Drugs and Behavior Psych

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Department
Psychology
Course
PSYCH 2220
Professor
myounglee
Semester
Fall

Description
Drugs/behavior 8/22 what is the drug’s...? -trade name/proprietary name =viagra (name given by company/capital letters) -generic name/cheaper to buy name/lots of companies use =sidenafil citrate -chemical name/named after what it looks like) = 5-[2-ethoxy-5-(4-methylpiperazin-1 etc -street name =”the blue pill”, vitamin v, blue diamond Basic concepts: -pharmacology- study the relationship between the drug and its effect ▯ -keep in mind the main effect/primary effect ▯ -side effect/adverse effects -how does a drug work to change behavior? Animals in Research -animals play an important role in pharmacological research Welfare vs. Rights Animal Welfare -human responsibility to all aspects of animal well being -moral obligation to healthy animals -scientific necessity of healthy animals Animal Rights -animals should have similar/the same rights as humans do: consent -opposition to animal research in any form, any purpose How can animals convey anything to humans? -depression can be seen in limbic system -changing limbic/nervous system can help -learned helplessness ▯ -dog in a box. isolated on one side and receives shocks ▯ -next day remove barrier and can escape shock ▯ -some dogs will still stay on the shocking side and shows they gave up ▯ -mimics signs of depression What animals are used? primates=.1% dogs/cats=.2% other small mammals=1.5% large mammals=1% fish, amphibians, reptiles, birds=15% rodents=82% What are the rules and laws? -Animal welfare act (1966)- sets standards and regulations for humane care and treatment of animals -requires.... ▯ -animal care and use committee (ACUC) ▯ -pain and stress are minimized ▯ -adequate veterinary care -enforcement by US department of agriculture (USDA) -exemptions to the AWA (ex: rats and mice) What should an ethical scientist do? -The 3 R’s ▯ -reducing (# of animals required) ▯ -replacing (replace animals with technology/cpus) ▯ -refining (refining experiment) Review questions: -jamie doesn’t want animals to suffer but she believes its necessary to do research with animals to understand disease. she supports the animal ___perspective. ▯ -Welfare -what is the role of the ACUC on a research campus like Mizzou? ▯ -makes it up to standards with government, adequate vet care, minimize stress n i a p d n ▯ a -Dr smith wants to follow the three Rs in her research program. give an example of what she should do for each R. ▯ -reduce amount of animals used, replace animals with something else, refine ▯ techniques so we can use fewer/no animals. EX: one group of mice received test drug and a second group receives placebo. The amount of food consumed after drug/placebo was then measured. -what’s the independent variable? ▯ =which mice for test drug/placebo -what’s the dependent variable? ▯ =the amount of food/placebo consumed (T/F) this is within subjects design ▯ =false. the same subject is getting the drug and the placebo. In between group design where some have one group and others have the other. Rules and guidelines for drugs: American history: before the 20th century... ▯ -patent medicines (patent refers to name of medication) -hostetter jitters stomach, wine, aspirin, bayer, heroin san francisco/cali=earliest drug laws on LOCAL level -chinese immigrants came in to help build -smoked opium -americans put laws on opium use in order to limit amount of chinese immigrants -marijuana laws targeted mexicans -cocaine restricted to target blacks -at federal level=no restrictions. local laws targeted minorities REVIEW: Dr. smith lives in the US in the 1870s and wants to sell an elixir to cute the common cold. what federal rules and regulations would he need to follow to sell this med? -get a patent and pay tax -Progressive movements: 1) -Sinclair’s the jungle and the muckraker journalists ▯ -took observations about meat packing in chicago ▯ ▯ -purpose: we need to protect the consumer, we need regulations on ▯ ▯ food/drug so we know what is in it or what effects are 2) Thalidomide (Kevadon) -not sure what it did, let’s just give it out -given to pregnant women since some said it helped morning sickness -babies were born stillborn/ -teratogenic effects ▯ -’little monster” “birth defects” ▯ -penguin like