PSY 351 EXAM 4 GUIDE Chapter 15-16
PSY 351 EXAM 4 GUIDE Chapter 15-16 351
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This 6 page Study Guide was uploaded by Benny Ye on Thursday December 10, 2015. The Study Guide belongs to 351 at University at Buffalo taught by Meyer, P in Fall 2015. Since its upload, it has received 53 views. For similar materials see Biopsychology in Psychlogy at University at Buffalo.
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Date Created: 12/10/15
Depression 1. Know Martin Seligmans’ conceptualization of explanatory styles that are associated with depression. He calls it the “common cold” Positive explanatory style is preferred Events explained via (universal, specific, permanence) 2. Know the different treatments for depression, including, TCA, MAOI, SSRI, ECT Cognitive behavioral therapy: changing negative thinking styles Interpersonal therapy: changing patients relationship with others ECT: very effective if other treatment do not work, a last resort for severe depression Medications: all of them react with dopamine, norepinephrine, & serotonin(5-HT)) TCA: inhibit reuptake of catecholamine 3. Know the structure of the serotonin synapse and how MAOI and SSRIs work there MAO inhibitors: breaks down monoamine oxidase Depression linked to decrease activity of monoaminergic neurons Cannot eat things with tyramine 4. Be able to explain why SSRIs take so long to have an effect on depression A procedure involving a low-tryptophan diet and a tryptophan-free amino acid “cocktail” that lowers brain tryptophan and consequently decreases the synthesis of 5-HT. 5. Know the animal models of depression, and what predictive validity is. Mouse tail suspension test or forced swim test Not very high validity because can one really ask what a mouse is feeling? 6. Know the evidence supporting that depression is a stress disorder. Environmental, childhood abuse is a factor 7. Know the hormones associated with HPA axis, and the negative feedback inhibition of this axis. Hypothalamus to pit to adrenal gland: release of cortisol 8. Know the changes in the hippocampus that occur after chronic stress High glucocorticoids leads to hippocampus damage more damage leads to weakening of the feedback loop higher uncontrollable glucocorticoid releases 9. Know how the serotonin transporter polymorphism is associated with depression, and how genetic differences in this gene are associated with sensitivity to stressful life events. 5 HTT gene transports serotonin to either short or long 5-HT(more promoter) SSRI has the least dangerous side effects 10. Know the hormones and brain areas associated with HPA axis, including corticotrophin releasing hormone(CRF) adrenocorticotropin (ACTH), glucocorticoids such as cortisol and corticosterone, and the negative feedback inhibition of this axis. CRF leads to ACTH -> cortisol released 11.What is the dexamethasone suppression test and what does it tell us about depression? Steroid that is a glucocorticoid: when injected brain should react with negative feedback, thus reducing the cortisol Schizophrenia 1. Know the two major categories of schizophrenic symptoms and examples of each Disordered thinking or inappropriate emotional responses, seeing hallucinations or delusions Positive: the addition of some strange behaviors Negative: the absence of some strange behaviors 2. Know the neurodevelopmental hypothesis of schizophrenia, and the evidence supporting that the brain changes in patients with schizophrenia. Less cells in prefrontal cortex, smaller hippocampus’s ventricles larger More instances of prognosis for those born in winter or early spring 3. Know the glutamate and dopamine hypotheses of the causes of schizophrenia, and the evidence for each. Blocking of dopamine receptors calm schizophrenia These drugs are neuroleptic 4. Know the glutamate and dopamine hypotheses of the causes of schizophrenia, and the evidence for each. What is phencyclidine (PCP), and how does it work? Know the D1-like and D2-like receptors and their roles in schizophrenia treatments. D1 & D5: excite or increase NT release D2 & D3: inhibit or decrease NT release Excite dopamine are located in striatum and nucleus accumbens, inhibit dopamine is in hypothalamus typically Schizophrenics have typically more inhibit dopamine receptors: D2 & D3 Glutamate: schizos tend to have less glutamate in their brains - Evidence found in that reduplicating the effects of low glutamate using PCP or ketamine 5. What do twin studies tell us about the heritability of schizophrenia? Monozygotic: 45-50% concordance Dizygotic: 16-20% concordance 6. Schizophrenics almost always smoke because nicotine can up their attention levels, Addiction 1. Know the negative reinforcement, positive reinforcement, and incentive motivational theories of addiction Positive reinforcement: - Positive reinforcement = pleasure? - View drugs as positive enforcers, we seek the pleasure derived from doing drugs Models: - Self-administration, conditioned place, taste reactivity Negative reinforcement: - Self-medication : presence of stress can be “mediated” with drugs - Physical dependence hypothesis :withdrawal avoidance, continued use has cause adaptations in brain reward system - preoccupation, anticipation, binge self- administration was formerly the criteria for drug addiction 2. Know how most drugs of abuse act on the brain, and the receptors and neurotransmitter systems involved Table 16.1 Drug and their receptor sites: Alcohol: NDMA Barbiturates(painkillers): GABA Cannabis: CB1 Nicotine: acetylcholine Opioids: opiate receptor Cocaine: blocking dopamine sites Amphetamine: releases extra dopamine at the sites Candidate genes: DAT1, DAT 2 DAT 4, OPRM1, GABA 3. Know the problems with euphoria models of addiction Wanting is not the same as liking, but dopamine is active in the seeking, motivation phase 4. Know how dopamine and endogenous opioids may mediate different aspects of the effects of addictive drugs. After a CS is introduced, the peak of dopamine happens before the award showing that dopamine activation is learning when to release, during pleasure or during seeking out the pleasure Endogenous opioids found on neurons that excite more dopamine release Opioids: pleasure Dopamine: incentive motivation 5. Know some of the treatments for drug addiction, and the brain areas on which these treatments act upon. - Cocaine, amp, meth are directly affecting the brain - Opioids, nicotine, alcohol are indirectly affecting Drugs to combat Addiction: - Methadone dosages for those addicted to heroin, morphine - Buprenorphrine of being an even better therapeutic agent for opiate addiction than methadone - Nicotine gum chewing - Bupropion an Anti-depress that treats nicotine - Varenicline especially used for nicotine - Opiate antagonists act to reduce reinforcing effect of alcohol (naltrexone) - Acamprosate NDMA antagonist to treat seizure disorders caused by alcohol withdrawal 6. Higher correlations for monozygotic twins than for dizygotic twins suggest a genetic influence for both drug and alcohol addiction
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