Study Guide Final Exam

Question 1

1. How do psychoactive drugs exert their influence on mental functioning?

Answer 1

Exert their influence through their actions on the nervous system, particularly
the brain and spinal cord.

Question 2

2. What are the four main categories of psychoactive drugs based on their effects on the central nervous system? Provide examples of drugs belonging to each category.

Answer 2

Depressants – slow down the function of the central nervous system
Alcohol, Xanax, Cannabis, Ketamine, Opioids
Hallucinogens – affect your senses and change the way you see, hear, taste,
smell or feel things
Cannabis, Ketamine, LSD, Psilocybin, PCP
Stimulants – speed up the function of the central nervous system.
Amphetamines, Caffeine, Cocaine, MDMA, Nicotine

Question 3

3. Why is the age group of 18-25 particularly vulnerable to illicit drug use? Explain from both societal and biological perspectives.

Answer 3

Societal explanation.
▪ Not easy/feasible to use drugs out
in the “real world”
▪ Peer influence
Biological explanation
▪ Our brain is wired to experience the
positive effects more and the
negative effects less.

Question 4

4. How does the concept of conditioned place preference help researchers study the rewarding effects of drugs in animals?

Answer 4

Conditioned Place Preference – Measures the
rewarding/aversive effects of a drug.

▪ Adolescents are less
sensitive to aversive effects
as measured using
conditioned place preference

Question 5

5. Differentiate between pharmacokinetics and pharmacodynamics. How do these concepts contribute to our understanding of drug effects?

Answer 5

Pharmacokinetics (drug action)
▪Study how a drug moves through the body, including process of absorption,
metabolism, distribution to tissues, and elimination.
Pharmacodynamics (drug effect)
▪Study of the ways in which a drug affects the living organism and the organs of
the body

Question 6

6. Explain how the route of drug administration influences its absorption and, consequently, its psychoactive effects.

Answer 6

Oral Ingestion—The administration of a drug through the mouth.
▪ The drug dissolves in the fluids of the mouth, esophagus, or stomach and is
carried to the intestines, where it is absorbed into the bloodstream.
▪ Most common for prescribed drugs
▪ Safest route of administration
▪ Effect of the drug is highly variable
Peripheral Injection
▪ Intramuscular (IM) injection—Injection of a drug into a muscle, usually the
shoulder, upper arm, thigh, or buttocks.
▪ Intraperitoneal (IP) injection—Injection of a drug through the abdominal wall
into the peritoneal cavity (space surrounding major organs).
▪ Intravenous (IV) injection—Injection of a drug into a vein.
▪Subcutaneous (SC) injection—Injection of a drug under the skin.
Central Injection
▪ Intracerebral injection—Injection of a drug directly into the brain.
▪ Intraventricular injection—Injection of a drug into the cerebral ventricles.
Inhalation–The administration of a drug through
the lungs.
Absorption—The administration of a drug by
absorption through the skin or mucous
membranes.

Question 7

Route of administration determines how quickly the
drug is in the blood

Answer 7

Pharmacokinetics effects:
Route can affect
psychoactive experience:
▪ Faster delivery is
associated with a greater
euphoric effect.

Question 8

7. Why is the blood-brain barrier crucial in determining whether a drug will produce psychoactive effects?

Answer 8

Ability to pass the Blood-Brain Barrier
▪ If too large it cannot pass and it will not produce a psychoactive effect.

Question 9

8. What is a drug’s half-life, and why is it an important consideration in understanding the duration of drug effects?

Answer 9

▪ Half-life: the amount of time required for the body to metabolize half the amount
of the drug.
▪ The longer the half-life the longer a drug continues to have a physiological
effect
▪ Cocaine : 0.5-1.5 hrs
▪ Amphetamine: 7-10 hours

Question 10

9. Describe the mechanisms of action of agonists and antagonists in relation to neurotransmitter receptors.

Answer 10

Agonist—A drug that mimics a neurotransmitter or enhances synaptic neurotransmission.
▪ Antagonist— A drug that blocks a neurotransmitter or inhibits synaptic neurotransmission.
▪ Can also distinguish between indirect vs direct agonist.

