Psyc4130 1nd EditionExam # 4 Study Guide Lectures: 22 - 36Lecture 22-26 (3/24, 3/26, 3/31, 4/02, 4/04)Chapter 11- Emotion EMOTIONS- Right/Lefo Right = More Emotional; Parallel Processor “Give a damn” side: integrates many little parts into big scene; projecting sympathy, empathy, and concern to outer world (primary emotions)o Lef = More Literal; Serial Processor Language (men are more lef-oriented for language), approach, outgoing, contentment, more fun-loving (preprocessing social emotions) Stroke of Insight (Jill Bolte-Taylor)o Results of Right Hemisphere Damage Indifference toward condition, diminished capacity for emotion in general, monotone speech, difficulty deciphering others’ non-verbals, deficient understanding of metaphor, simile, and sarcasm- Amygdala as “Fear Factor”o Lateral nucleus (LS) – inputs, especially from the vmPFC and hippocampus Ie. limbic system response from reading a booko Basal Nucleus (B) – assists LA in sending output to vmPFC and central nucleus of amygdalao Central Nucleus (CE) – output signals to hypothalamus and brainstem most important part for expression of emotional responses provoked by aversive stimuli; afer CE is destroyed, animals don’t show signs of fear Lateral hypothalamus → sympathetic activation, ↑ heart rate and BP, paleness VTA → behavioral fleeting from stressful situations (dopamine is released) Locus coeruleus → increased vigilance (norepinephrine) PAG (periaqueductal grey matter) → behavioral arrest (freezing) vmPFC can come to inhibit (override) CE during extinction of CER (conditioned emotional responses) Reciprocally connected and mutually inhibitory (inhibit each other) Lesions of vmPFC impair extinction (ECBs in amygdala required for extinction) vmPFC allows for extinction to occur (keeps amygdala in check) Extinction is not forgetting (spontaneous recovery and rapid reacquisition)--supressed response but have not forgetten it  Humans With Amygdala Damage → emotion generally intact, struggle interpreting subtle emotional cues or complex emotional situations, equally likely to remember emotional details, judgments of trustworthiness skewed from normal (broken sketch-radar)- Amygdala Activity When “Additional Processing Required”o The biggest increases in amygdala activity were observed when subjects were shown faces demonstrating fear or anger, but specifically when the emotional context was ambiguous (e.g. a terrified person is looking AT you when you have done nothing to make them fearful...this is confusing and the amygdala, ostensibly, is trying to motivate the rest of the brain to figure out what’s going on). On the other hand, if somebody is looking at you very angrily, amygdala activity goes up, but not as much as it goes up when the same face is looking at someone else with anger. The reasoning is that the “anger-averted” condition is more ambiguous and will require the brain to engage in more deliberative disambiguation.- vmPFC’s Role in Inhibiting Amygdala-Clinical Implicationso Holds amygdala in check = primary structure in control of extinguishing conditioned fear responses and is reciprocally connected with amygdala.o The types of rational and deliberative processing required in Cognitive-BehavioralTherapy (CBT), therefore, is believed to strengthen the vmPFC which ends up helping depression, anxiety disorders and other disorders (e.g. Borderline, et cetera) by inhibiting the activity of the amygdala. The amygdala doesn’t get to “run amok” and the patient, ostensibly, will not spiral out of control. - vmPFC Damage and Impersonal vs. Personal Moral Dilemmaso People with damage to the vmPFC are more likely to endorse the decision to personally cause someone else’s demise (e.g. throw the injured person out of thelifeboat) than are people with intact vmPFCs. - Proposed Circuitry for Moral Decision Making vmPFC → anterior cingulate cortex (ACC) → dorsolateral prefrontal cortex (dlPFC) vmPFC: detects “problem”/conflicts of interest ACC: evokes empathy (e.g. “do unto others”) dlPFC: develops plan(s) of action that are likely to lead to the best overall outcome- 5-HT and Impulsivity (Monkeys)o Low levels of 5-HT in monkeys → impulsivity and deatho Attempt longer leaps from branch to brancho Fail to show deference to social superiors/alphasLecture 27 (4/07)Chapter 13- Learning and Memory LTP and the Physiology of Learning - The whole brain/cortex is connected, project throughout entire brain, networks of interconnected neurons- HCF o CA Fields (CA1)- Entorhinal cortex  HCF  Amygdala- can activate hippocampus and vice versa  Hypothalamus (mammillary bodies) = “papez circuit”- LTPo NMDA glutamate receptor “coincidence detector”o Ketamine, PCP, Dextromethorphan, MK- 801 Alcohol Lecture 28-31 (4/09, 4/11, 4/14, 4/16)Chapter 15- Neurological Disorders  NEURODEGENERATIVE DISORDERS- Alzheimer’s Disease o Demographics @ age 65: 10% of population @ age 85: 50% of populationo Clinical Presentation 1st sign = excessive forgetfulness: ie. missing appointments, failing to remember common words, failure to recall peoples’ names 2nd = general trend toward ↑ confusion: ie. multitasking, balancing a checkbook, memory problems follow anterograde model Progressed stages = completely unable to care for themselves Diagnosis → death: 8 yearso Trajectory of the Disease Earliest pathologies are olfactory → limbic → neurons compromised throughout entire cerebral cortex, including regions of association cortex Sulci and fissures are deepened due to atrophy of neocortex Severe degeneration in olfactory cortex, entorhinal cortex and hippocampus, neocortex (especially association regions of frontal and temporal lobes) Vast degeneration in major neurotransmitter systems: nucleus basalis (ACh), locus coeruleus (NE), Raphe nuclei (5-HT)o PlaquesA-beta Stick to outside of neurons Include dense core of beta-amyloid protein surrounded by dead axons and dendrites Activated microglia and reactive astrocytes included too (seek destruction of damaged cells) Secretases and the snipping of APPs1. Β-secretase cuts tail off APP molecule2. ɣ-secretase cuts head offResult of secretases = molecule of Aβ containing 40-42 amino acids, determined by 2nd cut of ɣ-secretaseNormal brains: 90-95% shortAD