuronium

Answer

Vecuronium

Question 7

Which is a GABA transaminase inhibitor?

Accepted Answer

Valproate

Answer

TCA

Answer

Gabapentin

Answer

Sertraline

Question 8

Which anxiolytic acts through 5-HT1A receptor partial agonism without exhibiting significant anticonvulsant or muscle relaxant properties?

Accepted Answer

Buspirone

Answer

Diazepam

Answer

Zolpidem

Answer

Phenobarbitone

Question 9

Which dopamine receptor is known for its inhibitory action in the central nervous system?

Accepted Answer

Dopamine Receptor D2

Answer

Dopamine Receptor D5

Answer

No inhibitory dopamine receptor present

Answer

Dopamine Receptor D1

Question 10

Which of the following drugs is used for Smoking Cessation?

Accepted Answer

Bupropion

Answer

Methadone

Answer

Buprenorphine

Answer

Naltrexone

Central Nervous System Pharmacology — MCQs

Central Nervous System Pharmacology — MCQs

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