Biopsychology Study Guide Final Exam PDF

Study Guide Final Exam 1.​ How do psychoactive drugs exert their influence on mental functioning? a.​ Exert their influence through their actions on the nervous system, particularly the brain and spinal cord. 2.​ What are the four main categories of psychoactive drugs based on their eff...

Study Guide Final Exam 1.​ How do psychoactive drugs exert their influence on mental functioning? a.​ Exert their influence through their actions on the nervous system, particularly the brain and spinal cord. 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. a.​ 1. Depressants – slow down the function of the central nervous system i.​ Alcohol, Xanax, Cannabis, Ketamine, Opioids b.​ 2. Hallucinogens – affect your senses and change the way you see, hear, taste, smell or feel things i.​ Cannabis, Ketamine, LSD, Psilocybin, PCP c.​ 3.Stimulants – speed up the function of the central nervous system. i.​ Amphetamines, Caffeine, Cocaine, MDMA, Nicotine d.​ 4. Cannabis - Has both stimulant, depressant, and hallucinogenic properties e.​ Some drugs affect the body in many ways and can fall into more than one category 3.​ Why is the age group of 18-25 particularly vulnerable to illicit drug use? Explain from both societal and biological perspectives. a.​ Societal explanation: i.​ Not easy/feasible to use drugs out in the “real world” AND Peer influence b.​ Biological explanation: i.​ Our brain is wired to experience the positive effects more and the negative effects less. 4.​ How does the concept of conditioned place preference help researchers study the rewarding effects of drugs in animals? a.​ Two Distinct Environments: The animal is placed in an apparatus with two or more chambers that have different visual, tactile, or olfactory cues. i.​ Conditioning Phase → 1.​ Day 1, 3, 5, 7: Rat receives a dose of cocaine and is placed in Chamber A for 30 minutes. 2.​ Day 2, 4, 6, 8: Rat receives saline (no drug) and is placed in Chamber B. 1  ii.​ Test Phase (Drug-Free): → The animal is allowed to move freely between the chambers without receiving any drug. iii.​ If the animal spends more time in the drug-paired chamber, it indicates that the drug has rewarding properties, because the animal has developed a preference for the environment associated with the drug's effects. iv.​ ***CPP allows researchers to study the motivational and reinforcing effects of drugs without requiring animals to perform a task (unlike self-administration models).**** 5.​ Differentiate between pharmacokinetics and pharmacodynamics. How do these concepts contribute to our understanding of drug effects? a.​ Pharmacokinetics (DRUG ACTION) i.​ Study how a drug moves through the body, including process of absorption, metabolism, distribution to tissues, and elimination. b.​ Pharmacodynamics (drug effect) i.​ Study of the ways in which a drug affects the living organism and the organs of the body 6.​ Explain how the route of drug administration influences its absorption and, consequently, its psychoactive effects. a.​ Faster delivery of absorption into the bloodstream is associated with a greater euphoric effect. i.​ Oral Ingestion→ dissolves in fluids of mouth/esophagus/ stomach and is carried to the intestines, where it is absorbed into the bloodstream. ii.​ Peripheral Injection→ 1.​ Intramuscular (IM) injection—drug into a muscle, usually shoulder, upper arm, thigh, or buttocks. 2.​ Intraperitoneal (IP) injection—drug through the abdominal wall into the peritoneal cavity (space surrounding major organs). 3.​ Intravenous (IV) injection—Injection of a drug into a vein. 4.​ Subcutaneous (SC) injection—Injection of a drug under the skin. iii.​ Central Injection 1.​ Intracerebral injection—Injection of a drug directly into the brain. 2.​ Intraventricular injection—Injection of a drug into the cerebral ventricles. iv.​ Inhalation–The administration of a drug through the lungs. v.​ Absorption—absorption through the skin or mucous membranes 2 7.​ Why is the blood-brain barrier crucial in determining whether a drug will produce psychoactive effects? a.​ Factors that affect distribution of drug→ Lipid solubility of the drug i.​ More lipid soluble, the better able to cross cell membrane ii.​ If too large it cannot pass and it will not produce a psychoactive effect. 8.​ What is a drug's half-life, and why is it an important consideration in understanding the duration of drug effects? a.​ Enzymes breakdown drug and their metabolites are not normally going to produce psychoactive effects (similar to when a neurotransmitter is broken down). b.​ The more quickly the drug is metabolized, the more quickly the drug effects will disappear. c.​ Half-life: the amount of time required for the body to metabolize half the amount of the drug. i.​ The longer the half-life the longer a drug continues to have a physiological effect 1.​ Cocaine : 0.5-1.5 hrs 2.​ Amphetamine: 7-10 hours 9.​ Describe the mechanisms of action of agonists and antagonists in relation to neurotransmitter receptors. a.​ When an exogenous ligand such as a drug binds, it may activate the receptor, acting as an agonist b.​ Other ligands bind and block the receptor but do not activate it—antagonists (or receptor blockers) prevent the normal transmitter from binding c.​ Agonist—A drug that mimics a neurotransmitter or enhances synaptic neurotransmission. d.​ Antagonist— A drug that blocks a neurotransmitter or inhibits synaptic neurotransmission 10.​How can drugs influence both presynaptic and postsynaptic processes to modulate synaptic transmission? a.​ Presynaptic Effects: b.​ Synthesis→ Some drugs increase or decrease the production of neurotransmitters. i.​ Example: L-DOPA boosts dopamine synthesis in Parkinson’s treatment. c.​ Release→ Drugs may promote or inhibit neurotransmitter release into the synaptic cleft. i.​ BY blocking sodium channels (Na+) or release by blocking calcium (CA++) 3  d.​ Reuptake Inhibition→ Blocking reuptake increases neurotransmitter levels in the synaptic cleft. e.​ Postsynaptic Effects: f.​ Effects on transmitter receptors: i.​ Selective receptor antagonists block postsynaptic receptors from being activated by their neurotransmitter ii.