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PSYC 450 Final Exam Questions: Relapse and Drug-Seeking Behavior, Exams of Psychology

A comprehensive set of questions and answers related to relapse and drug-seeking behavior in the context of addiction. It explores various factors that contribute to relapse, including stress, drug cues, and priming effects. The document also delves into the neurobiological mechanisms underlying relapse, focusing on the role of dopamine and glutamate in specific brain regions. It examines different research methods used to study relapse, including animal models and human studies, highlighting their strengths and limitations. This resource is valuable for students studying addiction psychology, neuroscience, or related fields.

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PSYC 450 FINAL EXAM QUESTIONS WITH 100% CORRECT ANSWERS
"What are the main factors that can trigger a relapse? - CORRECT ANSWER Re-exposure to the
drug or other drugs: Even a brief re-exposure can prime relapse.
Cues associated with drug use: Includes objects (e.g., syringes), places, smells, or people linked to
drug use.
Stress: A commonly cited reason for relapse, as stress increases cravings.
Withdrawal symptoms: Conditioned withdrawal can trigger cravings even after the acute
withdrawal phase."
"What is the "priming effect" in the context of relapse? - CORRECT ANSWER The priming
effect occurs when a brief re-exposure to a drug (or a similar substance) reactivates cravings,
potentially leading to relapse. For example, medical exposure to opiates in someone with a
history of opioid use disorder."
"How are smartphones used to study relapse, and what are the challenges of this method? -
CORRECT ANSWER Users log emotions and cravings several times daily, but priming
individuals to report drug-related feelings can itself trigger cravings. Analyzing large, variable
datasets is also difficult."
"What methods are used to study the brain mechanisms of relapse in humans, and what are their
limitations? - CORRECT ANSWER Post-mortem studies, imaging (PET, fMRI), and magnetic
stimulation. These approaches have limited resolution and manipulation capabilities."
"Why is craving often used as a proxy for relapse in studies, and what is the limitation of this
approach? - CORRECT ANSWER Craving is measurable and often precedes relapse, but it does
not always result in relapse, as individuals can resist cravings."
"Why is the period of abstinence important when studying the effects of cues? - CORRECT
ANSWER The effects of drug-associated cues (e.g., paraphernalia, videos) are much stronger
when a user has been abstinent for a longer time, making the results more pronounced."
"What is an alternative method for studying relapse-related factors in abstinent users (Sinha et al
1999)? - CORRECT ANSWER Researchers assess the effects of stress by exposing participants
to stress-inducing, personalized scripts, which they develop with the participants. These scripts
simulate real-life stressful scenarios that the subjects imagine during testing."
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Download PSYC 450 Final Exam Questions: Relapse and Drug-Seeking Behavior and more Exams Psychology in PDF only on Docsity!

PSYC 450 FINAL EXAM QUESTIONS WITH 100% CORRECT ANSWERS

"What are the main factors that can trigger a relapse? - CORRECT ANSWER Re-exposure to the

drug or other drugs: Even a brief re-exposure can prime relapse. Cues associated with drug use: Includes objects (e.g., syringes), places, smells, or people linked to drug use. Stress: A commonly cited reason for relapse, as stress increases cravings. Withdrawal symptoms: Conditioned withdrawal can trigger cravings even after the acute withdrawal phase."

"What is the "priming effect" in the context of relapse? - CORRECT ANSWER The priming

effect occurs when a brief re-exposure to a drug (or a similar substance) reactivates cravings, potentially leading to relapse. For example, medical exposure to opiates in someone with a history of opioid use disorder."

"How are smartphones used to study relapse, and what are the challenges of this method? -

CORRECT ANSWER Users log emotions and cravings several times daily, but priming

individuals to report drug-related feelings can itself trigger cravings. Analyzing large, variable datasets is also difficult." "What methods are used to study the brain mechanisms of relapse in humans, and what are their

limitations? - CORRECT ANSWER Post-mortem studies, imaging (PET, fMRI), and magnetic

stimulation. These approaches have limited resolution and manipulation capabilities." "Why is craving often used as a proxy for relapse in studies, and what is the limitation of this

approach? - CORRECT ANSWER Craving is measurable and often precedes relapse, but it does

not always result in relapse, as individuals can resist cravings."