Question 11

10. How can drugs influence both presynaptic and postsynaptic processes to modulate synaptic transmission?

Answer 11

▪ Drugs work by enhancing or inhibiting these
processes.

Question 12

drugs influence both presynaptic

Answer 12

▪ Transmitter production—drugs may block synthesis
enzymes, axonal transport of raw materials, or the
ability to store the transmitter
▪ Transmitter release—drugs can block action
potentials by blocking sodium channels (Na+
) or
release by blocking calcium (CA++)
▪ Autoreceptors that monitor amount of release and
give feedback can also be affected by drugs
▪ Activate – less neurotransmitter
▪ Block – more neurotransmitter
▪ Transmitter clearance—drugs called reuptake
inhibitors can block reuptake of transmitter, while
others allow the tra

Question 13

10. How can drugs influence postsynaptic

Answer 13

A drug may alter the postsynaptic systems that respond to the released
transmitter
Effects on transmitter receptors:
▪ Selective receptor antagonists block postsynaptic receptors from being
activated by their neurotransmitter
▪ Selective receptor agonists bind to receptors and activate them, mimicking
the natural neurotransmitter
Drugs can also alter intracellular postsynaptic processes, such as number of
receptors and second-messenger systems

Question 14

11. Why is defining drug addiction a complex challenge? Discuss the limitations of early views that focused on moral failings or physical dependence.

Answer 14

-The term addiction has strong negative emotional associations for most of us
-As indicated in the DSM, the use must be maladaptive, which means that harm is
occurring to the user.
-

Question 15

12. How does the positive reinforcement model explain drug addiction? What are its strengths and limitations?

Answer 15

▪ Drug serves as a positive reinforcer. We use and abuse drugs because we “like” the
experience.
▪ The drug produces an intense euphoric effect that drives the person to seek out the
drug.
▪ Relapse occurs because individuals want to “re-experience” the euphoric effects.

Question 16

13. Explain the incentive-sensitization theory of addiction. How does it address some of the limitations of the positive reinforcement model?

Answer 16

Drugs produce not only negative and
positive reinforcing effects, but also
incentive motivational effects.
▪ Distinguishes between drug liking (that is,
the high) and drug-wanting (that is,
craving).

Question 17

14. Describe the contemporary biopsychological view of addiction. How does it differ from earlier perspectives?

Answer 17

The current view of “addiction” in biopsychology is that addiction is the result of long-term
neuroadaptations in the brain that are caused by chronic drug use.

Question 18

15. Why is relapse a significant challenge in addiction treatment? Explain the role of craving and environmental cues in relapse.

Answer 18

Vulnerability to addiction is heightened during early exposure to drug use.
▪ Drug addiction is a chronic and relapsing disorder
▪ Individuals remain “addicted” for long periods of time and drug-free periods
(remissions) are often followed by relapses in which drug use recurs and the
“vicious” cycle is started again.
▪ Relapse is driven by a strong urge or craving for the drug that can be elicited by
cues, the drug, or stress.

Question 19

16. Describe two commonly used animal models of addiction and explain what they measure

Answer 19

Self-Administration
▪ Like humans, rodents self-administer drugs
Conditioned Place Preference
▪ Prefer environments associated with drug
Locomotor Sensitization
▪ Show sensitized responses to drugs

Question 20

17. What is the mesolimbic dopamine system, and why is it considered the “reward pathway” in the brain?

Answer 20

The “rewarding” effects of drugs are attributed to dopamine within the mesolimbic system
(VTA to Nucleus accumbens)

Question 21

18. Explain the effects of alcohol on the central nervous system (CNS) in terms of its interaction with GABA, glutamate, and dopamine

Answer 21

Effects of Alcohol on the CNS:
▪ Alcohol enhances GABA (main inhibitory neurotransmitter) receptors by
enhancing GABA function (similar to Xanax and Valium – anxyolytics).
▪ Alcohol decreases glutamatergic transmission by inhibiting the NMDA
receptor and decreasing levels of glutamate (main excitatory
neurotransmitter)
▪ Alcohol elevates levels of dopamine by enhancing activity of the
mesolimbic pathway.
▪ Withdrawal from Alcohol (opposite effects on CNS):
▪ Decreased GABA function
▪ Increased Glutamate function
▪ Decreased dopamine function

