Psychopathopharmacology 1 MSN 671 quiz 3

Correct Answer:

A. Benzodiazepines

Explanation:

Benzodiazepines are well known to act on ionotropic receptors, specifically the GABA-A receptor, which is a chloride ion channel. By binding allosterically, benzodiazepines increase the frequency of chloride channel opening in response to GABA, leading to enhanced inhibitory signaling. This ionotropic mechanism allows benzodiazepines to take immediate clinical effects, such as sedation, anxiolysis, or anticonvulsant action, compared to drugs that act via slower metabotropic pathways.

Why Other Options Are Wrong:

B. Ionic compounds

This is incorrect because "ionic compounds" is not a drug class in psychopharmacology. It is a chemistry term referring to substances made of ions, not medications that act on receptors.

C. Antipsychotic

This is incorrect because most antipsychotics act on metabotropic G-protein-coupled receptors (GPCRs), such as dopamine D2 or serotonin 5-HT2A receptors. Their effects are slower and not mediated through ionotropic channels.

D. Antidepressants

This is incorrect because antidepressants, including SSRIs, SNRIs, and TCAs, primarily act by blocking neurotransmitter reuptake or influencing GPCR-mediated systems. They do not exert their main actions at ionotropic receptors and therefore do not produce immediate effects.

Correct Answer:

A. 5HT2C antagonism

Explanation:

While fluoxetine is primarily an SSRI (serotonin reuptake inhibitor), its early energizing effects are largely attributed to 5HT2C antagonism. The 5HT2C receptor normally inhibits dopamine and norepinephrine release in the prefrontal cortex. By blocking this receptor, fluoxetine disinhibits dopamine and norepinephrine release, leading to improvements in energy, attention, and cognition within days—much faster than the delayed mood-elevating effects from serotonin reuptake inhibition.

Why Other Options Are Wrong:

B. Norepi reuptake inhibition

This is incorrect because fluoxetine is not a norepinephrine reuptake inhibitor. Other antidepressants (e.g., SNRIs, TCAs) provide this effect, but fluoxetine does not significantly block norepinephrine transporters.

C. Serotonin reuptake inhibition

This is incorrect as the explanation for the rapid energizing effect. While fluoxetine does inhibit serotonin reuptake, those changes take weeks to translate into clinical mood improvement. The patient’s immediate boost in energy and cognition is better explained by 5HT2C antagonism.

Correct Answer:

C. Methylation

Explanation:

Methylation refers to the addition of methyl groups (–CH₃) to DNA (commonly at cytosine bases in CpG islands) or histone proteins. This process can silence or activate gene expression depending on the location and context. DNA methylation usually represses transcription by blocking transcription factor binding or recruiting repressor proteins, making it a key regulator in epigenetics.

Why Other Options Are Wrong:

A. Acetylation

This is incorrect because acetylation involves adding acetyl groups to histone tails, which typically loosens chromatin and activates gene expression, not methyl groups.

B. Transcription

This is incorrect because transcription is the process of synthesizing RNA from DNA, not a chemical modification of DNA or histones.

D. Epigenetic Modifications

This is incorrect because epigenetic modifications is a broad category that includes both methylation and acetylation (among others). The specific process of adding methyl groups is called methylation.

Correct Answer:

B. Communicates to the ventral tegmental area when cues related to drugs of abuse are present

Explanation:

The amygdala plays a crucial role in the emotional and cue-related aspects of substance abuse. It does not directly release dopamine but instead communicates with the ventral tegmental area (VTA) and other brain regions when environmental cues associated with drugs are encountered. This cue-induced activation can trigger craving and relapse. The dopamine release to the nucleus accumbens originates primarily from the VTA, not the amygdala, and drugs of abuse do not bind directly at the amygdala as their primary site of action.

Why Other Options Are Wrong:

A. Releases phasic bursts of dopamine to the nucleus accumbens when drugs of abuse are present

This is incorrect because phasic dopamine release comes from the VTA, not the amygdala.

C. Site of binding for most drugs of abuse

This is incorrect because drugs of abuse bind at their specific targets (e.g., opioid receptors, GABA-A, dopamine transporters) rather than directly at the amygdala.

D. A and B

This is incorrect because only B accurately describes the amygdala’s role, while A misattributes dopamine release.

E. A, B, and C

This is incorrect because neither A nor C is correct for the amygdala.

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:

A. Transduction

Explanation:

Signal transduction is the process in which a ligand (such as a hormone or neurotransmitter) binds to a receptor and activates intracellular molecules, ultimately leading to a specific cellular response. It acts as the “middle step” between reception of the signal and the actual cellular outcome.

Why Other Options Are Wrong:

B. Translation

This is incorrect because translation refers to the synthesis of proteins from mRNA on ribosomes, not receptor-mediated signaling.

C. Response

This is incorrect because the response is the final step of cell signaling (such as gene expression, secretion, or metabolic change), not the process of activating molecules inside the cell.

D. Reception

This is incorrect because reception is the first step, when the ligand binds to the receptor. Transduction follows this step.

Correct Answer:

B: Hypofunctioning NMDA receptors

Explanation:

The glutamate hypothesis, specifically NMDA receptor hypofunction, is the leading explanation for schizophrenia today. NMDA antagonists like ketamine and PCP can mimic both positive and negative symptoms of the disorder. Hypofunction of NMDA receptors on inhibitory interneurons disrupts excitatory–inhibitory balance, contributing to abnormal dopamine signaling.

Why Other Options Are Wrong:

A: Hyperfunctioning NMDA receptors

This is incorrect because schizophrenia is linked to reduced, not increased, NMDA receptor activity.

C: Hyperdopaminergic activity in mesolimbic pathways

This describes the older dopamine hypothesis of schizophrenia, which explains positive symptoms well, but it does not fully account for negative and cognitive symptoms.

D: Hypodopaminergic activity in mesocortical pathways

This is partially true since mesocortical dopamine deficits are linked to negative symptoms and cognitive dysfunction. However, the broader unifying hypothesis is NMDA receptor hypofunction, which influences both dopamine pathways.

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.

Correct Answer:

A. Ketamine

Explanation:

Ketamine, an NMDA receptor antagonist originally used as an anesthetic, has been found effective in treating treatment-resistant depression and rapidly reducing suicidal thoughts. Unlike traditional antidepressants that may take weeks to work, ketamine produces effects within hours. It is often administered intravenously in specialized clinics, and a related formulation, esketamine (Spravato®), is FDA-approved as a nasal spray for treatment-resistant depression.

Why Other Options Are Wrong:

B. Propofol

This is incorrect because propofol is an intravenous anesthetic used for induction and maintenance of anesthesia. It is not used in psychiatric treatment for depression or suicidality.

C. Hydroxyzine

This is incorrect because hydroxyzine is an antihistamine with sedative and anxiolytic properties. It may reduce anxiety but is not indicated for resistant depression or suicidal ideation.

D. Valium

This is incorrect because Valium (diazepam) is a benzodiazepine used for anxiety, muscle spasms, and seizures. It does not treat depression or suicidal thoughts and carries risks of dependence.