"Why is the period of abstinence important when studying the effects of cues? - CORRECT

ANSWER The effects of drug-associated cues (e.g., paraphernalia, videos) are much stronger

when a user has been abstinent for a longer time, making the results more pronounced." "What is an alternative method for studying relapse-related factors in abstinent users (Sinha et al

1999)? - CORRECT ANSWER Researchers assess the effects of stress by exposing participants

to stress-inducing, personalized scripts, which they develop with the participants. These scripts simulate real-life stressful scenarios that the subjects imagine during testing."

"Describe the procedure for the stress study involving abstinent subjects (Sinha et al 1999) -

CORRECT ANSWER Participants work with researchers to create personalized, stress-inducing

scripts based on real or familiar stressful scenarios. During testing, these scripts are read to participants, who imagine themselves in the scenario. Researchers measure physiological responses like heart rate and cortisol levels (a stress hormone that rises and falls over time). Participants also report their craving levels, which increase after imagining the stressful scenario." "What physiological and psychological effects are observed in abstinent users exposed to stress-

inducing scripts (Sinha et al 1999)? - CORRECT ANSWER Physiological effects include

increased heart rate and elevated cortisol levels that peak and decline during the recovery period. Psychologically, participants report heightened craving levels after imagining the stressful scenario."

"What are the limitations of studying abstinent users in stress experiments? - CORRECT

ANSWER Variables like craving are subjective and indirect.

Ethical restrictions limit the types of manipulations allowed. The population is difficult and expensive to work with, resulting in small sample sizes. Smartphone-based studies to track emotions and cravings provide large datasets but have limited depth and may inadvertently act as triggers."

"What are the main triggers for relapse in the Reinstatement Model? - CORRECT ANSWER

Stress: Mild footshocks irritate rats, increasing lever pressing. Priming Injection: A single drug dose induces lever pressing even without drug delivery. Cues: Reintroducing drug-associated cues (e.g., tones or lights) strongly reinstates lever pressing."

"What are the key triggers tested in the reinstatement procedure of drug-seeking behavior? -

CORRECT ANSWER Priming, cue exposure, and stress are used as triggers for reinstating drug-

seeking behavior in animals after extinction. Priming involves administering a small dose of the drug after the extinction phase to see if it reinstates drug-seeking behavior. Cue exposure refers to reintroducing environmental cues (like lights or sounds) previously associated with drug administration. Stress can also act as a powerful trigger for reinstatement, as it mimics conditions that might lead to relapse in humans."

"What is the effect of D2 receptor antagonists on heroin reinstatement (Shalam & Stewart 1996)?

- CORRECT ANSWER D2 receptor antagonists were tested, and even low doses effectively blocked reinstatement of drug-seeking behavior, suggesting that dopamine transmission through D2 receptors is also essential for priming-induced reinstatement." "What is the interpretation of the D1 and D2 receptor findings in reinstatement (Shalam &

Stewart 1996)? - CORRECT ANSWER DA is necessary for priming-induced reinstatement in

rats. Specifically: D1 receptors seem particularly important for priming effects. D2 receptors also play a role, with even low doses blocking reinstatement, highlighting the essential involvement of DA transmission in drug-seeking behavior." "What was the main goal of McFarland & Kalivas (2001) in their study on drug priming and

reinstatement of drug-seeking behavior? - CORRECT ANSWER The main goal was to examine

the role of specific brain regions, particularly the ventral tegmental area (VTA), nucleus accumbens (NAc), and prefrontal cortex (PFC), in cocaine priming-induced reinstatement of drug- seeking behavior. The study specifically investigated how dopamine (DA) and glutamate within these regions contribute to reinstatement of drug-seeking behavior after extinction." "How does cocaine priming influence reinstatement of drug-seeking behavior in animal models?