Question 22

19. What are the long-term consequences of chronic alcohol abuse on the brain and liver?

Answer 22

Tolerance and Dependence (withdrawal symptoms)
▪ For some, the withdrawal symptoms are very severe.
▪ 5-6 hrs post-drinking: tremors, headache, nausea,
sweating, vomiting, and abdominal cramps.
▪ 15-30 hrs: convulsive activity
▪ 24-48 hrs: delirium tremens – may last 3-4 days
▪ Disturbing hallucinations
▪ Bizarre delusions
▪ Confusion
▪ Tachycardia (rapid heart beat)
▪ Brain damage after many years of drinking can also
occur in part due to inadequate nutrition, particularly
thiamine (VitaminB1).
▪ Leads to Korsakoff’s syndrome (memory loss, sensory
and motor dysfunction, and eventually dementia)

Question 23

20. How does cocaine exert its stimulant effects on the brain? What are the potential risks associated with heavy cocaine use?

Answer 23

Cocaine was used as an anesthetic and
in soda (Coca Cola) but is highly
addictive because when smoked (crack)
or snorted it produces strong
pleasurable effects
▪ It acts by blocking reuptake of
monoamine transmitters so that they
accumulate in synapses throughout the
brain, boosting their effects
▪ heavy cocaine use raises the risk of
serious side effects like stroke,
psychosis, loss of gray matter, and
severe mood disturbances

Question 24

21. How does the concept of allostasis relate to the development of addiction?

Answer 24

Allostasis: The ability to achieve stability through change
“To obtain stability, an organism must vary all the parameters to its internal milieu and
match them appropriately to environmental demands”

Question 25

22. Describe the role of impulsivity and compulsivity in the transition from casual drug use to addiction.

Answer 25

IMPULSIVITY: An inability to resist urges and making unreflective decisions without regard for consequences. POSITIVE REINFORCEMENT: The process by which presentation of a stimulus such as drug increases the probability of a response like drug taking. NEGATIVE REINFOREMENT: The process by which removal of a stimulus produces negative feeling or emotion and then increases the probability of a response like taking drugs. COMPULSIVITY: Repeated behavior in the face of adverse consequences and repetitive behavior that are inappropriate to a particular situation. The transition from casual drug use to addiction has been neuro-biologically conceptualized as a shift from impulsive to compulsive use and driven by a transition from positive to negative reinforcement mechanisms

Question 26

23. Explain the three-stage cycle of addiction according to the conceptual model presented in the source.

Answer 26

binge/intoxication, withdrawal/negative affect, and preoccupation/anticipation (craving)—that worsens over time and involves neuroplastic changes in the brain reward, stress, and executive function systems

Question 27

24. How do changes in dopamine release in the nucleus accumbens contribute to the development of tolerance and the experience of withdrawal?

Answer 27

This activation of the opioid system directly or indirectly stimulates the VTA to release dopamine to the nucleus accumbens which reinforces the addiction. Cues, places, person, drug paraphernalia, mood can activate dopaminergic system to cause release of dopamine, resulting in motivation to seek drug use.

Question 28

25. Explain the role of the extended amygdala in the withdrawal/negative affect stage of addiction.

Answer 28

It follows the binge/intoxication stage and build up future binge and intoxication. Happens in the extended amygdala. Over time due to continued substance use the level of dopamine release from a certain dose of addictive substance reduces. The individual will need more dose to achieve the previous level of pleasure (Tolerance). When this happens or the drug is withdrawn temporarily or stopped, withdrawal and negative affect ensue.

Question 29

26. Describe the concept of "incentive salience" and its relevance to the preoccupation/anticipation stage of addiction.

Answer 29

In the prefrontal cortex- the executive region of the brain. It is a stage where the person may begin to seek substance again after a period of abstinence (craving). Prefrontal cortex- "Go system" "Stop system" "Go system" help in decision making planning and reacts to substance associated environmental cues (incentive salience). Exposure to cues dramatically increase the "Go system" prefrontal cortex activity. The over activation of the "Go system" in the prefrontal cortex promote habit like substance seeking and under activation of the "Stop system" of the prefrontal cortex promote impulsive and compulsive substance seeking.

