Week 31 / Nervous System - 2

Question 1

Question: What is a receptor in the context of neurons?

Answer 1

Answer: A receptor is a protein molecule that receives chemical signals from outside a cell.

Question 2

Question: What is a characteristic of receptor subtypes?

Answer 2

Answer: Receptor subtypes are widespread throughout the nervous system and provide a diversity of functions.

Question 3

Question: What types of receptors are commonly found in neurons?

Answer 3

Answer: Receptors can be either ligand-gated or G-protein coupled.

Question 4

Question: What is a ligand?

Answer 4

Answer: A ligand is a substance that forms a complex with a biomolecule to serve a biological purpose.

Question 5

Question: What is a prodrug?

Answer 5

Answer: A prodrug is a chemical compound that must undergo chemical conversion by metabolic processes before becoming an active pharmacological agent.

Question 6

Question: Which of the following is an example of a prodrug?
A) Morphine
B) Diamorphine
C) Dopamine
D) Serotonin

Answer 6

Answer: B) Diamorphine.

Question 6

Question: What happens to diamorphine when it enters the brain?

Answer 6

Answer: Diamorphine is converted into morphine, which binds to mu (μ) opioid receptors.

Question 7

Question: Which receptors does morphine bind to in the brain?

Answer 7

Answer: Morphine binds to mu (μ) opioid receptors.

Question 8

Question: What contributes to the side effects of a drug?
A) Its bioavailability
B) Its degree of affinity and specificity
C) Its efficacy
D) Its potency

Question: What is the primary action of diphenhydramine?
A) Histamine H1 receptor antagonist
B) Serotonin 5-HT2A receptor agonist
C) Muscarinic receptor antagonist
D) Adrenergic receptor antagonist

Question: How does diphenhydramine affect patients with Alzheimer’s disease?
A) It improves cognitive functions
B) It exacerbates cognitive and behavioral functions
C) It reduces memory loss
D) It promotes better sleep

Question: What side effects are associated with Mirtazapine?
A) Constipation, dry mouth, sleepiness, increased appetite, and weight gain
B) Increased alertness, insomnia, weight loss, and nausea
C) Tremors, dizziness, and blurred vision
D) Decreased appetite, dry skin, and fatigue

Question: What is the action of Mirtazapine as a receptor antagonist?
A) Serotonin 5-HT2A, 5-HT2C, 5-HT3, and Histamine H1 receptor antagonist
B) Dopamine D2 receptor antagonist
C) Muscarinic receptor antagonist
D) Adrenergic alpha 1 receptor antagonist

Question: Which of the following drugs is a potent anti-muscarinic that affects both histamine H1 and muscarinic receptors?
A) Mirtazapine
B) Diphenhydramine
C) Fluoxetine
D) Diazepam

Question: What is a potential side effect of Mirtazapine related to its effect on the H1 receptor?
A) Weight loss
B) Sleep disturbances
C) Sleepiness
D) Increased energy

Answer 8

Answer: B) Its degree of affinity and specificity
Answer: A) Histamine H1 receptor antagonist
Answer: B) It exacerbates cognitive and behavioral functions
Answer: A) Constipation, dry mouth, sleepiness, increased appetite, and weight gain
Answer: A) Serotonin 5-HT2A, 5-HT2C, 5-HT3, and Histamine H1 receptor antagonist
Answer: B) Diphenhydramine
Answer: C) Sleepiness

Question 8

Question: What does bioavailability refer to?

Question: What does affinity describe in pharmacology?

Question: What is efficacy in the context of drug-receptor interaction?

Question: How is potency defined in pharmacology?

Question: Which of the following describes how tightly a drug binds to its receptor?
A) Efficacy
B) Potency
C) Bioavailability
D) Affinity

Answer 8

Answer: Bioavailability refers to the extent and rate at which the active drug or metabolite enters systemic circulation.

Answer: Affinity describes how tightly a drug binds to its receptor.

Answer: Efficacy refers to the capacity of a drug to produce a change in a target cell or organ after binding to its receptor.