CORRECT ANSWER Cocaine priming involves administering a small dose of cocaine after

extinction of drug-seeking behavior. This priming injection leads to a significant reinstatement of drug-seeking behavior, measured by the number of responses during the extinction phase, indicating that the prior experience with the drug is reactivated by the priming injection." "What neurotransmitters and brain regions are involved in cocaine priming-induced

reinstatement according to McFarland & Kalivas (2001)? - CORRECT ANSWER Cocaine

priming-induced reinstatement is primarily influenced by DA and glutamate in specific brain regions: the VTA, NAc, and PFC. The study focuses on how these areas interact to control the return of drug-seeking behavior following extinction."

"How did researchers shut down the VTA in this study (McFarland & Kalivas 2001)? - CORRECT

ANSWER Baclofen and muscimol (GABA agonists) inhibited VTA activity, completely blocking

reinstatement by preventing dopamine release."

"How does DA in the dPFC affect cocaine priming-induced reinstatement (McFarland & Kalivas

2001)? - CORRECT ANSWER Injecting DA into the dPFC during VTA inhibition restored

reinstatement, showing that dopamine activity in the dPFC is critical for reinstatement." "How did researchers shut down the ventral tegmental area (VTA) in this study (McFarland &

Kalivas 2001)? - CORRECT ANSWER They used a mixture of baclofen (GABA-B agonist) and

muscimol (GABA-A agonist), which activate inhibitory GABA receptors to silence neurons in the VTA. This stopped dopamine release from the VTA and completely blocked cocaine-induced reinstatement." "What happened to cocaine reinstatement when the VTA was shut down (McFarland & Kalivas

2001)? - CORRECT ANSWER Cocaine reinstatement was completely blocked. This suggests

that the VTA's activity is necessary for reinstatement, likely through its dopamine projections to various targets like the PFC, NAc, and hippocampus." "What did the researchers demonstrate by injecting dopamine into the PFC after shutting down

the VTA (McFarland & Kalivas 2001)? - CORRECT ANSWER Reinstatement was rescued,

showing that DA activity in the PFC alone is sufficient to induce reinstatement, even without dopamine from the VTA targeting other brain regions." "Why was it surprising that a dopamine antagonist in the NAc core did not block reinstatement

(McFarland & Kalivas 2001)? - CORRECT ANSWER The NAc is a primary target of the

mesolimbic dopamine system, so it was unexpected that blocking dopamine in the NAc core had no effect on cocaine priming-induced reinstatement. This finding redirected focus to the role of the PFC and glutamate." "How are the core and shell of the NAc functionally different in addiction (McFarland & Kalivas

2001)? - CORRECT ANSWER Both regions receive different inputs and have distinct outputs.

The core is more critical for general and priming-induced reinstatement due to its glutamatergic input from the prelimbic cortex. The shell may be more involved in priming-induced reinstatement via dopamine." "What did the Kalivas group demonstrate about the NAc core and reinstatement (McFarland &

Kalivas 2001)? - CORRECT ANSWER They showed that glutamate, not DA, is critical for

priming-induced reinstatement in the NAc core. Blocking glutamatergic input from the prelimbic cortex to the core prevents reinstatement."

"What is the role of DA D1 receptors in context-induced reinstatement? - CORRECT ANSWER

In contrast to discrete cue-induced reinstatement, DA D1 receptors in the NAc lateral shell are crucial for context-induced reinstatement. When a DA D1 antagonist is injected into the NAc lateral shell during context exposure (such as placing the animal back in an environment associated with previous drug use), it effectively blocks the reinstatement of drug-seeking behavior. This suggests that the lateral shell plays a key role in processing contextual cues that trigger relapse." "How do the effects of DA D1 antagonists differ between discrete-cue and context-induced

reinstatement? - CORRECT ANSWER Discrete-cue Reinstatement: DA D1 receptors in the NAc

core are important for reinstatement in response to discrete cues. Context-induced Reinstatement: DA D1 receptors in the NAc lateral shell are important for reinstatement in response to contextual cues (environmental context), while the NAc core is not critical in this case."

"What can we conclude about the role of DA in cue-induced reinstatement? - CORRECT

ANSWER DA transmission, particularly through DA D1 receptors, is crucial for cue-induced

reinstatement of drug-seeking behavior. However, the specific subarea of the NAc involved (core vs. lateral shell) depends on the type of cue (discrete vs. contextual). DA transmission in the NAc core is vital for discrete-cue reinstatement, while the NAc lateral shell is important for context- induced reinstatement."