limbs, flipper arms, eye muscles, no ears/small ears -Frances Oldham Kelsey-worked for Gov., kept drug out of USA. lead to us needing more strict drug laws in USA. 3) Drugs and crime(?) -the “other” -social change and protest ▯ -(Drugs restricted to restrict people and control social change/protest) Laws for developing and selling THERAPEUTIC drugs: -pure food and drug act (1906) ▯ (first required companies to accurately label preparation, and required you to include if it was potentially addictive) -federal food, drug and cosmetic act 1938 (and its many amendments) - created the modern food and drug administration (responsible for drug safety and efficacy) - created distinction between prescription versus over the counter (drugs start as prescription then go to OTC) ex: claritin Laws for recreational drugs -Harrison tax act 1914=first big fed law to restrict drug access for rec purposes ▯ -controlled drugs by taxation -the Federal Comprehensive Drug Abuse Prevention and Control Act (1970) ▯ - also known as Controlled Substances Act ▯ ▯ -created scheduled vs. non scheduled drugs ▯ ▯ -enforced by Drug Enforcement Agency ▯ ▯ -alcohol and tobacco Review Questions: 1) under the pure food and drug act (1906), drug companies were required to: -label accurately -state if potentially addictive 2) The ___ is the government agency that regulates the development of new therapeutic drugs -FDA for therapeutics 3) why do we classify a drug as schedule 1? give example of schedule 1 -high risk of abuse, no medical benefits Schedule Drugs 1: drugs with high abuse potential and no accepted medial use ex: heroin, marijuana, hallucinogens 2: Drugs with high abuse potential but accepted medical use ex: morphine, cocaine, amphetamines 3: Drugs with moderate abuse potential and accepted medial use ex: barbiturates, anabolic steroids, higher grade narcotics 4: drugs with low abuse potential and accepted medical use ex: benzodiazepines 5: drugs with limited abuse potential and accepted medical use ex: low grade narcotics 8/27 amphetamine injection causes an increase in spontaneous motor behavior in mice. for several days a psychologist presents a light and injects the mice with amphetamine. later the light is lit, no injection is given and the mice show a decrease in motor behavior. US: injection of amphetamine UR increase motor behavior CS: light CR: decrease motor behavior Person uses cocaine, when in use they handle a crack pipe. They light the drug and feel good (UR). in lab they see crack pipe and it elicits a response. instead of feeling good CR, they feel craving/desire CR. review: you need a med to treat your back pain but you need a prescription: ?what government branch determines whether it’s a prescription or over the counter -FDA ?what factors determine whether it should be prescription or OTC? -is it habit forming? potential for abuse? whether it’s safe? side effects? how long it’s been on the market? ?what government branch determines where it’s scheduled? -DEA (drug enforcement agency) What are the differences between schedule 1 and schedule 2 drugs? -medically accepted schedule 1: no medical benefit, high abuse liability schedule 2345: beneficial use, abuse liability lower ex S1: marijuana, heroin S2: cocaine, morphine, amphetamine Basic and clinical evaluation of new drugs: drug development: -how do we bring a new drug to the market? -role of the food and drug administration ▯ -human subjects protection ▯ -safety (lethal dose/side effects) ▯ -efficacy(does the drug work for its purpose) what about “natural” remedies? -leptasol page -natural remedies not the responsibility of the FDA -buyer beware Stages of drug development 1) discovery/synthesis 2) characterization 3) human testing 4) marketing -enormous costs (800 million- 1.2 billion) ▯ -few reach market ▯ -money needed to pay for failures 1. drug discovery/synthesis -how do we find a new candidate? ▯ -modification (of an existing chemical) ▯ -random screening (test all drugs to see which interact well or poorly, time ▯ consuming) ▯ -rational drug design (computer, use what we know about brain/body/behavior to ▯ design new drug on computer) ▯ -biotechnology-working at genetic level to understand genome to come up with ▯ specific pharmacology. 