Question 30

27. Identify and explain three factors that increase vulnerability to relapse in addiction.

Answer 30

1. Brief exposure to ANY abusable drug or compulsive behavior (Dopamine release and dopamine receptor downregulation AKA Drug-induced Reinstatement/Relapse 2. Stress (Corticotropin Releasing Factor release and dopamine receptor downregulation) AKA Stress-induced Reinstatement/Relapse 3. Exposure to drug cues (glutamate release) AKA Cue-induced Reinstatement

Question 31

28. How does the concept of craving differ from simply "wanting" something? Explain the physiological basis of craving.

Answer 31

Increased stress = increased pleasure threshold = increased need for dopamine= midbrain thinks it is dying= CRAVING CRAVING is a physiological response to a neurochemical deficiency resulting in symptoms including sweating, stomach cramps, obsession, increased respirations, etc. No person can choose to crave or not. You don’t actually have to have drug use for the defective physiology of addiction to be active

Question 32

29. Outline the hierarchy of treatment for addiction. Why is addressing medical issues and detox a priority?

Answer 32

Treat most acute medical issues first * Detox * Quiet the midbrain with medication/abstinence * Restore Cortex * Give the person workable, credible tools to proactively manage stress and decrease craving * Coping skills * Stress Relief * Social Supports * Safe Environments

Question 33

30. How do animal models of addiction, such as self-administration and reinstatement paradigms, contribute to our understanding of relapse?

Answer 33

-Self-Administration primary reinforcement consummatory behavior -Reinstatement appetitive/approach behavior -Potent Non-Drug Reinforcer e.g., palatable sweet solution or food [i.e., sweetened condensed milk (SCM), glucose saccharin solution (GSS)] -Drug Reinforcer e.g., cocaine (COC), alcohol (EtOH), oxycodone

Question 34

31. What are the key components of emotion, and how do they interact to shape our emotional experiences?

Answer 34

Emotion is a subjective mental state that is usually accompanied by distinctive cognition, behaviors, and physiological changes. The physical sensations are the result of activation of the autonomic nervous system: ▪Sympathetic nervous system—“fight or flight” system; prepares the body for action ▪Parasympathetic nervous system—prepares the body to relax and recuperate

Question 35

32. Contrast the James-Lange and Cannon-Bard theories of emotion. How do they differ in their explanations of the relationship between physiological changes and emotional feelings?

Answer 35

▪ James–Lange theory—autonomic reaction triggers feeling ▪Cannon Bard theory—simultaneous autonomic reaction and feeling

Question 36

33. Explain Schachter's two-factor theory of emotion. How does it account for the influence of both physiological arousal and cognitive appraisal on emotional experience?

Answer 36

Schachter’s theory: ▪Emotional labels are attributed to sensations of physiological arousal. ▪Which emotion we feel depends on cognitive systems that assess the context of the current situation. The Schachter and Singer experiment showed that autonomic responses can intensify our emotions, but our cognitive analysis affects which emotion we experience.

Question 37

34. What is the basis for using polygraph tests to detect lying? What are the limitations and controversies surrounding their use?

Answer 37

The polygraph test measures activation of the sympathetic nervous system reflecting stress, not lying. Brain-imaging scans may prove more accurate in the future. But they are not very reliable just yet

Question 38

35. Discuss the evidence supporting the universality of emotional expressions. Are there cultural differences in how emotions are expressed and recognized?