"What is the significance of considering the type of cue used in addiction experiments? -

CORRECT ANSWER Findings on drug-seeking behavior vary depending on the type of cue

used. Discrete cues (such as a light or tone) and contextual cues (such as the environment where the drug is self-administered) engage different neural circuits, leading to different behavioral outcomes." "What is the traditional method for studying the contribution of brain areas to drug-seeking

behavior, and what are its drawbacks? - CORRECT ANSWER The traditional method is to lesion

brain areas, where researchers would destroy neurons in a specific area to observe changes in behavior. This method provides valuable insights but has the drawback of being nonspecific, and it causes permanent damage, making it difficult to draw conclusions about reversible brain functions."

"How can researchers temporarily shut down a brain area to study its role in behavior? -

CORRECT ANSWER Researchers can use tetrodotoxin (TTX), a neurotoxin that blocks Na+

channels and prevents neurons from firing action potentials. This inhibition is temporary, as the toxin is metabolized, and the brain area "comes back online" after a period."

"What was the goal of Grimm & See's 2000 study involving TTX, the BLA, and the NAc? -

CORRECT ANSWER They aimed to investigate the role of the BLA and NAc in cue-induced

reinstatement of drug-seeking behavior. They used TTX injections to temporarily shut down these brain areas and assess their contribution during cocaine self-administration and extinction." "What were the key findings during the extinction and cue-induced reinstatement phase of the

study with NAc inactivation? - CORRECT ANSWER Extinction: Rats showed a clear extinction

curve without any noticeable extinction bursts (unlike previous studies where animals showed frustration and an initial burst of responses). Cue-induced reinstatement: Despite shutting down the NAc with TTX during cue exposure, there was no effect on cue-induced reinstatement. The rats responded to the cues (light and tone) as expected, showing typical drug-seeking behavior."

"What did the lack of effect on cue-induced reinstatement after NAc inactivation suggest? -

CORRECT ANSWER The findings suggest that the NAc is not necessarily a critical component in

cue-induced reinstatement of drug-seeking behavior. However, it highlights the complexity of interpreting results from inactivation studies because shutting down a brain area with TTX may not always give clear answers—axons passing through the NAc could also be affected, complicating the interpretation."

"How did the NAc inactivation affect priming-induced reinstatement of drug-seeking behavior? -

CORRECT ANSWER After additional extinction sessions, when the rats were primed with a

cocaine injection, the vehicle group showed significant priming-induced reinstatement. However, the TTX-treated group that had their NAc shut down did not show priming-induced reinstatement, indicating that the NAc is critical for this form of reinstatement." "What conclusion was drawn from the experiment regarding the NAc's role in cue-induced and

priming-induced reinstatement? - CORRECT ANSWER The study concluded that the NAc is not

essential for cue-induced reinstatement but plays a critical role in priming-induced reinstatement. This underscores the idea that different brain areas may be involved in different forms of drug-seeking behavior, depending on whether the behavior is driven by cues or priming." "Why must researchers be cautious when interpreting results from studies that involve shutting

down brain areas with TTX? - CORRECT ANSWER Caution is needed because inactivation with

TTX may not only affect the targeted area but also any axons passing through it, which can lead to

Test Day: The animals are exposed to cocaine-associated cues again, leading to reinstatement of cocaine-seeking behavior, which demonstrates typical cue-induced reinstatement." "What is observed when the mPFC-NAc pathway is inhibited by yellow light during the test day

(Stefanik et al 2013)? - CORRECT ANSWER When the yellow light is activated to inhibit the

mPFC-NAc pathway, the cocaine-seeking behavior in response to cues is dramatically reduced, showing that this pathway is necessary for cue-induced reinstatement of cocaine-seeking behavior."

"What is the primary circuit involved in cue-induced reinstatement of drug-seeking behavior? -

CORRECT ANSWER DA (D1 receptors)

Glutamate transmission Brain regions: BLA, CeA, NAc, and mPFC."