Answer: Potency is a measure of drug activity expressed in terms of the amount required to produce an effect of given intensity.

Answer: D) Affinity

Question 9

What is the main pharmacological effect of inverse agonists?

Answer 9

Back:
Inverse agonists primarily act as receptor antagonists. Their effect on constitutive activity is only relevant if the system has spontaneous activity. In the absence of constitutive activity, inverse agonists behave as antagonists.

Question 10

Question: What is an agonist in pharmacology?
A) A drug that blocks receptor activity
B) A drug that mimics the action of a neurotransmitter and binds to its receptor
C) A drug that reduces the effects of a neurotransmitter
D) A neurotransmitter that binds to its antagonist

Question: What is the primary action of a neurotransmitter as an agonist?
A) It inhibits the post-synaptic neuron
B) It mimics the action of a drug
C) It binds to and activates its specific receptor
D) It reduces the activity of its corresponding receptor

Question: How does a partial agonist differ from a full agonist?
A) A partial agonist produces a lower response after binding to the receptor
B) A partial agonist always inhibits receptor activity
C) A partial agonist has no affinity for the receptor
D) A partial agonist produces the same response as a full agonist

Question: What effect can a partial agonist have in the presence of a full agonist?
A) It can act as a competitive antagonist
B) It enhances the response of the full agonist
C) It has no effect on the full agonist’s activity
D) It mimics the full agonist’s action

Question: An inverse agonist has what effect on the receptor?
A) It produces the same effect as an agonist
B) It blocks the receptor completely
C) It reduces the activity of the receptor below its basal level
D) It enhances the activity of the receptor

Question: Which of the following best describes the role of a neurotransmitter as an agonist?
A) It competes with other neurotransmitters for receptor binding
B) It mimics the effect of a drug by binding to its receptor
C) It blocks receptor sites from other neurotransmitters
D) It increases the breakdown of other neurotransmitters

Answer 10

Answer: B) A drug that mimics the action of a neurotransmitter and binds to its receptor

Answer: C) It binds to and activates its specific receptor

Answer: A) A partial agonist produces a lower response after binding to the receptor

Answer: A) It can act as a competitive antagonist

Answer: C) It reduces the activity of the receptor below its basal level

Answer: B) It mimics the effect of a drug by binding to its receptor

Question 11

What is constitutive activity?

Answer 11

Back:
Constitutive activity refers to the activation of receptors and the production of second messengers in the absence of an agonist.

Question 12

How do benzodiazepines work?

Answer 12

Back:
Benzodiazepines are agonists that enhance the effect of GABA by acting as allosteric modulators of the GABA receptor. This leads to anxiolysis and an antiepileptic effect.

Question 12

How do β-carbolines (e.g., norharmane) work?

Answer 12

Back:
β-carbolines act as inverse agonists at the GABA receptor, reducing the effect of GABA. This can cause anxiogenesis (increased anxiety) and seizures.

Question 13

What is the role of Flumazenil?

Answer 13

Back:
Flumazenil is a neutral antagonist that reverses both the sedative effects of benzodiazepines and the proconvulsant effects of β-carbolines. It has no activity in the absence of an agonist or inverse agonist but can block the activity of both.

Question 14

How do H2 antagonists like cimetidine, ranitidine, and famotidine work?

Answer 14

Back:
H2 antagonists reduce basal cAMP levels and behave as inverse agonists by decreasing the constitutive activity of H2 receptors.

Question 14

What is the effect of cetirizine and loratadine on H1 receptors?

Answer 14

Back:
Cetirizine and loratadine are H1 antagonists that reduce constitutive activity of H1 receptors. They behave as inverse agonists by stabilizing the inactive conformation of the H1 receptor.

Question 15

What are the effects of propranolol and nadolol?

Answer 15

Back:
Propranolol and nadolol are nonselective β-antagonists and inverse agonists. They reduce basal activity at β-receptors.

Question 16

How does inverse agonism explain the effects of carvedilol, naloxone, clozapine, and candesartan?