2) Characterization -determine a pharmacological profile ▯ -”high throughput screening”=get lots of info really quickly ▯ ▯ (-plastic plate size of deck with 96 holes, in each well put some drug, then ▯ ▯ card with drug goes into conveyer belt and over time that plate travels to ▯ ▯ other side and computer print out shows where it interacts in body ▯ -pharmacokinetics-how does drug move throughout body ▯ pharmacodynamics-what’s its mechanism of action. how does it treat? -animal research-no human subjects! -development of a lead compound-looks safe and should give $$ -no chemical can be certified as completely “safe” ▯ -estimate risk under specified conditions(these are conditions that are safe and ▯ not safe) -there are limitations to preclinical research ▯ -animals cant tell us everything, good in animals, but not good with humans -confounds in research ▯ -good research design 3. human testing -four phases of human trials ▯ -Notice of Claimed Investigational Exemption for a New Drug (IND) ▯ ▯ (given to FDA to get drug to humans, all data on drug) ▯ -phase 1-dose response (safety, side effects, how much can human handle, ▯ maybe 50-100 healthy people, we want to find dose limits/where effects seen) ▯ -phase 2-case study (find people with disease of interest, 100-200, test efficacy) ▯ -phase 3- large scale studies (thousands of ppl, all over world, diversity, efficacy) ▯ ▯ -New Drug Application (NDA)-you file a new application of all the new ▯ ▯ pos/neg data. sent to FDA. wait a few years for approval. approved for a ▯ ▯ certain use. ▯ -phase 4- Post Marketing Vigilance (keep an eye on safety) Timeline perfect timing=20 years ▯ year 0=chemical identified/patented ▯ year 4=end of characterization ▯ year 10-12= end of phase 1,2,3 ▯ year 20= end of phase 4/ generics possible ▯ after 20 years the drug can go to generic Review: ?your friend says she’s participating in a phase 2 human drug trial. What’s she likely experiencing? -a common disease that the drug is being used to treat 100-200 people ?When and why does a drug company prepare a New Drug Application? -phase 3, to note all new effects after using humans as subjects Aug 29th Pharmacology Methods a good pharmacology experiment must investigate multiple doses/concentrations (placebo--->effective concentration) ▯ -determine the dose-response relationships(what happens with dif doses) ▯ -minimal and maximal concentrations/doses (how much should be prescribed. minimal is best, but you need to know max where no more help is given, reduces waste, determines overdose, side effects) ▯ -potency and efficacy- terms of comparison. potent=amount of drug required to get effect efficacy-does the drug do its thing? how well does it do it? Research Design -dose/concentration response curve threshold dose=lowest concentration where desired effect is seen maximal effect=where no more results are seen and curve plateaus EC50 Value=dose of the drug that is effective in 50% of population. Therapeutic effect/side effect overlap solution: up the dosage to over mask side effect ▯ lower the dosage for drug so curves are separate Compare ED50 with LD50 LD50/ED50=therapeutic Index low index (4)=dangerous High index=safe!! Alcohol index= around 7..yikes what is each drugs ED50 value? 20 & 40 which drug is more potent? Drug A (20) more efficacious? Drug B higher % of subjects reported effects (look at plateau) what is each drugs LD50 value?60 & 80 what is each drugs therapeutic index? 3 & 2 based on index, which is safer? Drug A is safer since the index is higher Homeopathy -Humorism-our behavior is based on the relative level of 4 humors, black bile, yellow bile, blood, phlegm. Black bile= melancholic/irritable yellow bile=Choleric/angered Blood=sanguine/amorous Phlegm=Phlegmatic/calm -Samuel Hahnemann (1796)-disease state is due to chemical imbalance. we need stimulus for cure. body has ability to heal itself. need the spark! different natural products could do that. ▯ -Miasms responsible for disease -Law of similars ▯ -provings-natural products at high concentrations and report how subjects were feeling. now you know where it is targeting. ▯ -like cures like= high concentrations=bad. low concentrations=better Law of infinitesimals ▯ -1X=1/10 ▯ -1C= 1/100 avagadro’s number-smallest particle detectable ocillococcium=1/100e200 PLACEBO EFFECT Aug 31 Kinetics and Dynamics Pharmacokinetics what’s the time course? how long does it take a drug to reach a receptor? how long does it