​ Selective receptor agonists bind to receptors and activate them, mimicking the natural neurotransmitter g.​ Drugs can also alter intracellular postsynaptic processes, such as number ofreceptors and second-messenger systems Drug A and B have the same efficacy: response. ✅ True — Both reach the same maximum Drug A and C have the same efficacy: ❌ False — Drug C has a lower maximum response. Drug A has the highest affinity: ✅ True — It reaches 50% response at the lowest dose. Drug B has the highest affinity: ❌ False — It requires a higher dose than A. Drug C has the highest affinity: ❌ False — It requires the highest dose. 11.​Explain the three mechanisms of tolerance and the risks associated with high drug tolerance. a.​ Tolerance→ A decrease in response (effect) to a given dose of a drug after repeated treatment i.​ Need more of drug next time (leads to addiction/overdose bcs of high dosage) ii.​ DRUGS associated with TOLERANCE 1.​ Opioids: morphine, oxycodone, and heroin (body’s receptors become less responsive, leading to a need for higher doses to manage pain or achieve euphoria 4  2.​ Benzodiazepines: diazepam (Valium) and alprazolam (Xanax) are used to treat anxiety and insomnia. 3.​ Alcohol: Regular alcohol consumption results in tolerance, requiring higher quantities to achieve the same level of intoxication. 4.​ Stimulants: Drugs like amphetamines (used for ADHD) and cocaine lead to tolerance. Over time, their effects on alertness, energy, and euphoria diminish, increasing the risk of abuse and dependency. 5.​ Nicotine: Frequent use of nicotine, commonly through cigarettes or vaping, builds tolerance, requiring more frequent or higher doses to satisfy cravings. Nicotine tolerance contributes significantly to the difficulty of quitting smoking. b.​ Sensitization→ An increase in response to a given dose of drug after repeated administration i.​ Need less of drug neext time c.​ Mechanisms of Tolerance d.​ Metabolic→ Less drug is getting to the site of action due to an increase in the enzymes that break down the drug i.​ Example: alcohol dehydrogenase(Enzyme in the body that breaks down alcohol ) ↑ after repeated alcohol resulting in ↓ alcohol getting to the brain. e.​ Pharmacodynamic (mechanism) → Changes in structure or function at the site of action to compensate for drug i.​ Our body is constantly adapting to maintain equilibrium 1.​ Neurons down-regulate in response to agonist drug—fewer receptors available 2.​ They up-regulate in response to an antagonist f.​ Behavioral→ Adaptation to drug effects through learned behaviors and environmental cues, influenced by frequent use and specific contexts i.​ Tolerance that is influenced by learned Bx rather than just physiological changes. 12.​Why is defining drug addiction a complex challenge? Discuss the limitations of early views that focused on moral failings or physical dependence. a.​ Defining drug addiction is a complex challenge because it involves biological, psychological, social, and cultural factors—not just observable behaviors or symptoms. i.​ DSM IV used to distinguish between dependence and abuse. ii.​ In DSM V, the manual no longer distinguishes between these two. (Must have at least 2 symptoms 5  1.​ Criteria 1-9 focus on drug addiction Criteria 10/11 focus on tolerance and withdrawal b.​ Early views c.​ Drug dependence is a moral problem. i.​ Assume consumption is under voluntary control (individuals can stop if they “want” to. d.​ Physical dependence Once dependent due to repeated use, attempts at abstinence lead to highly unpleasant withdrawal symptoms. MEANT TO AVOID withdrawal symptoms i.​ Relief from withdrawal symptoms promotes drug-seeking behavior through a process of negative reinforcement, → continuous behavioral loop consisting of repeated abstinence attempts followed by relapses ii.​ CRITIQUES: cocaine doesn’t produce strong physical dependence 13.​How does the positive reinforcement model explain drug addiction? What are its strengths and limitations? a.​ Drug serves as a positive reinforcer. We use and abuse drugs because we “like” the experience. i.​ drug produces euphoric effect that drives the person to seek out the drug. ii.​ Relapse occurs because individuals want to “re-experience” the euphoric effects. b.​ Accounts for why people continue to take drugs when there are no withdrawal symptoms (e.g., cocaine). c.​ Criticisms of the Positive reinforcement model: i.​ Not all drugs that produce dependence produce euphoric effects (e.g., nicotine, alcohol). ii.​ A lot of individuals do not feel the euphoric effects anymore, but still feel compelled to take the drug. 14.​Explain the incentive-sensitization theory of addiction. How does it address some of the limitations of the positive reinforcement model? a.​ Drugs produce not only negative and positive reinforcing effects, but also incentive motivational effects. b.​ Distinguishes between drug liking (that is, the high) and drug wanting (that is, craving). c.​ When developing an addiction, there is a marked increase in wanting the drug even though there is no change or even a decrease in drug liking (because of tolerance for example) 6 15.​Describe the contemporary biopsychological view of addiction. How does it differ from earlier perspectives? a.​ Current view of “addiction” in biopsychology is that addiction is the result of long-term neuroadapations in the brain that are caused by chronic drug use. b.​ The brain changes as a result of repeated drug use. c.​ The disease model—“Addiction is a disease like heart disease” says the abuser requires medical treatment; however, an abnormal condition in abusers has not been identified d.​ Perhaps addiction is a result of damage to the No go system: Go (subcortical) vs. No Go (prefrontal cortex) – Hypofrontality e.​ Drug addiction is a chronic and relapsing disorder f.​ 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. g.​ Relapse is driven by a strong urge or craving for the drug that can be elicited by cues, the drug, or stress. 16.​Why is relapse a significant challenge in addiction treatment? Explain the role of craving and environmental cues in relapse. a.