How do we scientifically study emotion? Identify emotions as observable behavior Separate actions from internal feelings Operational definitions - valence (cognitive labels), observable behavior & physiology Must have consciousness to have emotion Ex. Absence seizures (brief bouts of epilepsy) Conscious awareness not necessary (ex. implicit memory based on emotion) Must have a fully functioning limbic and autonomic nervous system   Anatomy of the Limbic System Involved in motivation, emotion, learning, and memory Group of interlinked Structures: Olfactory bulb, hypothalamus, hippocampus, amygdala, and cingulate/prefrontal cortex Thalamus is not a part of the limbic system Cingulate cortex - pain and emotional regulation   Theories of Autonomic Activity and Emotion Commonsense View: Emotion causes responses People respond physiologically and behaviorally James-Lange Theory Physiological response to an event causes emotion Locked-In Syndrome is an example Cannon-Bard Theory Both physiological response and emotional response occur simultaneously but independently This enables variability between different people's emotional response Schacter-Singer Theory (two-factor theory) Similar to Cannon-Bard theory Change in physiological response determines the quantity of an emotion, but cognitive appraisal is needed to determine the type of emotion   The Effects of Stress on Emotion Stress - a nonspecific response of the body to any demand made upon it Targets for stress: Rapid target - Autonomic Nervous System Target over time - HPA Axis (produces hormones like cortisol) HPA Axis - hypothalamus, pituitary gland, adrenal cortex  Stages of Stress (General Adaptation Syndrome) 1. Alarm Reaction (to stressor) Sympathetic nervous system activity Mobilize resources for immediate recovery (short-term stress) 2. Resistance Cope with stress Autonomic functions maintained Hormones released for sustained stress (long-term) 3. Exhaustion Sympathetic nervous system starts to fail (really long-term) Body’s reserves depleted More susceptible to illness   Disorders Related to Stress Involving Autonomic Nervous System Psychosomatic Illnesses “Stress to the system” Ulcers, Heart Disease Voodoo Deaths Overwhelming emotions stop the heart Implicated by excess parasympathetic activity after sympathetic onset during overwhelming helplessness HPA Effects - Heart Disease, immune system, memory loss   The Brain and Emotion: The Hypothalamus Testosterone facilitates activity of the VMH (ventromedial hypothalamus) Stimulation of the VMH = Increase in aggressive behaviors What behavior is dependent on what area is stimulated   Brain Areas for Aggression: The Amygdala Stimulation in Amygdala Aggressive, affective attacks Higher association with fear   Clinical Significance in regards to the Amygdala and Aggression Rabies Attacks the temporal lobe (where the Amygdala is located) Leads to furious, violent behavior Focal Seizure (Seizure Originating) from the Amygdala Increase in aggressive behavior Temporal Lobe Epilepsy Possible increase in aggression More generalized than focal seizure in amygdala Lesion/Removal of the Amygdala Tameness, placidity (decrease in aggression) Kluver-Bucy Syndrome Bilateral damage (lesions) to the amygdala Dramatic emotional changes, including reduction of fear and anxiety

Basic Definitions Agonist - a substance that initiates a physiological response when combined with a receptor Antagonist - a substance that interferes with or inhibits the physiological action of another Temporal lobe - location of the amygdala   What is Anxiety? Fear vs. Anxiety (Two Types of Escape Emotions) Fear: temporary experience, usually escapable Anxiety: long-lasting, less escapable   How We Measure Anxiety Escape behaviors - a way to observe fear/anxiety Innate Fears Startle reflex Reaction modified by mood or past experience Conditioned fear response Measure physiological behavior during a fearful stimulus Pair another stimulus shortly before the fear-evoking stimulus Upon repetition, subjects will respond to the originally non-threatening stimulus as though it’s anticipating a fearful response   Human Amygdala and Fear Experimental Evidence Viewing fearful faces - increased activity in amygdala Clinical Evidence Urbach-Wiethe Disease Calcium accumulation kills cells in amygdala No experience of fear Trouble identifying or drawing fearful expressions   Amygdala and Chemicals Involved in Anxiety   CCK (Cholecystokinin) Main excitatory amygdala neurotransmitter CCK agonist (increase in CCK) = increase in startle reflex GABA (Gamma Amino Butyric Acid) Main inhibitory amygdala neurotransmitter GABA antagonist (decreased GABA) = symptoms of panic Extremely low levels of GABA possibly related to panic disorder       Mechanism Behind Anxiety-Reducing Drugs Benzodiazepines and Alcohol Both act on GABA receptors (changes its shape) Facilitates the binding of GABA receptors (inhibitory) Exhibit cross-tolerance