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Drugs and Behavior Exam 2 review

by: Becca Sehnert

Drugs and Behavior Exam 2 review PSYC 265

Marketplace > University of Nebraska Lincoln > Psychology (PSYC) > PSYC 265 > Drugs and Behavior Exam 2 review
Becca Sehnert
GPA 3.9

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About this Document

This is the study guide for exam two.
Drugs and Behavior
Dr. Stoltenberg
Study Guide
Drugs, behavior, exam, review, Psychology
50 ?




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This 2 page Study Guide was uploaded by Becca Sehnert on Monday October 10, 2016. The Study Guide belongs to PSYC 265 at University of Nebraska Lincoln taught by Dr. Stoltenberg in Fall 2016. Since its upload, it has received 52 views. For similar materials see Drugs and Behavior in Psychology (PSYC) at University of Nebraska Lincoln.


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Date Created: 10/10/16
Drugs and Behavior Exam 2 review Cerebellum 1. Has 70% all neurons in brain 2. Regulates movement a. Maintain posture b. Coordinate head and eye movement c. Fine tuning muscle movement 3. Brain damage has uncoordinated gait 4. First affected by alcohol 5. Field sobriety tests Nucleus accumbens and VTA 1. Addictive drugs release dopamine in nucleus accumbens a. Other reinforces too –food and sex 2. Dopamine neurons originate in VTA (ventral tegmental area) 3. Part of “reward pathway” Agonist and Antagonists 1. Agonist –facilitate neurotransmitter action a. Increase synthesis b. Inhibit degradation c. Increase release d. Activate post-synaptic receptors e. Block reuptake transporters 2. Antagonist –reduces neurotransmitter action a. Decrease synthesis b. Keep from being packaged into vesicles c. Block neurotransmitter binding Alcohol (EtOH) 1. GABA –inhibitory neurotransmitter (Ethanol increases GABA release [agonist]) 2. Glutamate –excitatory neurotransmitter (Ethanol inhibits glutamate release [antagonist]) Neuroadaptation 1. If it increases dopamine released in nucleus accumbens, want to stop being over stimulated 2. Neuro systems adapt by altering a. Production b. Number of receptors c. Reuptake, etc 3. Then begin taking more of the substance to feel the same affects Alcohol metabolism genes 1. How genes increase risk for alcohol dependence 2. Alcohol dehydrogenase (ADH-4q) 3. Aldehyde dehydrogenase (ALDH-12q) a. 2 mutated versions Protects from alcoholism, wont become addicted to alcohol because your liver doesn’t break it down properly and you get a flushing response and feel bad b. Genetic variant of ADH that works faster so have too much acetaldehyde in system (toxic) and lowers risk of alcoholism 4. Antibuse (disulveram) a. Block ALDH enzyme and makes you feel sick cuz build up of acetaldehyde Animal models for convergent evidence 1. Can breed for genes in mice 2. Result of selecting for genes has affect on ethanol consumption 3. This means that genes do have an affect on alcohol consumption 4. Eliminate function of gene  behavior outcome a. Seratonin receptor blocked –mice more aggressive and drink more Motivational model of alcohol use 1. Drinkers regulate emotions and moods by using alcohol 2. Coping –make bad feelings go away, reduce negative emotion a. Using substance is primary way to cope 3. Enhancement –increase positive emotions 4. Most use both motives depending on context 5. Rely primarily on one motive or another Wernicke-Korsakoff Syndrome 1. Caused by prolonged thiamine (Vit. B1) deficiency a. Diet of mostly alcohol, has carbs but no vitamins b. Brain needs this to metabolize glucose c. Lead to loss or shrinkage of neurons 2. Symptoms a. Ataxia (cerebellar damage) b. Retrograde and anterograde amnesia (declarative memory) c. Confabulation (make up stories to fill lost memories) Alcohol myopia: more attention to short term impulses than to long term interests 1. Intoxicated individuals –not alcoholics 2. Consumption impairs controlled effortful cognitive processing 3. Narrows attention 4. Resources remaining go to easiest, immediate cues 5. Hostile situations, lead to aggression and less non-provocative cues


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