"What is the role of the mPFC in cue-induced reinstatement of drug-seeking behavior? -

CORRECT ANSWER The input from the dorsal mPFC to the NAc is glutamatergic. This pathway

is critical for cue-induced reinstatement of cocaine-seeking behavior, as blocking this pathway inhibits reinstatement." "What are the core components of the circuit involved in cue-induced reinstatement of drug-

seeking behavior? - CORRECT ANSWER VTA, PFC,

NAc, Ventral Pallidum, BLA, CeA"

"How does DA contribute to cue-induced reinstatement? - CORRECT ANSWER DA plays a

critical role in cue-induced reinstatement, particularly in the NAc, depending on where it is injected (core or shell). The effect of DA varies based on the type of cue (contextual vs. discrete). In general, DA in the NAc is important for triggering reinstatement."

"How does the cue-induced reinstatement circuit vary for different triggers? - CORRECT

ANSWER There is some overlap between the different parts of the circuit, but each trigger (e.g.,

cocaine cue, contextual cue) may involve specific additions to the circuit. Despite this complexity, there appears to be a common pathway out, though the specific route taken can vary depending on the type of trigger." "Why is the role of the HPA axis in stress-induced reinstatement different for heroin and cocaine?

- CORRECT ANSWER In heroin-induced reinstatement, the absence of corticosterone does not affect the reinstatement response. However, in cocaine-induced reinstatement, a baseline level

of corticosterone is needed for the reinstatement to occur, even though the stress-induced increase in corticosterone is not necessary. The exact reasons for this difference are not fully understood."

"How does the role of CRF differ in stress-induced reinstatement? - CORRECT ANSWER CRF is

not only a hormone involved in the HPA axis but also acts as a neurotransmitter in the brain. It is released at synapses and binds to specific CRF receptors. Researchers began to investigate its role in stress-induced reinstatement, as it is implicated in stress responses outside of the hormonal pathway." "How does norepinephrine (NE) contribute to stress-induced reinstatement of drug-seeking

behavior? - CORRECT ANSWER NE is released during stress or excitement and is involved in

the stress response. It plays a significant role in modulating stress-induced reinstatement of drug- seeking behavior, alongside CRF."

"Which brain regions are involved in stress-induced reinstatement of drug-seeking behavior? -

CORRECT ANSWER The bed nucleus of the stria terminalis (BNST), amygdala, and the release

of CRF, NE, DA, and 5-HT (serotonin). These regions and neurotransmitters coordinate to influence the reinstatement of drug-seeking behavior following stress." "What are the major neurotransmitters involved in the stress response related to drug-seeking

behavior? - CORRECT ANSWER CRF (Corticotropin-Releasing Factor)

Norepinephrine (NE) Dopamine (DA) Serotonin (5-HT)These neurotransmitters interact with brain regions like the BNST and amygdala to modulate stress and drug-seeking behavior."

"What was the focus of the Erb et al., 1998 study? - CORRECT ANSWER The study investigated

the role of CRF receptors in stress-induced reinstatement of drug-seeking behavior, specifically following footshock and priming-induced reinstatement of cocaine and heroin seeking in animals."

"What were the experimental groups in the Erb et al., 1998 study? - CORRECT ANSWER The

animals were trained to self-administer cocaine and then underwent extinction training. Before the test, they were injected with a CRF receptor antagonist (D-Phe) at different doses. Some animals received saline (control), while others received different doses of D-Phe before the test."

"What were the results for the saline group in the Erb et al., 1998 study? - CORRECT ANSWER

The animals in the saline group, who went through the test without receiving any CRF receptor

"How can FOS expression be used to study stress-induced reinstatement? - CORRECT

ANSWER FOS expression identifies neuronal activity in regions involved in the behavior, such as

the BNST following reinstatement."

"What is the effect of infusing a CRF antagonist into the BNST? - CORRECT ANSWER It blocks

stress-induced reinstatement, showing the critical role of CRF in the BNST for this behavior."