Answer 38

Darwin suggested that expressions of emotions are universal among all people. The similarity in facial expressions in human and nonhuman primates suggests a common ancestor. Noted nonhuman primates have the same facial muscles as humans Redican described nonhuman primate expressions including a play face, homologous to the human laugh. Emotions act as motivational programs that evolved to coordinate responses to solve adaptive problems. ▪Responding to dangerous situations with a fear program—improved survival ▪The emotion of fear shifts our perception, attention, cognition, and action ▪ Avoiding body fluids after another individual expresses disgust for them— reduced rates of infection

Question 39

36. Describe the role of facial muscles, cranial nerves, and CNS pathways in mediating facial expressions.

Answer 39

Facial expressions are mediated by muscles, cranial nerves, and CNS pathways. Two categories of facial muscles: ▪Superficial facial muscles—attach between points of facial skin ▪Deep facial muscles—attach to bone; produce larger movements, like chewing Facial muscles are innervated by two cranial nerves: the facial nerve (VII) and the motor branch of the trigeminal nerve (V). Paul Ekman and his collaborators say there are distinctive expressions for anger, sadness, happiness, fear, disgust, contempt, and embarrassment Other researchers include affection and expectation in the core group of facial expressions that are interpreted similarly across many cultures. Cross-cultural similarity is noted in the production of expressions of specific emotions, yet some isolated groups do not agree on expressions of surprise and disgust. Subtle cultural differences suggest that cultural conditioning enforces prescribed rules for facial expression.

Question 40

37. Explain the facial feedback hypothesis and its implications for the James-Lange theory of emotion.

Answer 40

The facial feedback hypothesis suggests that sensory feedback from our facial expressions can affect our mood. ▪ Lends support to the James–Lange theory People performing a task who take on a happy or sad face report stronger feelings of the emotions they were simulating. Botox injections, which paralyze facial muscles, cause people to experience emotions less intensely. Yet, when a stressful situation compels someone to display false emotional expressions it can be detrimental to their well-being and happiness at work

Question 41

38. How does electrical brain stimulation provide insights into the neural circuits involved in emotion?

Answer 41

Electrical brain stimulation can produce emotional effects. Brain self-stimulation—animals (including humans) will work to receive electrical stimulation to their brain. Brain sites that support self-stimulation have been mapped. Most are subcortical, concentrated in the medial forebrain bundle. Medial forebrain bundle—the tract that rises from the midbrain through the hypothalamus; affected at many self-stimulation sites Nucleus accumbens—important target for axons of medial forebrain bundle; major component of the reward circuit; release of dopamine here produces very pleasurable feelings

Question 42

39. Describe the role of the amygdala in fear learning and the processing of fear-provoking stimuli.

Answer 42

Classical conditioning can elicit fear, including behaviors and autonomic changes, by pairing a stimulus with an aversive stimulus, like shock. Studies of fear conditioning identified the amygdala, located in the temporal lobe, as a key structure in the mediation of fear. Fear-provoking stimuli reach the thalamus and are directed to the amygdala via the “low road,” bypassing conscious processing and allowing immediate reactions to stimuli. Another route that processes fear-provoking stimuli after the thalamus is the "high road" that goes through sensory cortex. Processing here allows for a slower conscious perception that can integrate with the higher-level cognitive functions of learning and memory. Neural mechanisms of fear conditioning are implicated in posttraumatic stress disorder (PTSD). Sensory cues that a memory once linked with a horrible event will later intrusively evoke the same autonomic and psychological fear symptoms originally produced by the traumatic event. Extinction of the fear learning is a goal of treatment

Question 43

40. What evidence suggests that different brain regions are involved in processing different emotions? Is there a simple one-to-one mapping of specific emotions to specific brain areas?

Answer 43

Feeling love can bilaterally increase activity in the insula and anterior cingulate cortex and decrease activity in the posterior cingulate and prefrontal cortices. A study comparing brain activation during sadness, happiness, anger, and fear showed activation of the insula, cingulate cortex, and prefrontal cortex. ▪ There is no simple, one-to-one relation between a specific emotion and changed activity of particular brain regions.

Question 44

41. What are the core characteristics of major depressive disorder (MDD)? How do these symptoms affect an individual's daily functioning?

Answer 44

Depression is characterized by: ▪Unhappy mood ▪ Loss of interests, reduced energy ▪Changes in appetite and sleep patterns ▪Difficulty in concentration ▪Restless agitation or torpor ▪Pessimism and thoughts of death Depression may last for several months. Inheritance is a determinant in depression.

Question 45

42. Discuss the biological factors that may contribute to the development of depression, including brain chemistry, hormones, and genetics.