​ Relapse is a significant challenge in addiction treatment because addiction is a chronic, relapsing brain disorder—not simply a matter of willpower. Even after detox or initial treatment, many individuals return to drug use due to long-lasting changes in brain function and behavior. b.​ Persistent Brain Changes: i.​ Addiction alters brain regions related to reward, impulse control, and stress regulation (e.g., prefrontal cortex, amygdala, nucleus accumbens) → can last long after drug use c.​ Craving: i.​ powerful, overwhelming urge to use the drug can be triggered by internal states (stress, emotions, mood) or external cues. ii.​ Craving activates the same brain circuits that were engaged during drug use, reinforcing the behavior. d.​ Environmental Cues (Conditioned Triggers): i.​ Through classical conditioning, the brain links person/place/thing with drug’s effects. ii.​ Even after long periods of abstinence, exposure to cues can trigger intense cravings and relapse. e.​ Example: A former smoker smells cigarette smoke and feels a sudden urge to smoke 7  f.​ Stress and Emotional Dysregulation: i.​ Stress can reactivate drug-seeking behaviors by altering brain chemistry and weakening impulse control. g.​ Why This Makes Relapse Difficult to Prevent: i.​ Relapse is not failure, but a sign that treatment must be ongoing and adaptable. ii.​ Many traditional treatments don’t address psychological triggers or provide long-term coping strategies. iii.​ Cravings and cues can appear unexpectedly, even after years of sobriety. 17.​Describe two commonly used animal models of addiction and explain what they measure. a.​ Self-Administration→ Like humans, rodents self-administer drugs i.​ Animals (usually rats or monkeys) are trained to perform an action (e.g., press a lever) to receive a drug, often via intravenous infusion. b.​ Conditioned Place Preference→ Prefer environments associated with drug i.​ animals are repeatedly exposed to a drug in one distinct environment (chamber) and a placebo in another. Later, they are allowed to choose between the two chambers. c.​ Locomotor Sensitization→ Show sensitized responses to drugs 18.​What is the mesolimbic dopamine system, and why is it considered the "reward pathway" in the brain? a.​ DEF: The mesolimbic dopamine system is a major brain pathway responsible for reward, motivation, and pleasure (inputs from the ventral tegmental area) b.​ Why It's Called the “Reward Pathway”: i.​ Dopamine Release: When a person experiences something rewarding, dopamine is released from the VTA into the nucleus accumbens. This surge is associated with pleasure, learning, and motivation to repeat the behavior. ii.​ Drugs of Abuse: Many addictive substances (e.g., cocaine, opioids, nicotine) hijack this pathway by artificially boosting dopamine levels—much more than natural rewards—leading to reinforcement of drug-seeking behavior. iii.​ Learning and Conditioning: The system also helps the brain learn which behaviors and cues are associated with rewards, increasing the likelihood of repeating them. 8 19.​Explain the effects of alcohol on the central nervous system (CNS) in terms of its interaction with GABA, glutamate, and dopamine. a.​ 1. GABA (Gamma-Aminobutyric Acid) – Inhibitory Neurotransmitter i.​ Alcohol enhances GABA (Inhibitory) receptors by enhancing GABA function (similar to Xanax and Valium – anxiolytics (alleviate anxiety) ii.​ decreases glutamatergic transmission by inhibiting the NMDA receptor and decreasing levels of glutamate (main excitatory NT) elevates levels of dopamine by enhancing activity of the mesolimbic pathway iii.​ Withdrawal from Alcohol (opposite effects on CNS): 1.​ Decreased GABA function 2.​ Increased Glutamate function 3.​ Decreased dopamine function 20.​What are the long-term consequences of chronic alcohol abuse on the brain and liver? a.​ Withdrawal symptoms are sometimes very severe. i.​ 5-6 hrs post-drinking: tremors, headache, nausea, vomiting, and abdominal cramps. ii.​ 15-30 hrs: convulsive activity iii.​ 24-48 hrs: delirium tremens – may last 3-4 days, Disturbing hallucinations/delusions iv.​ Tachycardia (rapid heart beat) b.​ Long-Term Effects on the Brain: i.​ Brain damage can also accur bcs of low thiamine (VitaminB1). ii.​ Leads to Korsakoff’s syndrome (memory loss, sensory and motor dysfunction, and eventually dementia) 1.​ Risk of Wernicke-Korsakoff syndrome (caused by thiamine deficiency): 2.​ Wernicke’s encephalopathy: Confusion, eye movement problems, loss of coordination. 3.​ Korsakoff’s psychosis: Severe memory loss and inability to form new memories. iii.​ Mood and Mental Health Disorders→ Increased risk of depression, anxiety, and alcohol-induced psychosis. 1.​ Impaired emotional regulation and social functioning. iv.​ Addiction and Brain Plasticity Changes→ Long-term disruption of dopamine signaling in the reward system. 9  1.​ Altered brain circuits that reinforce compulsive drinking and reduce impulse control. c.​ Long-Term Effects on the Liver: i.​ Fatty Liver (Steatosis): ii.​ Fibrosis and Cirrhosis:--> Fibrosis: Scar tissue begins to replace healthy liver tissue. 1.​ Cirrhosis: Advanced, irreversible scarring that severely impairs liver function. iii.​ Alcoholic Hepatitis→ Inflammation of the liver with symptoms like jaundice, abdominal pain, and nausea. iv.​ Fetal alcohol syndrome (pregnant women abusing alcohol, with permanent damage to the fetus) v.​ In adults, alcohol abuse affects the frontal lobes, though effects are reversible with abstinence vi.​ Bingeing may cause brain damage and reduces the rate of neurogenesis 21.​How does cocaine exert its stimulant effects on the brain? What are the potential risks associated with heavy cocaine use? a.​ Cocaine is a powerful central nervous system stimulant that primarily affects the dopamine system, but also influences norepinephrine and serotonin. i.​ blocking reuptake of monoamine transmitters so that they accumulate in synapses throughout the brain, boosting their effects b.​ heavy cocaine use→ Stroke, psychosis, loss of gray matter, and severe mood disturbances c.​ Mechanism of Action: i.​ Cocaine blocks the reuptake of dopamine, norepinephrine, and serotonin by binding to their transporters leads to increased levels of these NT’s in the synaptic clef d.