"What happens when CRF is injected into the BNST? - CORRECT ANSWER It induces

reinstatement, confirming the importance of CRF transmission in the BNST." "What evidence supports the amygdala → BNST CRF pathway's role in stress-induced

reinstatement? - CORRECT ANSWER Massive CRF innervation from the amygdala to the BNST.

Blocking CRF in the BNST prevents reinstatement. Injecting CRF in the BNST induces reinstatement."

"Why are both NE and CRF considered important in stress-induced reinstatement? - CORRECT

ANSWER NE acts upstream, while CRF in the BNST is the critical downstream mediator of

reinstatement."

"Why are neurotransmitter-specific manipulations preferable to lesion studies? - CORRECT

ANSWER They allow precise targeting of pathways, avoiding nonspecific effects that lesions

might cause."

"What did FOS expression studies reveal about the BNST? - CORRECT ANSWER The BNST is

highly active following stress-induced reinstatement, highlighting its role in the behavior."

"What are the contrasting effects of blocking or activating CRF in the BNST? - CORRECT

ANSWER Blocking CRF: Prevents reinstatement.

Injecting CRF: Induces reinstatement."

"What is the critical source of NE for stress-induced reinstatement? - CORRECT ANSWER The

LTA is the important source of NE, with other sources being less critical." "What are the key brain regions and neurotransmitters involved in stress-induced reinstatement?

- CORRECT ANSWER Regions: Bed nucleus of the stria terminalis (BNST), amygdala. Neurotransmitters: CRF, NE, DA."

"What is the primary goal of the "disconnection" study (Erb et al 2001)? - CORRECT ANSWER

To test whether the amygdala → BNST pathway is critical for stress-induced reinstatement by using manipulations in both hemispheres."

"What assumption is critical for the disconnection study's logic (Erb et al 2001)? - CORRECT

ANSWER The amygdala → BNST pathways in each hemisphere operate independently without

significant cross-innervation."

"What manipulations were performed in the disconnection study (Erb et al 2001)? - CORRECT

ANSWER Injecting TTX to inhibit the amygdala in one hemisphere.

Injecting a CRF antagonist in the BNST of the opposite hemisphere." "What happens when only one side of the amygdala → BNST pathway is disrupted (Erb et al

2001)? - CORRECT ANSWER Footshock-induced reinstatement is unaffected, as the pathway

on the other side compensates." "What happens when both the amygdala and BNST are disrupted on opposite sides (Erb et al

2001)? - CORRECT ANSWER Stress-induced reinstatement is attenuated, demonstrating the

importance of the amygdala → BNST pathway." "What does the disconnection study conclude about the amygdala → BNST pathway (Erb et al

2001)? - CORRECT ANSWER It is critical for stress-induced reinstatement, as disrupting both

pathways prevents the behavior."

"Why does the disconnection study depend on pathways being primarily unilateral? - CORRECT

ANSWER Cross-innervation would allow compensation, invalidating the results of the

manipulations."

"What modern techniques could confirm the findings of the disconnection study? - CORRECT

ANSWER Optogenetics or chemogenetics could specifically manipulate the amygdala → BNST

pathways."

"Why do single-sided manipulations serve as a control in the disconnection study? - CORRECT

ANSWER They show that the behavior persists when only one pathway is disrupted, ensuring

that effects seen with dual manipulations are specific."

"Why is stress-induced reinstatement not completely blocked when the amygdala → BNST

pathway is partially disrupted (Shaham & Stewart 1996)? - CORRECT ANSWER Other

pathways or contributors are likely involved in stress-induced reinstatement, as demonstrated by the persistent effect of footshock even after disrupting the amygdala → BNST pathway."

"How would these experiments be conducted more elegantly today? - CORRECT ANSWER By

using optogenetics or chemogenetics, which allow for precise manipulation of specific pathways, such as the amygdala → BNST pathway, without affecting other regions."

"How do heroin priming and stress differ in their effects on reinstatement? - CORRECT

ANSWER Stress-induced reinstatement is unaffected by blocking opioid receptors, while heroin

priming involves the opioid system."

"What was the focus of the Tobin et al. 2013 study on drug-seeking behavior? - CORRECT

ANSWER The study investigated acute food deprivation-induced reinstatement of heroin

seeking after 21 hours of food deprivation."