Answer 45

Unfortunately, the causes remain unknown. A variety of factors may be involved ▪ Biological Differences ▪ People with depression may have physical differences in their brain. ▪ Brain Chemistry ▪ Changes in the production, function, and effects of certain neurotransmitters (brain chemicals). ▪ Hormones ▪ Changes in the body’s balance of hormones. ▪ Genetics ▪ Depression is more common in people whose blood relatives also have this condition

Question 46

43. Describe the brain changes associated with depression, including alterations in brain activity, blood flow, and structure.

Answer 46

Brain changes with depression: ▪ Increased activation in ▪ Frontal lobes, during cognitive tasks ▪Amygdala, during emotional processing ▪Decreased blood flow to areas implicated in attention ▪ Dysfunction of the lateral habenula by the pineal gland, possibly making it an "antireward center" of lost pleasure. ▪Cortex of the right hemisphere is thinner

Question 47

44. Explain the monoamine hypothesis of depression. What evidence supports this hypothesis, and what are its limitations?

Answer 47

▪ Inhibitors of monoamine oxidase (MAO), enzyme that inactivates the monoamines: norepinephrine, dopamine, and serotonin ▪The first antidepressant drugs o MAO inhibitors raise the level of monoamines at the synapse o Efficacy led to monoamine hypothesis of depression ▪Tricyclics—another type of antidepressant; inhibit reuptake of monoamines ▪Selective serotonin reuptake inhibitors (SSRIs)—block the reuptake of serotonin in the brain

Question 48

45. Describe the mechanisms of action of different classes of antidepressant medications. How do they affect neurotransmission in the brain?

Answer 48

A Wide Variety of Treatments Are Available for Depression Problems with idea that reduced serotonin stimulation causes depression: ▪ Long lag-time (often weeks) between treatment and reduction of symptoms ▪Not everyone responds to SSRIs ▪Some SSRI benefits are attributable to placebo effect ▪ Increased risk of suicide in children and adolescents using SSRIs

Question 49

46. What are the potential benefits and limitations of cognitive-behavioral therapy (CBT) in treating depression?

Answer 49

Cognitive behavioral therapy (CBT) can be as effective as SSRIs, and when used together are more effective than either alone. Other treatments being researched: ▪Ketamine and leptin ▪ Psychedelic drugs: psilocybin and LSD ▪ Vagal nerve stimulation ▪Deep brain stimulation (DBS)—through a surgically implanted electrode

Question 50

47. How does depression affect sleep patterns? Describe the specific changes in sleep stages observed in individuals with depression.

Answer 50

Sleep is altered by depression: ▪Stage 3 of slow-wave sleep is reduced ▪Patients enter REM sleep very quickly, with an increase of REM sleep in the first half of the night

Question 51

48. What are the challenges in developing animal models of depression? Briefly describe two approaches used to study depression-like behaviors in animals.

Answer 51

Some signs of depression are observable behaviors: ▪ In learned helplessness, an animal is exposed to a repetitive stressful stimulus that it cannot escape. ▪ Linked to a decrease in serotonin function ▪After removal of olfactory bulbs, rodents show irritability, alcohol preference, and elevated stress hormones

Question 52

49. What are the key characteristics of bipolar disorder? How does it differ from major depressive disorder?

Answer 52

Bipolar disorder is characterized by periods of depression alternating with periods of expansive mood (mania). The rate of alternation between moods varies. ▪ Rapid-cycling consists of four or more cycles per year (though some have as many as several per day). Men and women are equally affected, and the disorder is heritable.

Question 53

50. Explain the role of the HPA axis in anxiety. How does chronic stress affect the HPA axis and contribute to anxiety disorders?

Answer 53

Anxiety is a normal reaction to stress. Mild levels of anxiety can be beneficial. ▪ alert us to dangers and help us prepare to pay attention. Anxiety refers to anticipation of a future concern. Fear is an emotional response to an immediate threat and is associated with a fight or flight reaction HPA Axis represents the interaction between the hypothalamus, pituitary gland, and adrenal glands and plays an important role in the body's response to stress, and the pathway results in the production of cortisol.