Neurotransmitters and Receptors — MCQs
Which of the following neurotransmitters has only inhibitory action?
Which of the following is a G protein coupled receptor?
Which of the following neurotransmitters is primarily released from the sympathetic nervous system to increase heart rate in response to a DECREASE in blood pressure?
Which dopamine receptor is known for its inhibitory action in the central nervous system?
Which drug is suitable for epilepsy related to a brain tumor?
What neurotransmitter is mainly involved in obsessive-compulsive disorder (OCD)?
What is the treatment for extrapyramidal side effects induced by Haloperidol?
What neurotransmitter is found in increased quantities in mania?
Which of the following is the primary neurotransmitter involved in the transmission of pain signals in the spinal cord?
A 30-year-old shows delusions, hallucinations, and marked thought disorder. Labs reveal anti-NMDA receptor antibodies. Best initial treatment?
Neurotransmitters and Receptors Indian Medical PG Practice Questions and MCQs
Question 1: Which of the following neurotransmitters has only inhibitory action?
- A. Glutamine
- B. All of the options
- C. GABA (Correct Answer)
- D. Aspartate
Explanation: ***GABA*** - **Gamma-aminobutyric acid (GABA)** is the primary **inhibitory neurotransmitter** in the central nervous system. - It works by reducing neuronal excitability, often by allowing **chloride ions** into the cell, leading to hyperpolarization. *Glutamine* - **Glutamine** is an **amino acid** that is a precursor to the excitatory neurotransmitter **glutamate** and the inhibitory neurotransmitter GABA, but it is not a neurotransmitter itself. - It plays a crucial role in the **glutamate-GABA cycle**, but its direct action is not neurotransmission. *All of the options* - This option is incorrect because only GABA among the choices has a solely inhibitory action; **glutamine** is a precursor, and **aspartate** is primarily excitatory. - Not all substances listed are neurotransmitters, nor do they all have purely inhibitory actions. *Aspartate* - **Aspartate** is an **excitatory neurotransmitter** and plays a role in synaptic plasticity and learning. - It primarily acts on **NMDA receptors**, similar to glutamate, to depolarize neurons.
Question 2: Which of the following is a G protein coupled receptor?
- A. M2 muscarinic receptor (Correct Answer)
- B. NMDA receptor
- C. Insulin receptors
- D. Steroid receptors
Explanation: ***M2 muscarinic receptor***- The **M2 muscarinic receptor** is a classic example of a **G protein-coupled receptor (GPCR)** [1]. When a ligand binds to a G-protein-coupled receptor, it triggers a mechanism where GDP is exchanged for GTP, causing the G-protein's alpha subunit to separate and initiate signaling pathways [1]. These heterotrimeric G-proteins couple cell surface receptors to catalytic units that form second messengers or directly to ion channels [1]. GPCRs are important regulators of nerve activity in the CNS and are receptors for neurotransmitters of the peripheral autonomic nervous system, with acetylcholine (ACh) being a ligand that regulates functions of glands and smooth muscle [2]. The **M2 muscarinic receptor** specifically activates an **inhibitory G protein (G_i)**, leading to a decrease in **cAMP** and opening of **potassium channels**. The effects of metabotropic receptors, like GPCRs, can last tens of seconds to minutes, contrasting with the brief effects of ionotropic receptors [4].*NMDA receptor*- The **NMDA receptor** is a **ligand-gated ion channel** that allows the influx of calcium and sodium ions [3]. It does not couple to G proteins, but directly mediates ion flow upon activation by **glutamate** and **glycine**. Ligand-gated ion channels open a central transmembrane ion channel when a neurotransmitter binds to sites on its extracellular domain [3].*Steroid*- **Steroid hormones** primarily act on **intracellular receptors** that, once activated, translocate to the nucleus to regulate gene expression. They are not cell surface receptors and do not utilize G protein signaling.*Insulin receptors*- **Insulin receptors** are **receptor tyrosine kinases** that, upon binding insulin, undergo autophosphorylation and activate intracellular signaling pathways. They signal through a cascade of protein phosphorylations, not through G proteins.
Question 3: Which of the following neurotransmitters is primarily released from the sympathetic nervous system to increase heart rate in response to a DECREASE in blood pressure?
- A. Norepinephrine (Correct Answer)
- B. Dopamine
- C. Acetylcholine
- D. Epinephrine
Explanation: ***Norepinephrine*** - **Norepinephrine** is the primary neurotransmitter released by **postganglionic sympathetic neurons** directly onto the heart to increase heart rate and contractility in response to a drop in blood pressure. - It acts on **beta-1 adrenergic receptors** in the sinoatrial (SA) node, atria, and ventricles, leading to increased chronotropy (heart rate) and inotropy (contractility). *Dopamine* - While **dopamine** can have cardiovascular effects, particularly at high doses, it is not the primary neurotransmitter released by the sympathetic nervous system for direct heart rate regulation. - Dopamine is a precursor to norepinephrine and epinephrine, but its main physiological roles involve **renal blood flow regulation** and central nervous system functions. *Acetylcholine* - **Acetylcholine** is the primary neurotransmitter of the **parasympathetic nervous system**, which generally acts to **decrease heart rate** (bradycardia) through muscarinic receptors. - It is also released by **preganglionic sympathetic fibers**, but these do not directly innervate the heart to produce the desired effect of increasing heart rate. *Epinephrine* - **Epinephrine** (adrenaline) is primarily a **hormone** released from the **adrenal medulla** into the bloodstream, not directly from postganglionic sympathetic nerve terminals to the heart. - Although it has strong effects on beta-1 receptors in the heart, its release is more generalized and slower than the direct neuronal release of norepinephrine.
