Psychopathopharmacology 1 MSN 671 quiz 3

Correct Answer:

C. Serotonin 2A recept

Explanation:

The serotonin 2A (5-HT2A) receptor is the principal binding site for hallucinogens such as LSD, psilocybin, and MDMA. Activation of these receptors in the cortex alters perception, cognition, and mood, producing hallucinations and psychotic-like symptoms. This receptor is strongly implicated in the pathophysiology of psychosis and is also a target for many atypical antipsychotics, which block 5-HT2A receptors.

Why Other Options Are Wrong:

A. GABA-A receptor

This is incorrect because GABA-A receptors mediate inhibitory neurotransmission and are targeted by drugs like benzodiazepines and alcohol, not hallucinogens.

B. Cannabinoid 1 receptor

This is incorrect because cannabinoid receptors are activated by THC and synthetic cannabinoids, producing different effects such as relaxation, altered perception, and appetite stimulation, but they are not the main hallucinogen binding site.

D. Serotonin 2C receptor

This is incorrect because while 5-HT2C receptors modulate appetite, mood, and anxiety, they are not the primary receptor mediating hallucinogen-induced psychotic-like effects—the 5-HT2A receptor is central.

Correct Answer:

A. Phase I

Explanation:

Phase I clinical trials are the first stage of testing in humans and typically involve a small group (20–100) of healthy volunteers. The primary goal is to evaluate safety, tolerability, dosage ranges, and pharmacokinetics of the drug. This phase answers the question: Is the drug safe in humans?

Why Other Options Are Wrong:

B. Phase IV

This is incorrect because Phase IV occurs after FDA approval, focusing on post-marketing surveillance to monitor long-term safety and rare adverse effects in the general population.

C. Phase III

This is incorrect because Phase III involves large randomized controlled trials in patients with the target condition to confirm efficacy, monitor side effects, and compare with standard treatments.

D. Phase II

This is incorrect because Phase II involves a larger group of patients with the disease to test efficacy and further assess safety, not healthy volunteers.

Correct Answer:

B. Ligand

Explanation:

A ligand is any molecule, such as a neurotransmitter, drug, or hormone, that binds specifically to a receptor. When the ligand binds, it induces a conformational change in the receptor, which may open ion channels or activate intracellular signaling pathways. For example, GABA acts as a ligand for GABA receptors, opening chloride channels to inhibit neuronal activity.

Why Other Options Are Wrong:

Presynaptic

This is incorrect because "presynaptic" refers to the neuron releasing the neurotransmitter, not the molecule binding to a receptor.

Voltage

This is incorrect because "voltage" refers to electrical potential differences across the membrane, not the binding molecule.

Isomer

This is incorrect because an isomer is a molecule with the same chemical formula as another but with a different structure. It is unrelated to receptor binding.

Correct Answer:

A. Via voltage-sensitive sodium channels until it reaches voltage-sensitive calcium channels and consequent calcium influx causes neurotransmitter release into the synapse

Explanation:

The action potential starts with sodium influx through voltage-gated sodium channels, depolarizing the axon. This depolarization wave travels along the axon until it reaches the presynaptic terminal, where voltage-gated calcium channels open. Calcium ions flow into the terminal, and this influx of calcium triggers synaptic vesicles to fuse with the membrane, releasing neurotransmitters into the synapse.

Why Other Options Are Wrong:

B. Via voltage-sensitive calcium channels until it reaches voltage-sensitive sodium channels and consequent sodium influx causes neurotransmitter release into the synapse

This is incorrect because calcium entry does not initiate the action potential. Sodium influx depolarizes the membrane first; calcium entry only occurs at the terminal to trigger neurotransmitter release.

C. Via voltage-sensitive potassium channels until it reaches a sodium channel and consequent sodium influx causes neurotransmitter release into the synapse

This is incorrect because potassium channels are responsible for repolarization after depolarization. They do not drive the action potential forward or cause neurotransmitter release.

D. None of the above

This is incorrect because option A correctly describes the physiological order and ion flow that leads to neurotransmitter release.

Correct Answer:

C. Positive Allosteric

Explanation:

A positive allosteric modulator (PAM) binds to a site on the receptor different from the agonist’s binding site and enhances the receptor’s response when the agonist is present. This increases receptor sensitivity without directly activating it. A key example is benzodiazepines, which are positive allosteric modulators of the GABA-A receptor, making the receptor more responsive to GABA.