stay there? drug onset: behavior to change behavior, drug must enter the central nervous system ▯ -via the blood ▯ -how does the drug get into the blood? (brain/spinal cord) what is the drug’s therapeutic window-range of doses where we see effects of drug oral digestion-takes longer to work therapeutic window shifts up or down ▯ -change in body weight ▯ -build up of tolerance Review questions: what is the appropriate time course for a drug to manage a chronic disorder (e.g. depression) ▯ -to get “high” (e.g. produce euphoria) we want drug to stay in system for awhile because psychiatric illness is 24/7 so the drug should be too. we don’t want tolerance to build up or the therapeutic window to change how might formulation effect abuse-by changing the formulation, the release time, etc adderall-slow release if swallowed. but high release if otherwise consistent regimen for taking drug once it reaches a plateau keep it there keep dose low Pharmacokinetics four basic processes Absorption-how does drug get into the body? distribution- how does the drug move throughout the body? metabolism-the pill you swallow will change. how does drug change in body? elimination-we want it to wear off in a certain amount of time Absorption -get in the blood-through CNS/blood what’s the best route? ▯ -do we want fast or slow drug onset? ▯ -is the drug stable with the desired route?-chemically can we do it? ▯ -is the route safe? ▯ -will we have good compliance?-will patient follow directions Parenteral(needle/syringe) administration ▯ -invention of hypodermic needle and syringe ▯ low duration high learning ▯ (decrease duration between response and outcome=high learning) ▯ -vehicle textbook review: describe___ injection. when is it used? -subcutaneous (s.c)-right under the skin. depot of skin/tent/bubble-inject -intramuscular (i.m.)-put into muscle where there’s lots of blood so it works faster -intraperitoneal (i.p)-peritoneal cavity (abs)- put insulin inside then drug is absorbed in stomach and our intestines. -intravenous (i.v)-put into veins directly so it’ll directly hit bloodstream. vein could collapse, dangerous, risky, can leave body quicker so you need to keep IV in. Inhalation administration - -speed (FASTEST) -diffusion ([high concentration] -->[low concentration]) gets absorbed into blood -damage to tissues if inhaled Peroral administration (p.o) swallowing -easy and hard -stomach-intestines -how quickly/slowly it goes to intestines from stomach Review Questions: which route of administration would be best and why? what might limit that route? get a quick euphoric high-inhalation because it works quickly and gets to CNS fast management of the symptoms of a chronic anxiety disorder-subcutaneous since it lasts longer, oral administration is easy and it absorbs slower. Review: Dr smith wants to train a monkey to respond on a FR schedule to receive an infusion of heroin. Describe the monkey’s pattern of responding ▯ -what if Dr. Smith switches to VR, FI, or VI what are real world examples of FR, VR, FI and VI schedules absorption -drugs need to pass through membranes ▯ -lipids -will a drug be absorbed through a membrane? ▯ -small molecule ▯ -lipid soluble (lipophilicity) ▯ -ionized Review what pKa value is Distribution -drugs don’t always move evenly -transport mechanisms ▯ -passive transport mechanism ▯ -active transport system -binding proteins Blood-brain barrier ▯ -glial cells (astrocytes) -placenta▯ ▯ -teratogenic effects? Metabolism and Excretion Drug--> enzyme-->metabolite -enzymes metabolize drugs ▯ -monoamine oxidase and cytochrome p-450 for example -liver -first pass metabolism -drug metabolism does not necessarily mean inactivation Drug-->active metabolite-->inactive metabolite Review: when janelle started college, she would feel intoxicated after half a beer. After six semesters of drinking, she needs eight beers to start to get a buzz. How can metabolism explain her transition? Pharmacokinetics: how does the drug work (chemical communication) -neuron is stimulated, releases a chemical, chemical works on another neuron and affects how that next neuron fires etc. drugs interfere with this process. they can increase/decrease amt of chemical -study of interaction of ligands(chemicals) and receptors -not all ligands interact with all receptors -1st step: ligand needs to be recognized by receptor (binding/recognition) Hormone, neurotransmitter, drug( all need to be recognized by receptor)--> -2nd step: transduction (something needs to change ex ion channel open/close, stimulation of nearby protein) gives signal value -3rd step: amplification (signal goes from receptor thru neuron then through neural circuit to other parts of brain then body etc) changes communication/increase/decrease amt of protein, release of neuroactive agents, etc. or change at genetic level, transcription lead to dna change. 