​ Potential Risks Associated with Heavy Cocaine Use: i.​ 1. Cardiovascular Risks→ Increased heart rate, blood pressure, and vasoconstriction (narrowing of blood vessels) ii.​ 2. Neurological and Psychological Effects→ Anxiety, paranoia, hallucinations, and agitation 1.​ Cocaine-induced psychosis (especially with chronic or binge use) 2.​ Long-term changes in brain function, including dopamine system depletion—leading to anhedonia (inability to feel pleasure 10  iii.​ 3. Addiction and Dependence: Cocaine is highly addictive due to its intense, short-lived high and strong reinforcement of drug-taking behavior 1.​ Difficult withdrawal symptoms: fatigue, depression, irritability, and intense drug craving 22.​How does the concept of allostasis relate to the development of addiction? a.​ Allostasis: The ability to achieve stability through change i.​ active changes in the body’s systems to meet chronic demands or stressors ii.​ ****Addiction is not just about chasing pleasure—it becomes about escaping pain caused by the brain’s allostatic changes**** b.​ EXPLAINS HOW the brain and body adapt to repeated drug use, contributing to the development and persistence of addiction i.​ Initial Drug Use – Positive Reinforcement: drug use increases dopamine/pleasure. 1.​ brain adapts by reducing dopamine sensitivity --- beginning of allostatic change. ii.​ Chronic Use – Shift to Negative Reinforcement: 1.​ Over time, the brain's set point for reward and mood lowers. 2.​ The individual needs the drug not just to feel high—but to feel “normal” or avoid withdrawal and emotional pain. 3.​ This shift reflects a new, unhealthy allostatic state: the brain now functions abnormally without the drug. iii.​ Stress and Anti-Reward Systems →Chronic drug use activates the stress systems 1.​ The “anti-reward” system becomes overactive, increasing anxiety, irritability, and dysphoria when not using the drug. 2.​ This further drives compulsive drug seeking as a way to avoid these negative states 23.​Describe the role of impulsivity and compulsivity in the transition from casual drug use to addiction. a.​ IMPULSIVITY: An inability to resist urges and making unreflective decision without regard for consequences b.​ COMPULSIVITY: Repeated behavior in the face of adverse consequences and repetitive behavior that are inappropriate to a particular situation c.​ transition from casual drug use to addiction same as shift from impulsive to compulsive use and driven by a transition from positive to negative reinforcement mechanisms. 11 24.​Explain the three-stage cycle of addiction according to the conceptual model presented in the source. a.​ 🔁 1. Binge/Intoxication Stage i.​ Person uses the drug and experiences its rewarding effects ii.​ Basal ganglia ((nucleus accumbens (reward circuit)) →Dopamine release reinforces the behavior iii.​ Positive reinforcement—the drug is taken to feel good iv.​ BRAIN ASSOCIATED DRUG WITH REWARD/GOOD b.​ 😖 2. Withdrawal/Negative Affect Stage i.​ person experiences unpleasant emotional and physical symptoms when drug wears off ii.​ Negative reinforcement—the drug is taken to avoid or relieve these negative feelings 1.​ Withdrawal comes from 2 sources a.​ Extended amygdala→ Decrease in dopamine, increase in stress hormone b.​ stress systems become overactive, and the person feels worse without the drug. c.​ 🔁 3. Preoccupation/Anticipation (Craving) Stage i.​ preoccupied with obtaining and using the drug again, often triggered ii.​ Prefrontal cortex impaired→ weakening self-control iii.​ Craving and loss of control iv.​ Drug-seeking behavior resumes, even after periods of abstinence this contributes to relapse 25.​How do changes in dopamine release in the nucleus accumbens contribute to the development of tolerance and the experience of withdrawal? a.​ Tolerance i.​ Early drug use triggers a large surge of dopamine in the nucleus accumbens, producing intense pleasure or euphoria. ii.​ amount of dopamine released after drug decreases→ need more of drug next time b.​ Withdrawal i.​ When drug use stops, the reduced baseline dopamine activity in the nucleus accumbens leads to:Negative mood states, lack of pleasure, no motivation 12  ii.​ This "crash" in dopamine function contributes to the emotional and physical discomfort of withdrawal, especially in the withdrawal/negative affect stage of the addiction cycle. iii.​ The person may resume drug use to relieve these symptoms, reinforcing the addiction through negative reinforcement. 26.​Explain the role of the extended amygdala in the withdrawal/negative affect stage of addiction. a.​ Extended amygdala→ Decrease in dopamine, increase in stress hormone b.​ This imbalance—low reward, high stress—creates a powerful drive to use the drug again to relieve the discomfort. c.​ The person learns to use the drug not for pleasure, but to escape negative emotions caused by withdrawal. d.​ This shift from positive reinforcement (using to feel good) to negative reinforcement (using to feel less bad) is a hallmark of addiction’s progression 27.​Describe the concept of "incentive salience" and its relevance to the preoccupation/anticipation stage of addiction. a.​ Incentive salience is the process by which certain stimuli—especially those associated with drug use—become powerfully “wanted” or craved, even if they are no longer genuinely pleasurable. b.​ Prefrontal cortex (executive region)- "Go system" "Stop system" i.​ "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. c.​ Relevance to preoccupation/anticipation stage i.​ The prefrontal cortex, responsible for decision-making and impulse control, is impaired. ii.​ Cravings, triggered by cues that have acquired incentive salience, drive compulsive drug-seeking behavior 28.​28. Identify and explain three factors that increase vulnerability to relapse in addiction a.​ 1. Drug Re-exposure: Dopamine release and dopamine receptor downregulation​ Even a single small dose of the previously used drug can trigger full-blown relapse. i.​ AKA Drug-induced Reinstatement/Relapse b.​ 2. Stress: Corticotropin-Releasing Factor release and dopamine receptor downregulation) i.