Answer 16

Back:
Inverse agonism may explain the beneficial effects of carvedilol (in heart failure), naloxone (in opioid withdrawal), clozapine (in psychosis), and candesartan (in cardiac hypertrophy) by reducing the basal activity of their respective receptors.

Question 17

What is the role of Pimavanserin?

Answer 17

Back:
Pimavanserin is an inverse agonist and antagonist of the 5-HT2A receptor. It is approved to treat Parkinson’s disease psychosis and also reduces psychosis in various dementia subtypes.

Question 18

What is an antagonist in pharmacology?

Answer 18

Back:
An antagonist is a drug that has affinity for a neurotransmitter receptor and prevents the neurotransmitter from binding to its receptor, thus inhibiting its action.

Question 19

What is physiological antagonism?

Answer 19

Back:
Physiological antagonism occurs when a drug binds to a different receptor and produces a response that opposes the effect of an agonist-bound receptor.
Example: Histamine (agonist) stimulates acid secretion, while omeprazole inhibits acid secretion by blocking the proton pump.

Question 20

What is an inhibitor in biological activity?

Answer 20

Back:
An inhibitor is a substance that interferes with a chemical reaction, growth, or other biological activity. Typically, it binds to an enzyme and decreases its activity.
Some neurotransmitters or drugs act as inhibitors by (1) hyperpolarizing a neuron or (2) blocking the binding of a neurotransmitter to its receptor.

Question 21

Which neurotransmitters use the reuptake process?

Answer 21

Back: GABA and Glutamate use the reuptake process to return neurotransmitters to the presynaptic nerve terminals or surrounding glial cells.

Question 21

How is the action of a neurotransmitter terminated? [3]

Answer 21

Back: The action of a neurotransmitter is terminated through the following mechanisms: Enzymatic degradation – The neurotransmitter is degraded either intracellularly or in the synaptic cleft by enzymes. Reuptake – Neurotransmitter molecules are removed from the synaptic cleft and returned to the presynaptic nerve terminal or surrounding glial cells. Autoreceptors – Receptors located on the presynaptic neuron that inhibit further neurotransmitter release once an adequate level has been reached.

Question 22

How is dopamine (DA) synthesized from tyrosine?

Answer 22

Back: Tyrosine hydroxylase converts the amino acid tyrosine into DOPA. DOPA decarboxylase then converts DOPA into dopamine (DA).

Question 22

How is the action of norepinephrine (NA) and dopamine (DA) terminated in the synaptic cleft?

Answer 22

Back: The action of NA and DA is mainly terminated by reuptake into the presynaptic neuron. DA and NA can also be degraded intracellularly or in the synaptic cleft by the enzymes: Monoamine oxidase (MAO) Catechol-O-methyltransferase (COMT)

Question 22

How is norepinephrine (NA) synthesized from dopamine (DA)?

Answer 22

Back: Dopamine beta-hydroxylase (DBH) converts dopamine (DA) into norepinephrine (NA).

Question 22

What is the precursor in the biosynthesis of serotonin (5-HT)?

Answer 22

Back: The precursor for serotonin is tryptophan, not tyrosine.

Question 23

How is serotonin (5-HT) synthesized?

Answer 23

Back: Tryptophan is converted to 5-hydroxytryptophan by the enzyme tryptophan hydroxylase. 5-hydroxytryptophan can cross the blood-brain barrier (BBB) to increase central levels of serotonin (5-HT). 5-hydroxytryptophan is then decarboxylated to form 5-HT (serotonin) by dopa decarboxylase.

Question 24

How is serotonin (5-HT) action terminated?

Answer 24

Back: Reuptake of serotonin (5-HT) from the synaptic cleft into the presynaptic neuron is the primary method of termination. In the synaptic cleft, MAO-A (monoamine oxidase-A) deactivates serotonin by converting it into 5-hydroxyindoleacetic acid.

Question 25

How is acetylcholine (ACh) synthesized?