"How does DA influence stress-induced reinstatement of heroin seeking (Tobin et al 2013)? -

CORRECT ANSWER DA plays a critical role, particularly via D1 receptors in the NAc shell.

Blocking these receptors reduces stress-induced heroin-seeking behavior."

"How was the DA D1 receptor antagonist administered in the Tobin et al. 2013 study? -

CORRECT ANSWER The DA D1 receptor antagonist was injected directly into the NAc shell."

"What was the effect of injecting a DA D1 receptor antagonist into the NAc shell (Tobin et al. 2013

study)? - CORRECT ANSWER It blocked stress-induced reinstatement of heroin seeking during

acute food deprivation, indicating the importance of D1 receptors in the NAc shell." "How does the effect of systemic DA antagonist injections compare to localized NAc shell

injections (Tobin et al. 2013 study)? - CORRECT ANSWER Systemic injections of DA antagonists

also block stress-induced reinstatement, but the specific targeting of D1 receptors in the NAc shell provides more precise evidence of the receptor's role." "What does acute food deprivation (21 hours) do to heroin-seeking behavior (Tobin et al. 2013

study)? - CORRECT ANSWER It increases heroin-seeking behavior, which can be blocked by a

DA D1 receptor antagonist in the NAc shell."

"What was the role of flupenthixol in stress-induced reinstatement studies (Tobin et al. 2013

study)? - CORRECT ANSWER Flupenthixol, a nonspecific dopamine antagonist, blocks stress-

induced reinstatement of heroin seeking when administered systemically."

"What is the overall summary of DA's role in stress-induced reinstatement of heroin seeking? -

CORRECT ANSWER DA is crucial for stress-induced reinstatement. Blocking D1 receptors in

the NAc shell specifically reduces heroin-seeking behavior during acute food deprivation, highlighting the importance of the mesolimbic dopamine pathway."

"What did studies on the disconnection between the amygdala and the BNST reveal? - CORRECT

ANSWER These studies revealed that while the amygdala-BNST pathway is important, other

areas also contribute to stress-induced reinstatement, highlighting a broader network involvement."

"What is the function of a microdialysis probe in drug-seeking behavior studies? - CORRECT

ANSWER A microdialysis probe collects extracellular molecules from the brain and can also

infuse substances, like a CRF antagonist, into specific brain regions to study their effects."

"How was a microdialysis probe used to study CRF's role in the VTA? - CORRECT ANSWER The

probe was implanted into the VTA to infuse CRF antagonist, allowing researchers to investigate how blocking CRF affects stress-induced drug-seeking behavior."

"What is the significance of the VTA in drug-seeking behavior? - CORRECT ANSWER The VTA is

crucial for reward and stress-related behaviors. Manipulating CRF or dopamine in this area can affect stress-induced reinstatement of drug seeking."

"What brain regions and neurotransmitters are involved in stress-induced reinstatement? -

CORRECT ANSWER The bed nucleus of the stria terminalis (BNST), amygdala, CRF, NE, DA, and

glutamate play key roles in stress-induced reinstatement."

"What is the effect of footshock on CRF release in the VTA according to Wang et al., 2005? -

CORRECT ANSWER Footshock induces a robust release of CRF in the VTA, which is part of the

stress response. This release occurs in both cocaine-trained and cocaine-naive rats."

"How does CRF affect glutamate release in cocaine-trained rats (Wang et al., 2005)? - CORRECT

ANSWER CRF controls glutamate release in the VTA only in cocaine-trained rats, not in cocaine-

naive rats. This glutamate release activates the mesolimbic dopamine system, triggering reinstatement."