​ AKA Stress-induced Reinstatement/Relapse c.​ 3. Exposure to drug cues (glutamate release) AKA Cue-induced Reinstatement 13 29.​How does the concept of craving differ from simply "wanting" something? Explain the physiological basis of craving. a.​ Increased stress →increased pleasure threshold →increased need for dopamine→midbrain thinks it is dying→CRAVING b.​ CRAVING is a physiological response to a neurochemical deficiency resulting in symptoms including sweating, stomach cramps, obsession, increased respirations, etc. c.​ The midbrain hijacks the abilities of the frontal cortex… i.​ The brain will utilize the most likely reasoning to get the addict to feel like they have to use ii.​ Pain (won’t cause death) iii.​ Anxiety (won’t cause death) iv.​ Stress (won’t cause death) v.​ Specific people or events/reservations (ALWAYS a choice) 30.​Outline the hierarchy of treatment for addiction. Why is addressing medical issues and detox a priority? a.​ 1. Treat most acute medical issues first & DETOX i.​ Medical issues like infections, organ damage, or malnutrition must be addressed before any psychological or behavioral treatment can be effective. ii.​ The brain and body must be stabilized as Ignoring medical problems can lead to life-threatening complications b.​ 2. Quiet the midbrain with medication/abstinence i.​ Medications for Opioid Use Disorder 1.​ Buprenorphine: partial agonist at the mu-opioid receptor 2.​ Methadone: mu-opioid receptor agonist 3.​ Naltrexone: opioid receptor antagonist (primarily mu-opioid receptor) ii.​ Medications for Alcohol Use Disorder 1.​ Acamprosate: NMDA receptor modulator 2.​ Disulfiram: irreversively inhibits alcohol dehydrogenase, Naltrexone iii.​ Medications for Tobacco Use Disorder 1.​ Nicotine replacement therapy, Bupropion: inhibits dopamine and norepinephrine reuptake transporters 14  c.​ 3. Restore Cortex i.​ Give the person tools to proactively manage stress and decrease craving ii.​ Coping skills Stress Relief Social Supports Safe Environments 31.​How do animal models of addiction, such as self-administration and reinstatement paradigms, contribute to our understanding of relapse? a.​ Self-administration paradigm (Models voluntary drug use) →Animals trained to press a lever/perform task to receive drug (cocaine, heroin, alcohol) i.​ Relevance to relapse: After animals learn the behavior, the drug is removed (extinction), and researchers can then test what triggers relapse b.​ Reinstatement Paradigm→researchers test what causes drug-seeking to return or reinstatement after drug is taken away i.​ Three common triggers are tested: 1.​ Drug-induced reinstatement (giving a small dose of the drug) 2.​ Cue-induced reinstatement (light, sound, or smell associated with the drug prior) 3.​ Stress-induced reinstatement ( foot shock or loud noise) ii.​ Relevance to relapse: Shows that different relapse triggers activate distinct neural pathways (ex: glutamate for cues, corticotropin-releasing factor (CRF) for stress). c.​ Both mirror real-life patterns of human relapse i.​ Craving triggered by cues→ Relapse after stress → Relapse after “just one hit” 32.​What are the key components of emotion, and how do they interact to shape our emotional experiences? Emotion involves a complex interplay of: a.​ 1. Physiological Arousal→ bodily changes triggered by the autonomic nervous system b.​ 2. Cognitive Appraisal→ Involves how we interpret or evaluate a situation. c.​ 3. Subjective experience → how it feels internally (e.g., joy, anger, fear). d.​ 4. Expressive behavior→ outward signs of emotion (facial expressions, body language, tone) e.​ 5. BX response→ Emotions motivate us to act (escaping danger when afraid, seeking comfort when sad) 15 33.​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? a.​ James-Lange Theory→ We feel emotion because we experience physiological changes i.​ Emotion is felt after interpreting these body changes (e.g., “I feel afraid because my heart is pounding”). ii.​ EX: “I’m sad because I’m crying,” not “I cry because I’m sad.” b.​ Cannon-Bard Theory→ We feel emotion and experience physiological changes at the same time, but independently i.​ The brain generates emotion, not the body alone ii.​ EX: Seeing a bear causes both fear and a pounding heart at once, but neither causes the other. Key Differences: Feature ​ ​ James-Lange​ Cannon-Bard Sequence​ Arousal → Emotion Arousal + Emotion occur simultaneously Role of Body​ Body drives emotion Brain initiates both emotion and arousal Timing ​ Emotion is after bodily changes Emotion and arousal happen together Example​ "i know I’m afraid because I tremble." "I tremble and feel afraid at the same time." 34.​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? a.​ *****Schachter’s theory: Emotion = Arousal + Interpretation***** i.​ Physiological arousal →increased heart rate ii.​ interpreting the arousal based on the situation or context b.​ STEPS: Stimulus (e.g., loud noise) i.​ → Physiological arousal (e.g., heart races) 1.​ →Cognitive appraisal (e.g., “This is dangerous!”) a.​ = Emotion (e.g., fear) 35.​What is the basis for using polygraph tests to detect lying? What are the limitations and controversies surrounding their use? a.​ polygraph test measures activation of the SYMPATHETIC NS,reflecting stress, NOT LYING 16  i.​ Based on the assumption that people have an emotional response when lying because they fear detection and/or feel guilty 1.​ emotions are usually accompanied by bodily responses 36.​Discuss the evidence supporting the universality of emotional expressions. Are there cultural differences in how emotions are expressed and recognized? a.​ Darwin→ expressions of emotions are universal &nonhuman primates have the same facial muscles as humans b.​ Redican→ primate expressions including a play face, homologous to the human laugh i.​ Mice make facial expressions related to emotions. c.​ Emotions act as motivational programs that evolved to coordinate responses problems i.​ Ex: Responding to dangerous situations with a fear program—improved survival d.​ Plutchik suggests eight basic emotions, in four pairs of opposites: i.​ ▪ Joy/sadness ▪ Affection/disgust ▪ Anger/fear ▪ Expectation/surprise e.