If you develop a tolerance for one, you will have one for the other   Anxiety Disorders Generalized Anxiety Disorder Symptoms common, persistence abnormal ⅔ of sufferers are women (results may be skewed) Attention shifts from worry to worry (with physical symptoms) No identification for cause of worries Panic Disorder Occurs suddenly, very intense, then disappears Marked by frequent panic attacks Symptoms: racing heart, shortness of breath, dizziness, etc. Often accompanied by agoraphobia Phobias Irrational fears that disrupt “normal” functioning Can be specific or general (ex. social) Most common anxiety disorder Obsessive-Compulsive Disorder Based on repetitive thoughts (obsessions) and behaviors (compulsions) Anxiety reduction based on negative reinforcement Interferes with everyday functioning Ex. Howard Hughes, 'As Good As it Gets' Post-Traumatic Stress Disorder Direct experience with an extremely fearful event  Uncontrollable sense of fear, helplessness, and horror Must be at least 6 months after an event Marked by excessive drug abuse, lashing out, hallucinations Benzodiazepines  Ex. Valium, Librium, Xanax Serve as tranquilizers Amygdala and hypothalamus: anti-anxiety effects Cortex and thalamus: sleepiness and memory impairment Perspectives of Anxiety Disorders Learning Classical conditioning Reinforcement Generalization Observational learning Biological Natural selection Genes Physiology

Basic Definitions Proband - an individual affected with a disorder who is the first subject in a study (as of a genetic character in a family lineage) Proband study - studies genetics of mental illness through number of occurrences within a family tree Concordance rates - the probability that a pair of individuals will both have a certain characteristic, given that one of the pair has the characteristic; usually means the likelihood of presence of the same trait in both members of a  pair of twins Reuptake - The reabsorption of a secreted substance by the cell that originally produced and secreted it Catecholamines - dopamine, epinephrine, and norepinephrine Major Depressive Disorder Feelings of sadness and helplessness every day for at least 2 weeks Little energy, feelings of worthlessness, contemplating suicide, trouble sleeping & concentrating 2x more women than men Can happen across lifespan Most cases of depression are episodic Main neurotransmitters - dopamine, serotonin, norepinephrine   Major Depressive Disorder (Genetic Evidence) Runs in families Adopted children resemble biological parents Higher risk if parents have severe, long-lasting depression before age 30 Sex difference, but hard to explain Questionable effects from hormones No differences in social influences (unreported cases) No isolated gene for depression   Major Depressive Disorder (Neuroanatomical and Physiological Bases) Lateralization effects Happy mood elicits high activity in left prefrontal lobe Depressed mood elicits high activity in right prefrontal lobe Left hemisphere damage correlates with depression Right hemisphere damage correlates with mania   Antidepressant Drugs Tricyclics 2nd course of treatment in depression Example: Tofranil Prevent reuptake of serotonin and catecholamines Increases the production of serotonin, norepinephrine, and dopamine Major side effects: Histamine receptors - drowsiness Acetylcholine receptors - dry mouth, difficulty urinating Sodium channels - heart irregularities SSRIs (Selective Serotonin Reuptake Inhibitors) First course of treatment in depression (and often anxiety) Examples: Prozac, Zoloft, Celexa, Luvox, Paxil (generics end in ‘-ine’ or ‘-pram’) Similar to tricyclics but specifically prevent serotonin reuptake Nausea, headaches, nervousness (more mild side effects) MAOIs (Monoamine Oxidase Inhibitors) Last course of treatment for depression (due to side effects) Example: Phenelzine (Nardil) Blocks the enzyme Monoamine Oxidase (MAO) MAO inactivates catecholamines and serotonin in axon terminal Avoid foods containing tyramine (cheese, raisins, liver, pickles) Consumption can lead to death (increases blood pressure)   Why Don’t Antidepressants Cure All Depressive Disorders? Physiological confounds Mood = combination of neurotransmitters Time course between behavioral and psychological effects Mechanisms of long-term effects not characterized Placebo effects Other factors Depression may be due to different factors in different people Environmental influences Only ⅔ of patients show benefits from antidepressants   Electroconvulsive Therapy (ECT) Patients who don’t respond to drugs Electrically induces seizure, usually every other day for 2 weeks Memory problems (limited with right hemisphere shock) Downfall: huge relapse effect (50%)   Bipolar Disorder Fluctuations between mania and depression Mania: extreme activity, excitement, loss of inhibition Fluctuations and ages may vary Possible genetic effect Treatments: Lithium (a salt) Mechanism not well understood (possibly on 2nd messengers) Dose important - too high may be toxic Anticonvulsant drugs ( ex. Valproic Acid, or Depakene) Blocks 2nd messenger systems   Seasonal Affective Disorder (SAD) Depression during a particular season (winter) Occurs most severely in areas near the poles (subtle effects in moderate climates) Depressed patients - phase advanced SAD patients - phase-delayed Related to circadian rhythms (different from depression) Treatment: very bright lights 1+ hours a day   Schizophrenia Characterized by: Gross distortions of thoughts and perceptions Loss of contact with reality (Different from multiple personalities) 1% of Americans exhibit over lifetime Most common in United States Equal number of men and women Average age of onset: Men = 18 to 25 years old Women = 26 to 45 years old Can be chronic or acute The more acute, the more likely a recovery can occur Diagnosed through differential means   Schizophrenia Major Symptoms Incoherent thinking Delusions Hallucinations Disturbance of affect Bizarre Behavior   Neuroanatomical Hypothesis of Schizophrenia Various brain regions are smaller in schizophrenics Prefrontal cortex, hippocampus, amygdala, temporal cortex Areas involved with emotion, coherent thought, perceptions Ventricles are larger in schizophrenics Lateralization of schizophrenia Lower activity of regions on the left Development of larger areas (including planum temporale) on right Differences do not progress Question: if this is the case, why don’t symptoms appear earlier in life?   Dopamine Hypothesis of Schizophrenia Excess dopamine receptor activity at synapse contributes to symptoms of schizophrenia Supporting evidence: Antipsychotics (ex. Thorazine), and neuroleptic drugs (ex. Haloperidol, or Haldol) Certain drugs = increase in dopamine activity (cocaine, amphetamines, meth, LSD) Downsides: Time course discrepancies Receptor differences questionable   Glutamate Hypothesis of Schizophrenia Deficient activity at glutamate synapses in the prefrontal cortex and hippocampus contribute to symptoms of schizophrenia Supporting evidence: Antagonistic effects between glutamate and dopamine (Supported by antipsychotic drugs) PCP (phencyclidine) effects are close to schizophrenia (inhibits glutamate) Produces little effects in prepubescent monkeys, significant effects later on Produces specific and long-lasting effects (in comparison to drugs that stimulate dopamine) Downside: Glutamate treatment will overstimulate cells to death  

Emotion and Anxiety Disorders 1.) Define emotion and describe what is required (and not required) to scientifically study emotional behavior.  Provide example for each of these criteria. 2.) Identify the limbic system (as well as its parts) and its general role in emotion. 3.) Describe the relationship between emotion (we used fear as a working example) and physiological responses (or readiness for action) and describe all theories (and examples) that attempt to explain such a relationship. 4.) Define stress and distinguish between short-term and long-term stress on the basis of what part of the nervous system is involved. 5.) Describe all disorders that are related to short-term and long-term stress 6.) Identify different brain regions that are involved with emotions like aggression/fear and provide examples to support such claims. 7.) Identify different ways that we express our emotions as describe how these expressions (and how we perceive these expressions) can vary in a number of ways. 8.) Describe the role of hormones and neurotransmitters in aggressive behaviors as well as provide an example to support this claim. 9.)  Distinguish between fear and anxiety as emotions (this is covered in Chapter 16 in more detail). 10.) Distinguish between fear and anxiety. 11.) Describe how fear (and anxiety) can be measured/manipulated as well as factors that may affect such a response. 12.) Describe the role of different chemicals on the amygdala, and inevitably, anxiety. Cite examples that support such claims. 13.) Identify different benzodiazepines that are found to reduce anxiety as well as describe the way in which they work (and where their effects are found in the brain). 14.) Describe what is meant by “cross-tolerance.” 15.) Characterize all different anxiety disorders that were mentioned in class 16.) Describe how anxiety disorders might develop in someone (biologically and psychologically)   Mood Disorders  1.) Characterize the symptoms of major depression. 2.) Describe how major depression may or may not be genetically based. 3.) Identify the three major classes of antidepressants on the basis of a.) examples; b.) neurotransmitters involved; and c.) side effects from each. 4.) Describe why antidepressants may not work as well as one would think and provide one other type of treatment for major depression. 5.) Describe the symptoms of bipolar disorder/seasonal affect disorder (SAD), their possible causes, and possible treatments.