"What procedure was followed for studying stress-induced reinstatement in cocaine-trained rats

(Wang et al 2005)? - CORRECT ANSWER Rats were trained to self-administer cocaine,

underwent extinction (drug removal), and were then exposed to footshock to test reinstatement." "What happens when a CRF receptor antagonist (α-H-CRF) is infused in cocaine-trained rats

(Wang et al 2005)? - CORRECT ANSWER The footshock-induced reinstatement of cocaine-

seeking behavior is blocked, indicating that CRF release is critical for reinstatement." "What does the blocking of reinstatement by a CRF receptor antagonist demonstrate (Wang et al

2005)? - CORRECT ANSWER It shows that the increase in CRF caused by footshock is essential

for triggering the reinstatement of cocaine-seeking behavior." "How does a CRF receptor antagonist affect glutamate levels in the VTA after footshock (Wang et

al 2005)? - CORRECT ANSWER The CRF antagonist reduces or almost blocks the footshock-

induced increase in glutamate levels in cocaine-trained rats." "How does a CRF receptor antagonist affect dopamine levels in the VTA after footshock (Wang et

al 2005)? - CORRECT ANSWER The CRF antagonist also blocks the footshock-induced increase

in dopamine levels in cocaine-trained rats."

"What is the first step in the cascade of events following footshock (Wang et al 2005)? -

CORRECT ANSWER Footshock triggers an increase in CRF in the VTA, a stress response that is

independent of the rats' history with cocaine."

"What happens after CRF is released in the VTA during footshock (Wang et al 2005)? - CORRECT

ANSWER CRF activates its receptors, leading to an increase in glutamate release in cocaine-

trained rats."

"What does the increase in glutamate lead to in cocaine-trained rats (Wang et al 2005)? -

CORRECT ANSWER The glutamate release activates the mesolimbic dopamine system,

resulting in increased dopamine levels in the VTA."

"What is the effect of blocking CRF transmission on the cascade (Wang et al 2005)? - CORRECT

ANSWER Blocking CRF receptors prevents the increases in glutamate and dopamine, and blocks

the reinstatement of cocaine-seeking behavior."

"Why is CRF considered critical in stress-induced reinstatement (Wang et al 2005)? - CORRECT

ANSWER CRF release initiates the cascade leading to increases in glutamate and dopamine,

which are necessary for the reinstatement of cocaine-seeking behavior in trained rats." "How are glutamate and dopamine responses different in cocaine-trained vs. naive rats during

footshock (Wang et al 2005)? - CORRECT ANSWER Increases in glutamate and dopamine

occur only in cocaine-trained rats, highlighting cocaine-induced neural adaptations."

"What is the sequence of events in stress-induced reinstatement (Wang et al 2005)? - CORRECT

ANSWER Footshock → CRF release → CRF receptor activation → Glutamate release →

Dopamine release → Reinstatement of cocaine-seeking behavior." "How does footshock-induced glutamate release differ between cocaine-trained rats and naive

rats? (Wang et al 2005)? - CORRECT ANSWER In cocaine-trained rats, footshock causes a

significant increase in glutamate release, which is not observed in naive animals. While naive rats experience a stress response, they do not show the glutamate increase seen in trained animals, indicating that cocaine history modifies glutamate system responses." "What was the outcome of infusing a nonspecific glutamate receptor antagonist (Kynurenic acid)

in cocaine-trained rats (Wang et al 2005)? - CORRECT ANSWER Infusion of Kynurenic acid

blocked reinstatement of cocaine-seeking behavior following footshock. The antagonist inhibits postsynaptic glutamate receptors, preventing glutamate's action, but it does not affect glutamate release itself." "How does Kynurenic acid affect glutamate and dopamine responses to footshock in cocaine-

trained rats (Wang et al 2005)? - CORRECT ANSWER Glutamate: Kynurenic acid does not block

the increase in glutamate because it only targets postsynaptic receptors, leaving presynaptic glutamate release unaffected. Dopamine: Blocking glutamate receptors prevents the downstream increase in dopamine levels, which is crucial for reinstatement." "Why does glutamate release remain unchanged even when postsynaptic receptors are blocked

(Wang et al 2005)? - CORRECT ANSWER Glutamate release is presynaptic and unaffected by

receptor blockade. All groups exposed to footshock show an increase in glutamate release." "What happens to DA levels if glutamate receptors are blocked during footshock exposure (Wang

et al 2005)? - CORRECT ANSWER Blocking glutamate receptors prevents the increase in

dopamine, which is critical for reinstatement of cocaine-seeking behavior."