​ Paul Ekman→ basic emotions with universally recognized facial expressions: i.​ Happiness ⇼ Sadness ⇼Fear ⇼Anger ⇼Contempt ⇼Disgust ⇼Embarrassment f.​ Other researchers include affection and expectation in the core group of facial expressions that are interpreted similarly across many cultures. g.​ 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. h.​ Subtle cultural differences suggest that cultural conditioning enforces prescribed rules for facial expression. 37.​Describe the role of facial muscles, cranial nerves, and CNS pathways in mediating facial expressions. a.​ Two categories of facial muscles: i.​ ▪ Superficial facial muscles—the facial nerve (VII) 1.​ attach between points of facial skin for expressions ii.​ ▪ Deep facial muscles—trigeminal nerve (V) (motor branch) 1.​ attach to bone; larger movements, like chewing b.​ STRUCTURE ROLE 17  FACIAL NERVES VISIBLE face EXPRESSION CRANIAL NERVE VII SEND MOTOR SIGNALS to muscles CNS (MOTOR CORTEX) CONTROL VOLUNTARY FACIAL EXPRESSIONS. CNS (LIMBIC SYSTEM) GENERATES INVOLUNTARY EMOTIONAL EXPRESSION EX: suprise 38.​Explain the facial feedback hypothesis and its implications for the James-Lange theory of emotion. a.​ facial feedback hypothesis suggests that sensory feedback from our facial expressions can affect our mood. i.​ muscle activity in the face sends signals to the brain, which helps the brain interpret or even generate emotional states ii.​ Lends support to the James–Lange theory (I’m sad because I’m crying) b.​ STUDY→ Participants who were forced to smile by holding a pen in their teeth rated cartoons as funnier Vs those w/o pencil c.​ Botox studies: People with Botox (which limits facial muscle movement) often report reduced emotional intensity, especially with negative emotions. d.​ BUUUTTT when a stressful situation forces someone to display false emotional expressions, it can be detrimental to their well-being and happiness at work. 39.​How does electrical brain stimulation provide insights into the neural circuits involved in emotion? a.​ Brain self-stimulation—animals (including humans) will work to receive electrical stimulation to their brain. b.​ Brain sites that support self-stimulation have been mapped. Most are subcortical, concentrated in the medial forebrain bundle → rises from the midbrain through the hypothalamus; affected at many self-stimulation sites c.​ Nucleus accumbens—important target for axons of medial forebrain bundle major component of the reward circuit; release of dopamine here produces very pleasurable feelings d.​ 1. Identification of "Pleasure Centers" i.​ Stimulation of the medial forebrain bundle (especially the nucleus accumbens and ventral tegmental area or VTA) produces intense feelings of pleasure in animals and humans. 18  ii.​ Animals will press a lever repeatedly to self-stimulate these areas—this is known as intracranial self-stimulation (ICSS).--> This supports the idea that the mesolimbic dopamine system is central to reward and positive emotion. e.​ 2. Mapping Fear etc→ Stimulation of amygdala evoke fear, anxiety, or defensive behaviors. f.​ 3. Role of the Hypothalamus→ trigger aggression, rage, sexual arousal, depending on site suggests the hypothalamus helps coordinate autonomic and emotional responses. g.​ 4. Human Reports During Surgery i.​ Patients undergoing awake brain surgery (e.g., for epilepsy) sometimes report emotional experiences (e.g., sudden joy, fear, or déjà vu) when specific brain areas are stimulated—especially the temporal lobe and limbic regions. 40.​Describe the role of the amygdala in fear learning and the processing of fear-provoking stimuli. a.​ fear conditioning: a neutral stimulus (a tone) becomes associated with an aversive event (shock), eventually triggering a fear response on its own i.​ Lateral nucleus (LA): Receives sensory input (tone, shock) and forms the association between the neutral and aversive stimuli. ii.​ Central nucleus (CeA): Outputs signals to the hypothalamus and brainstem to initiate fear responses (e.g., freezing, increased heart rate). iii.​ This circuit enables the brain to learn quickly which cues signal danger and respond rapidly in the future. b.​ 🧠 Pathways: i.​ "Low Road" (fast, crude): Thalamus → Amygdala (quick reaction before detailed processing) ii.​ "High Road" (slower, refined): Thalamus → Sensory cortex → Amygdala (conscious evaluation) c.​ SUMMARY→ i.​ amygdala activates the autonomic nervous system via hypothalamus, → to physical symptoms of fear (sweating, rapid heartbeat). 1.​ interacts with hippocampus (context) and prefrontal cortex (regulation). 19 41.​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? a.​ Feeling love can bilaterally increase activity in the insula and anterior cingulate cortex and decrease activity in the posterior cingulate and prefrontal cortices. b.​ brain activation during sadness, happiness, anger, and fear showed activation of the insula, cingulate cortex, and prefrontal cortex. i.​ Fear → activates the amygdala ⇼ Disgust → associated with the insula ⇼Sadness → often linked with the subgenual anterior cingulate cortex (ACC) ⇼Happiness and reward → involve the ventral striatum and nucleus accumbens ⇼ Anger → may engage the orbitofrontal cortex (OFC) and anterior cingulate cortex 2. c.​ People with amygdala damage (patient S.M.) show impaired recognition and experience of fear i.​ Damage to the insula impairs recognition of disgust (Huntington’s disease) ii.​ Prefrontal cortex lesions may affect emotion regulation, moral judgment, or aggression d.​ Electrical Brain Stimulation→ Stimulating different regions can evoke distinct emotional experiences (e.g., fear via the amygdala, pleasure via the nucleus accumbens). e.​ ❌ Why There's No One-to-One Mapping i.​ Emotions are complex and involve multiple components: physiological arousal, subjective feeling, cognitive appraisal, and behavior. ii.​ The same region (amygdala) may be active in multiple emotions, depending on context. iii.​ Emotions are constructed by dynamic patterns of brain activity rather than fixed "emotion centers." 1.​ Example: The amygdala is most known for fear, but it also responds to positive stimuli, novelty, and salience 42.