1. recognition where does ligand stick 2. how does chemical signal change 3. how do we move thru system (neurons entire brain or body 4. response receptor--> transport of ions/molecules, enzyme activation/deactivation, release of neuroactive agents, transcription-->protein synthesis--> Behavioral response Brain and behavior: the neuron doctrine (Ramon Y Cajal) ▯ -1900 ▯ -nervous system is not random. rational organization ▯ -consistent communication between nerve cells. predictable. changeable. ▯ -behavior from neurons. behavior occurs because of communication of nervous ▯ system. Drugs alter behavior by interacting with neuronal communication The neuron: what is in it-multipolar neuron/typical. soma(cell body) in center which has lysosomes, mitochondria etc. dendrites come off cell body which can be simple or complex. depends on incoming communication. job is to receive info from other neurons. that signal is then integrated as excitatory or inhibitory in cell body then msg goes to axon Axon- which is inside myelin sheath. info travels down it to the terminal buttons. terminal buttons-where one neuron communicates with the next one. they link to dendrites of next neuron. cerebellum-balance and coordination. axons are short. Review: what is a neuron’s resting membrane potential? -where the neuron is while it is at rest. before it is changed by stimulus. -70 at rest between inside and outside of neuron. what causes resting membrane potential? -differences in # of sodium potassium ions of inside and outside. dif in electrical charge between inside and outside. what keeps difference in sodium and potassium? -uses energy to segregate sodium and potassium to create electrical difference in ions. What does it mean when the membrane becomes hyper polarized? -it will hinder an action potential ex action potential is -70 and it goes to -90. polarized=away from zero. resting potential is polarized. hyper-polarized=even further away from zero depolarized=get closer to 0. membrane is hyper-polarized -70 if we have enough depolarizing, we have reached threshold. it is a particular potential (if we hit it) we have action potential. specific types of NA+ and K channels open up. signal goes down axon and allows communication. -signal jumps from node to node (node of ranvier) until it reaches terminal buttons. -myelin sheath speeds it up and saves energy. The synapse: how one neuron communicate with another. secretes neurotransmitter that goes and affects activity of next neuron. action potential moves down axon, releases chemical neurotransmitter then affects next neuron and increases/decreases probability of next action potential. -synaptic cleft/synapse-small channel between neurons. neurons are not connected. goes through presynaptic then synapse then postsynaptic. inside presynaptic, neurotransmitters are in vesicles. they are storage unit for NT. they don't go into synapse. Types of receptors: -on post synaptic they interact with receptor. 2 types: metabotropic & ionotropic ionotropic: “fast or quick receptors” when nt binds, you see transduction. almost immediate change. 5 transmembrane domains. can be apart and ions pass, or together and no ions pass through. think of fingers on hand. metabotropic-slow receptors. when nt binds it is coupled to proteins. where it binds is G protein. (signaling protein) then it activates enzyme(turns something into something else) enzyme activates second messenger. (intracellular signal) neurotransmitter( extracellular signal) second messenger opens ion channel, can go to nucleus and other parts of cell, (nucleus makes stuff) 2nd messengers can change protein synthesis! change structure/long term function of neuron. ex)antidepressants: why does it take time for them to work? second messengers! they need time to change nervous system. review: solarcaine is a sodium channel blocker