Question 4: Which dopamine receptor is known for its inhibitory action in the central nervous system?
- A. Dopamine Receptor D5
- B. No inhibitory dopamine receptor present
- C. Dopamine Receptor D2 (Correct Answer)
- D. Dopamine Receptor D1
Explanation: ***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.
Question 5: Which drug is suitable for epilepsy related to a brain tumor?
- A. Levetiracetam (Correct Answer)
- B. Phenytoin
- C. Phenobarbitone
- D. Carbamazepine
Explanation: ***Levetiracetam*** - Levetiracetam is often preferred for **tumor-related epilepsy** due to its favorable **pharmacokinetic profile**, minimal **drug-drug interactions**, and broad spectrum of activity against various seizure types. - It does not significantly induce or inhibit hepatic enzymes, making it a safer option for patients who may be on other medications for their tumor or cancer treatment. *Phenytoin* - **Phenytoin** has a narrow **therapeutic window** and significant **drug-drug interactions** due to its potent hepatic enzyme induction, which can complicate concomitant use with **chemotherapy** or other medications. - It also has a dose-dependent non-linear pharmacokinetic profile, making dose adjustments challenging and increasing the risk of **toxicity**. *Phenobarbitone* - **Phenobarbitone** is a potent enzyme inducer and has a high potential for **sedation** and cognitive side effects, which can significantly impair the quality of life for patients. - Its long half-life and propensity for **drug interactions** make it less desirable, especially in patients with brain tumors who may experience other neurological deficits. *Carbamazepine* - **Carbamazepine** is another potent **enzyme inducer** that can lead to significant **drug interactions**, particularly with chemotherapy agents, altering their metabolism and efficacy. - It often causes side effects like **drowsiness**, **dizziness**, and can lead to **hyponatremia**, which may be problematic in patients who are already compromised.
Question 6: What neurotransmitter is mainly involved in obsessive-compulsive disorder (OCD)?
- A. GABA
- B. NE
- C. Dopamine
- D. Serotonin (Correct Answer)
Explanation: ***Serotonin*** - The **serotonin system** is consistently implicated in the pathophysiology of OCD, and selective serotonin reuptake inhibitors (**SSRIs**) are the first-line pharmacotherapy. - Dysregulation in **serotonin levels** and receptor function is thought to contribute to the repetitive thoughts and compulsive behaviors characteristic of the disorder. *GABA* - **Gamma-aminobutyric acid (GABA)** is the primary inhibitory neurotransmitter in the brain and is mainly associated with anxiety disorders. - While anxiety is often comorbid with OCD, GABA dysregulation is not considered the primary neurochemical basis for the core symptoms of OCD. *NE* - **Norepinephrine (NE)** is a neurotransmitter involved in the 'fight or flight' response, attention, and mood. - While NE imbalances can contribute to anxiety and mood disorders, it is not considered the main neurotransmitter primarily implicated in the core pathology of OCD. *Dopamine* - **Dopamine** is mainly associated with reward, motivation, and motor control, and plays a role in conditions like schizophrenia and Parkinson's disease. - While dopamine has a **significant secondary role** in OCD (especially in the cortico-striato-thalamo-cortical circuits) and dopamine antagonists are used as augmentation therapy in treatment-resistant cases, **serotonin remains the primary neurotransmitter** implicated in OCD pathophysiology.
Question 7: What is the treatment for extrapyramidal side effects induced by Haloperidol?
- A. Barbiturates
- B. SSRIs
- C. Benzodiazepines
- D. Anticholinergic drugs (Correct Answer)
Explanation: ***Anticholinergic drugs (effective treatment)*** - **Anticholinergic medications**, such as **benztropine** or **diphenhydramine**, are the primary treatment for **acute extrapyramidal symptoms (EPS)** like dystonia and parkinsonism induced by antipsychotics like haloperidol. - They work by **blocking muscarinic acetylcholine receptors**, helping to restore the balance between dopamine and acetylcholine in the basal ganglia. *Benzodiazepines (used for anxiety and muscle relaxation)* - While benzodiazepines can offer some relief for **akathisia** (a form of EPS characterized by restlessness) due to their sedative and muscle relaxant properties, they are **not the first-line treatment for other acute EPS** such as dystonia or parkinsonism. - They primarily enhance **GABAergic transmission** and are effective for anxiety and seizure control rather than direct antagonism of EPS mechanisms. *Barbiturates (used as sedative-hypnotic drugs)* - **Barbiturates** are strong central nervous system depressants used for sedation, anesthesia, and seizure control, but are **not indicated for the treatment of EPS**. - Their significant **sedative and addictive potential**, along with a narrow therapeutic index, makes them unsuitable for this purpose. *SSRIs (used for depression and anxiety)* - **SSRIs (Selective Serotonin Reuptake Inhibitors)** are antidepressants that work by increasing serotonin levels in the brain and are used to treat depression, anxiety, and obsessive-compulsive disorder. - They **do not have a direct role** in ameliorating dopamine-acetylcholine imbalance responsible for haloperidol-induced EPS.