​What are the core characteristics of major depressive disorder (MDD)? How do these symptoms affect an individual's daily functioning? a.​ Unhappy mood ▪ Loss of interests, reduced energy ▪ Changes in appetite and sleep patterns b.​ ▪ Difficulty in concentration ▪ Restless agitation or torpor ▪ Pessimism and thoughts of death c.​ Depression may last for several months. Inheritance is a determinant in depression. d.​ An individual with MDD might: ▪ Struggle to get out of bed in the morning ▪ Stop attending classes or work ▪ Avoid friends and family 20 43.​Discuss the biological factors that may contribute to the development of depression, including brain chemistry, hormones, and genetics. a.​ Biological Differences ▪ People with depression may have physical differences in their brain i.​ Reduced volume in the hippocampus (memory, emotion regulation) ii.​ Overactivity in the amygdala (fear and emotional processing) iii.​ ​Dysfunction in the prefrontal cortex (decision-making, inhibition) b.​ Brain Chemistry ▪ Changes in the production, function, and effects of certain neurotransmitters (brain chemicals). Serotonin (5-HT): Regulates Norepinephrine (NE): Involved in Dopamine (DA): Central to motivation mood/sleep/appetite/pain. Low energy/attention/stress response. and reward. Reduced dopamine activity levels are commonly associated Dysregulation can lead to fatigue may contribute to anhedonia (loss of with depression. and cognitive dysfunction. pleasure). c.​ Hormones ▪ Changes in the body’s balance of hormones i.​ Hypothalamic-pituitary-adrenal (HPA) axis dysregulation is common in depressed individuals. ii.​ Chronic stress → ↑ Cortisol (a stress hormone) → impacts brain areas like the hippocampus and amygdala. d.​ Genetics ▪ Depression is more common in people whose blood relatives also have this condition 44.​Describe the brain changes associated with depression, including alterations in brain activity, blood flow, and structure. a.​ Increased activation in: i.​ Frontal lobes, during cognitive tasks ii.​ Amygdala, during emotional processin b.​ Decreased blood flow to areas implicated in attention c.​ Dysfunction of the lateral habenula by the pineal gland, possibly making it an "antireward center" of lost pleasure. d.​ Cortex of the right hemisphere is thinner Brain Region Observed Change Implication Prefrontal Cortex ↓ Activity, ↓ Volume Poor regulation of mood and decision-making Amygdala ↑ Activity Increased emotional reactivity, negativity bias Hippocampus ↓ Volume Impaired memory, stress sensitivity Anterior Cingulate Altered activity (↑ or ↓) Mood dysregulation, cognitive-emotional Cortex conflict Blood Flow ↑ in limbic areas, ↓ in frontal areas Emotional overdrive, reduced cognitive control 21 45.​Explain the monoamine hypothesis of depression. What evidence supports this hypothesis, and what are its limitations? a.​ The hypothesis suggests that: i.​ ↓ serotonin → sadness, anxiety, and irritability. ii.​ ↓ norepinephrine →low energy, fatigue, and poor concentration. iii.​ ↓ dopamine → anhedonia (loss of pleasure) and lack of motivation. b.​ Inhibitors of monoamine oxidase (MAO) ​ WHICH inactivate monoamines i.​ Ex: norepinephrine, dopamine, and serotonin→ The first antidepressant drugs c.​ MAO inhibitors raise the level of monoamines at the synapse→ Efficacy led to monoamine hypothesis of depression d.​ Evidence Supporting the Hypothesis i.​ Tricyclics—blocking the reuptake of Norepinephrine (NE) and serotonin (5-HT) ii.​ Selective serotonin reuptake inhibitors (SSRIs)—block the reuptake of serotonin in the brain and increase monoamine levels e.​ LIMITATIONS→ f.​ Antidepressants increase monoamines within hours, but clinical relief often takes weeks, suggesting other mechanisms are involved (e.g., neuroplasticity). g.​ ▪ Not everyone responds to SSRIs ▪ Some SSRI benefits are attributable to placebo effect h.​ ▪ Increased risk of suicide in children and adolescents using SSRIs 46.​Describe the mechanisms of action of different classes of antidepressant medications. How do they affect neurotransmission in the brain? a.​ Antidepressants not given to children as depression goes long with low energy→ if given drug then client will have the energy to attempt suicide. Moral dilema→ need the drug to feel better but might kill themselves if given the drug b.​ Selective Serotonin Reuptake Inhibitors (SSRIs)→ SSRIs block the reuptake of serotonin into the presynaptic neuron, increasing serotonin levels in the synaptic cleft. c.​ Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs) → Block the reuptake of both serotonin and norepinephrine, increasing their availability. (Improve mood, energy, and focus) d.​ Tricyclic (TCAs)→ Inhibit the reuptake of norepinephrine and serotonin (Boost monoamine levels) 22  e.​ Monoamine Oxidase Inhibitors (MAOIs) → Inhibit the enzyme monoamine oxidase, which breaks down serotonin, norepinephrine, and dopamine. (Increases thet hree levels) 47.​What are the potential benefits and limitations of cognitive-behavioral therapy (CBT) in treating depression? a.​ Potential Benefits: i.​ Cognitive behavioral therapy (CBT) can be as effective as SSRIs, and when used together are more effective than either alone. ii.​ CBT teaches individuals how to recognize and challenge distorted thoughts, develop coping skills, and reduce negative behaviors, fostering lasting improvement. iii.​ CBT does not produce negative physical side effects iv.​ CBT targets thought patterns, patients maintain progress and prevent relapse v.​ CBT can be delivered in individual, group, or online formats, and can be tailored for specific populations (e.g., adolescents, older adults). b.​ Limitations i.​ CBT tasks like journaling require energy. People w/ severe depression may have llow energy, concentration, or motivation ii.​ CBT typically requires weekly sessions and homework, which may not be accessible iii.​ Availability of trained CBT therapists may be limited, insurance coverage issues iv.​ CBT doesn't work for everyone 48.​How does depression affect sleep patterns? Describe the specific changes in sleep stages observed in individuals with depression. a.​ Stage 3 of slow-wave sleep is reduced i.