Why Other Options Are Wrong:

A. Acetylcholine modulator

This is incorrect because “acetylcholine modulator” is not a precise pharmacological classification. Acetylcholine itself is a neurotransmitter, not a modulator.

B. Nicotinic modulator

This is incorrect because “nicotinic modulator” is not a standard category. Nicotinic receptors respond to acetylcholine or nicotine, but the modulation is not specifically termed this way.

D. Negative Allosteric

This is incorrect because negative allosteric modulators decrease receptor activity in the presence of an agonist by reducing sensitivity or efficacy, which is the opposite of boosting activity.

Correct Answer:

C. Both A and B

Explanation:

Excitation-secretion coupling in neurotransmission is the process that links an action potential to the release of neurotransmitters at the synaptic cleft.

Voltage-sensitive sodium channels are critical for generating and propagating the action potential along the axon.

Voltage-sensitive calcium channels open when the action potential reaches the presynaptic terminal, allowing calcium influx. This calcium entry triggers synaptic vesicle fusion and neurotransmitter release.

Thus, both sodium and calcium channels are required for efficient excitation-secretion coupling.

Why Other Options Are Wrong:

A. Voltage-sensitive sodium channels

This is incorrect alone because sodium channels propagate the action potential but do not directly cause neurotransmitter release without calcium entry.

B. Voltage-sensitive calcium channels

This is incorrect alone because calcium influx is essential for vesicle release, but without sodium channel–mediated action potential propagation, the depolarization would not reach the terminal.

D. Neither A nor B

This is incorrect because both channel types are central to the process of excitation-secretion coupling.

Correct Answer:

B. Resensitization of nicotinic receptors

Explanation:

Nicotine binds to nicotinic acetylcholine receptors (nAChRs) in the brain, causing receptor activation and dopamine release, which produces reinforcement. After nicotine exposure, nAChRs become desensitized and stop responding despite nicotine being present. Over time (about every 1–2 hours), the receptors resensitize, becoming responsive again. This resensitization drives craving and withdrawal because the brain seeks nicotine to re-activate the now-sensitive receptors, creating the cycle of dependence.

Why Other Options Are Wrong:

A. Desensitization of nicotinic receptors

This is incorrect because desensitization occurs right after smoking, not when cravings emerge. Cravings arise when receptors resensitize.

C. Desensitization of muscarinic receptors

This is incorrect because muscarinic acetylcholine receptors are not the primary target of nicotine in addiction. Nicotine acts on nicotinic receptors, not muscarinic ones.

D. Resensitization of muscarinic receptors

This is incorrect because muscarinic receptors are not central to nicotine craving and withdrawal. The addiction mechanism involves nicotinic receptor cycles, not muscarinic receptor activity.

Correct Answer:

C. Ratio between toxic dose and effective dose

Explanation:

The Therapeutic Index (TI) is a measure of a drug’s safety margin. It is calculated as the ratio between the toxic dose (TD₅₀ or LD₅₀) and the effective dose (ED₅₀). A higher TI means the drug is relatively safe because the toxic dose is much higher than the effective dose, while a low TI indicates a narrow safety margin, requiring close monitoring.

Why Other Options Are Wrong:

A. Ratio between absorption and distribution

This is incorrect because these are pharmacokinetic processes, not measures of drug safety.

B. Ratio between metabolism and excretion

This is incorrect because metabolism and excretion describe drug clearance, not the therapeutic safety margin.

D. Ratio between chemical and generic names

This is incorrect because therapeutic index has nothing to do with drug nomenclature.

Correct Answer:

C. Receptor Tyrosine Kinases

Explanation:

Receptor Tyrosine Kinases (RTKs) are transmembrane receptors that have intrinsic enzymatic activity. When ligands such as growth factors bind, RTKs dimerize and autophosphorylate on tyrosine residues. These phosphorylated sites act as docking points for intracellular signaling proteins, triggering cascades like the MAPK or PI3K pathways.

Why Other Options Are Wrong:

A. Ion Channel Receptors

This is incorrect because ion channel receptors allow ions to pass through the membrane in response to ligand binding or voltage changes but do not have intrinsic enzyme activity.

B. Transmembrane Receptors

This is incorrect because “transmembrane receptors” is a broad category that includes GPCRs, ion channels, and RTKs. Not all transmembrane receptors have enzymatic activity; the specific type with kinase activity is RTKs.

D. G Receptors

This is incorrect because G protein-coupled receptors (GPCRs) do not have intrinsic enzyme activity. Instead, they activate heterotrimeric G proteins, which then trigger downstream signaling pathways.