Question 8: What neurotransmitter is found in increased quantities in mania?
- A. Noradrenaline
- B. Serotonin
- C. GABA
- D. Dopamine (Correct Answer)
Explanation: ***Dopamine*** - **Dopamine levels are consistently elevated during manic episodes**, representing one of the most robust neurobiological findings in mania. - Increased dopaminergic activity contributes to **psychomotor agitation**, **goal-directed behavior**, **reward-seeking**, **decreased need for sleep**, and **psychotic features** (delusions, hallucinations). - **Dopamine antagonists** (antipsychotics like haloperidol, olanzapine) are **first-line treatments** for acute mania, supporting the dopamine hypothesis. - The dopamine hypothesis of mania is well-established in psychiatric literature and supported by neuroimaging studies. *Noradrenaline* - Noradrenergic hyperactivity is also implicated in mania, contributing to increased arousal, energy, and reduced sleep. - However, while elevated, the evidence is less consistent than for dopamine, and noradrenaline's role appears more modulatory. - The question asks for the neurotransmitter "found in increased quantities" - both are elevated, but dopamine has stronger evidence. *Serotonin* - Serotonin dysfunction is implicated in mood disorders, but manic episodes are generally associated with **reduced or dysregulated serotonin activity**, not an increase. - Low serotonin may contribute to impulsivity and mood instability in bipolar disorder. *GABA* - **GABA** (gamma-aminobutyric acid) is the primary **inhibitory neurotransmitter** in the CNS. - **Reduced GABAergic activity** has been reported in mania (not increased), which may contribute to disinhibition and hyperexcitability. - GABAergic drugs (e.g., benzodiazepines, valproate) are used as adjuncts in mania, supporting reduced GABA activity.
Question 9: Which of the following is the primary neurotransmitter involved in the transmission of pain signals in the spinal cord?
- A. Substance P (Correct Answer)
- B. Dopamine
- C. Serotonin
- D. Gamma-aminobutyric acid (GABA)
Explanation: ***Substance P*** - **Substance P** is a neuropeptide that plays a crucial role in the transmission of **nociceptive (pain) signals** from the periphery to the central nervous system, particularly in the **spinal cord**. - It is released by primary afferent neurons during painful stimuli and contributes to the sensation of pain and **neurogenic inflammation**. *Dopamine* - **Dopamine** is primarily involved in **reward**, motivation, motor control, and pleasure. - While dopamine can influence pain perception, it is not considered the primary neurotransmitter directly responsible for the **transmission of pain signals** in the spinal cord. *Serotonin* - **Serotonin (5-HT)** is involved in mood, sleep, appetite, and a wide range of other functions, including modulation of pain. - Although it can have both **pro-nociceptive and anti-nociceptive effects** depending on its receptor subtype and location, it is not the primary neurotransmitter for pain signal transmission. *Gamma-aminobutyric acid (GABA)* - **GABA** is the main **inhibitory neurotransmitter** in the central nervous system, reducing neuronal excitability. - Its role in pain is primarily to **modulate and inhibit pain signals**, rather than to transmit them.
Question 10: A 30-year-old shows delusions, hallucinations, and marked thought disorder. Labs reveal anti-NMDA receptor antibodies. Best initial treatment?
- A. Immunotherapy (Correct Answer)
- B. Benzodiazepines
- C. ECT
- D. Antipsychotics
Explanation: ***Immunotherapy*** - The presence of **anti-NMDA receptor antibodies** indicates an autoimmune etiology for the psychiatric symptoms, making **immunotherapy** (e.g., corticosteroids, IVIG, plasmapheresis) the definitive first-line treatment. - Immunotherapy aims to reduce inflammation and remove autoantibodies, thereby reversing the neurological and psychiatric manifestations. *Benzodiazepines* - While useful for acute agitation or catatonia in psychiatric disorders, **benzodiazepines** do not address the underlying autoimmune pathology of anti-NMDA receptor encephalitis. - They would provide only symptomatic relief and would not prevent disease progression or long-term neurological damage. *ECT* - **Electroconvulsive therapy (ECT)** is a treatment for severe, refractory mood disorders or catatonia, which might be present in anti-NMDA receptor encephalitis. - However, ECT is a symptomatic treatment and does not target the autoimmune cause, making it less appropriate as the **initial definitive treatment**. *Antipsychotics* - **Antipsychotics** are used to manage psychosis, delusions, and hallucinations, which are prominent in anti-NMDA receptor encephalitis. - However, they do not treat the underlying **autoimmune inflammation** and may worsen some symptoms, such as autonomic instability or seizures, in this specific condition.
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