​ REM occurs earlier and dominates early in the night. ii.​ Deep sleep is suppressed, reducing the brain’s recovery time. iii.​ Relieve anxiety of the day during rem sleep b.​ Changes may result from dysregulation in monoamine neurotransmitters (like serotonin) and cortisol (linked to stress), contribute to emotional dysregulation, poor concentration, and worsening mood. 49.​What are the challenges in developing animal models of depression? Briefly describe two approaches used to study depression-like behaviors in animals. a.​ Challenges 23  i.​ Core symptoms like sadness, guilt, and suicidal thoughts can’t be directly assessed in animals. ii.​ hard to ensure animal behaviors accurately reflect human depressive symptoms. iii.​ Many models do not fully represent the biological or psychological causes of human depression. iv.​ A valid model should respond to antidepressants in a way similar to humans—which not all do. b.​ 🧪 Two Approaches to Studying Depression-Like Behaviors in Animals c.​ 1. Forced Swim Test (FST) / Tail Suspension Test (TST) → measures Behavioral despair or helplessness. i.​ Procedure: Animals are placed in an inescapable situation (like a water tank or suspended by the tail). Over time, they stop struggling and become immobile. ii.​ Relevance: Immobility is interpreted as a model of despair; antidepressants reduce immobility, which supports predictive validity. d.​ 2. Chronic Mild Stress (CMS) Model→ measures: Anhedonia (loss of pleasure) i.​ Procedure: Animals exposed to unpredictable stressors (wet bedding, tilted cages) over weeks. They are then tested for reduced interest in rewarding stimuli (like sweetened water) ii.​ Relevance: Decreased sucrose consumption reflects anhedonia; response to antidepressants restores normal behavior, adding construct and predictive validity 50.​What are the key characteristics of bipolar disorder? How does it differ from major depressive disorder? a.​ Bipolar disorder is characterized by periods of depression alternating with periods of expansive mood (mania). b.​ The rate of alternation between moods varies. i.​ ▪ Rapid-cycling consists of four or more cycles per year (though some have as many as several per day). Feature Bipolar Disorder Major Depressive Disorder (MDD) Mood Episodes Both depressive and manic/hypomanic episodes Only depressive episodes 24 Mania/Hypomania Present (defining feature) Absent Mood Swing Pattern Alternating highs and lows Persistent low mood only Onset Typically earlier (late teens to early 20s) Slightly later (20s to 30s) Treatment Mood stabilizers, antipsychotics, and Primarily antidepressants antidepressants cautiously and psychotherapy Risk of Misdiagnosis Often mistaken for unipolar depression during Less frequently depressive phase misdiagnosed c.​ Brain changes are similar to those seen in schizophrenia—enlarged ventricles and reduced gray matter. d.​ The element lithium is an effective treatment that has been reported to increase gray matter in patients’ brains, but its use must be carefully monitored for toxic side effects of overdose. 51.​Explain the role of the HPA axis in anxiety. How does chronic stress affect the HPA axis and contribute to anxiety disorders? a.​ Anxiety refers to future concern.| Fear is an emotional response to an immediate threat i.​ Anxiety disorders cause people to avoid situations that trigger or worsen symptoms. ii.​ to be diagnosed with an anxiety disorder, the fear or anxiety must: 1.​ ▪ Be out of proportion to the situation or be age- inappropriate 2.​ ▪ Hinder their ability to function normally b.​ Generalized Anxiety Disorder ▪ involves persistent and excessive worry that interferes with daily activities. c.​ Panic Disorder ▪ The core symptom of panic disorder is recurrent panic attacks, an overwhelming combination of physical and psychological distress d.​ Obsessive Compulsive Disorder ▪ characterized by unwanted thoughts (obsessions) and repetitive behaviors (compulsions) e.​ Phobias ▪ A phobia is excessive and persistent fear of a specific object, situation or activity that is generally not harmful. f.​ Social Anxiety Disorder ▪ significant anxiety and discomfort about being embarrassed, humiliated, rejected or looked down on in social interactions. g.​ HPA Axis (Hypothalamic–Pituitary–Adrenal 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. 25  h.​ Activation Under Stress: i.​ Hypothalamus releases CRF (corticotropin-releasing factor) ii.​ CRF stimulates the pituitary gland to secrete ACTH (adrenocorticotropic hormone) iii.​ ACTH prompts the adrenal glands to release cortisol (primary stress hormone) i.​ Cortisol’s Effects: i.​ Mobilizes energy (glucose), increases alertness, suppresses non-essential functions (like digestion) ii.​ In normal situations, negative feedback regulates cortisol levels once the threat is gone 1.​ EX: When body temperature rises, the brain sends signals to sweat glands to produce sweat, which cools the body through evaporation. Conversely, if body temperature drops, the brain triggers shivering to generate heat. j.​ In Anxiety: i.​ The HPA axis may become overactive or dysregulated ii.​ Elevated or prolonged cortisol levels enhance fear responses, increase vigilance, and heighten emotional reactivity, particularly via effects on the amygdala and hippocampus Chronic Stress and HPA Axis Dysregulation Chronic Stress Effects How It Contributes to Anxiety Persistent CRF and cortisol secretion Maintains a constant state of hypervigilance and arousal Desensitization of cortisol receptors Impairs negative feedback, worsening stress reactivity Amygdala sensitization Heightens fear and threat detection Hippocampal damage Affects memory, emotion regulation, and feedback control Prefrontal cortex impairment Reduces rational control over fear and stress responses k.​ Link to Anxiety Disorders: i.​ Generalized Anxiety Disorder (GAD), Panic Disorder, and PTSD often show abnormal HPA axis function, such as: ii.​ Elevated baseline cortisol 26  iii.​ Blunted or exaggerated cortisol responses iv.​ Altered CRF activity in cerebrospinal fluid Affinity→ the strength of the attraction or binding between two molecules, typically a ligand and its target 27