Answer 25

Back: ACh is synthesized from choline and acetyl-CoA by the enzyme Choline acetyltransferase (ChAT). Choline is derived from dietary and intraneuronal sources. Acetyl-CoA is made from glucose in the mitochondria of neurons.

Question 26

How is the action of acetylcholine (ACh) terminated?

Answer 26

Back: The action of ACh is terminated by the enzyme acetylcholinesterase (AChE), which is found primarily in the synaptic cleft. AChE rapidly breaks down ACh into acetate and choline.

Question 27

What happens to choline after ACh breakdown?

Answer 27

Back: Choline is immediately taken back up into the presynaptic terminal, where it is combined with acetate ions to form ACh again.

Question 28

How is glutamate (Glu) synthesized?

Answer 28

Back: Glutamate (Glu) is synthesized from glutamine. The enzyme glutaminase, present in mitochondria, converts glutamine into glutamate.

Question 29

What happens to glutamate after it is released into the synaptic cleft?

Answer 29

Back: After release in the synaptic cleft, glutamate is taken up by astroglia cells. In astroglia cells, glutamate is converted back to glutamine, which is inactive and cannot activate glutamate receptors. Glutamine is released from the glial cells into the extracellular fluid.

Question 30

How is GABA synthesized?

Answer 30

Back: GABA is synthesized in the presynaptic neuron from the precursor glutamate. The enzyme glutamate decarboxylase (GAD), which uses vitamin B6 (pyridoxine) as a cofactor, converts glutamate to GABA.

Question 31

What happens to glutamine after it is released from glial cells?

Answer 31

Back: Glutamine is taken up by nerve terminals, where it is converted back into glutamate.

Question 32

What happens to GABA after it is released?

Answer 32

Back: After release, GABA is rapidly taken up by surrounding astrocytes and neurons. It is then degraded by the enzyme GABA transaminase, regenerating glutamate and glutamine.

Question 33

How do astrocytes contribute to GABA handling?

Answer 33

Back: Astrocytes, a subtype of glial cells, can synthesize and release GABA, and also reuptake GABA from the synaptic cleft.

Question 34

Front: What is the difference between an antagonist and an inhibitor? A) Antagonists block receptors; inhibitors block enzyme activity. B) Antagonists inhibit enzyme activity; inhibitors block receptors. C) Both antagonists and inhibitors bind to receptors to activate them. D) Both antagonists and inhibitors increase biological activity. Front: Are GABA, enkephalin, diazepam, and morphine agonists or antagonists? A) Agonists B) Antagonists C) Both agonists and antagonists D) Neither agonists nor antagonists Front: What does Nifedipine do, and how is it classified? A) It increases calcium ion influx, classified as a channel opener. B) It inhibits calcium ion influx, classified as a calcium channel blocker and antagonist. C) It blocks sodium channels, classified as an antagonist. D) It stimulates muscle contraction, classified as an agonist. Front: What is Atenolol, and how does it function? A) Atenolol inhibits alpha receptors, classified as an antagonist. B) Atenolol inhibits beta-1 adrenergic receptors, classified as an antagonist. C) Atenolol stimulates beta-2 receptors, classified as an agonist. D) Atenolol inhibits alpha-2 adrenergic receptors, classified as an antagonist. Front: How does Aspirin (acetylsalicylic acid) work as an inhibitor? A) It inhibits cyclooxygenase enzymes, reducing prostaglandin and thromboxane production. B) It stimulates cyclooxygenase enzymes, increasing prostaglandin production. C) It blocks calcium channels, preventing inflammation. D) It blocks beta-adrenergic receptors to reduce inflammation.

Answer 34

Back: A) Antagonists block receptors; inhibitors block enzyme activity. Back: A) Agonists Back: B) It inhibits calcium ion influx, classified as a calcium channel blocker and antagonist. Back: B) Atenolol inhibits beta-1 adrenergic receptors, classified as an antagonist. Back: A) It inhibits cyclooxygenase enzymes, reducing prostaglandin and thromboxane production.