that minimizes pain by changing nervous system activity. why/how does it work? much research on drug addiction focuses on the second messenger cAMP in the cns. why might cAMP play a role? -sodium ions needs to exchange places with an ion. so in order to have an action potential or regulate potential you need to blow sodium across. Pka- is the ph where half the drug is ionized. ionized means the drug has a charge to it (+ or -) when drug is put in solution some degree of the molecule will be ionized. absorption: best if not ionized. lss ionized=better! very lipophilic, small molecule, little ionization. September 14th -a ligand can bind and affect activity of receptor -some drugs produce effects at allosteric sites can enhance or minimize how agonist works -do not work at same site (agonist and allosteric) Ionotropic modulation: Gaba binds to receptor and chloride ions pass through. How many ions pass through? -take GABA and measure activity. Put in placebo and have no effects, no ions passing through. Gaba binds to agonist binding site and opens ion channel and 100 ions pass through. An antagonist comes in and has no effect alone but with agonist---antagonist blocks some of agonist effect Gaba+diazepam-150 ions passing through. Possible targets for drugs: 1. change rate of synthesis 2. change amount of NT released 3. alter NT storage 4. change rate of metabolism 5. bind to receptor 6. change NT uptake 7. serve as neurotoxin September 17th Theories of addiction 3 & 5 Review: define and give example of: -acute tolerance =body gets used to it (tolerance) tolerance that develops on a single administration. ex)alcohol as you drink the level of intoxication go up and down -tachyphylaxis =several administrations ex) development of tolerance develops with several administrations. number of administrations is what matters. -cross tolerance =tolerance to morphine might transfer to another opiate -metabolic tolerance =the body gets better at metabolizing the drug so it has less of an effect. tolerance to caffeine, more coffee needed to get same effect. -pharmacodynamic tolerance =change in number of vesicles that release NTS. change in body that affects drug. presence of a drug might change an auto receptor, (up and down regulation) in UP=increase in number of receptors, the more we use the more receptors Down=decrease in number of receptors, as we use drug the number of receptors goes down. Why do people use drugs? Drug use: -when is it a problem? ▯ -society’s views ▯ (cigarettes and alcohol are acceptable. weed is not. Government says it is not ▯ okay. Pharmacologically between the three there’s not a huge difference. ) ▯ ▯ -transition from use to “addiction” Progression of drug use: circumstantial situational use experimental compulsive use use social recreational use relapse withdrawal transition in the type of drug used? ▯ -gateway hypothesis “socially accepted substances (tobacco and beer) leads to harder substances like marijuana leads to illicit substances like cocaine, heroin, lsd our goal is to stop cycle before people move onto weed. That’s why we are so strict on weed right now!! Review: lisa rarely smokes but when she is stress she smokes weed. - circumstantial situational when at a party you drink -social recreational when kelly wakes up she has to have a drink compulsive Drug abuse and dependence: -how do clinical psychologists and psychiatrists study and define problems with drugs? ▯ -Diagnostic and Statistical Manual of Mental Disorders (DSM) ▯ -published by the American Psychiatric Association -this book is continually changing. -up until 1969 homosexuality was considered to be disease how does DSM view problems with drugs: substance abuse- 1. a maladaptive pattern of substance use leading to significant impairment or distress by one or more of the following within 12 months ▯ -recurrent substance use resulting in failure to fulfill major role obligations ▯ -recurrent substance use in situations in which it is physically hazardous ▯ -recurrent substance related legal problems ▯ -continued substance use despite having persistent or recurrent social or interpersonal problems caused/exacerbated by the effects of the substance 2. the symptoms have never met the criteria for Substance Dependence for this class of substance Substance dependence- three or more of the following any time during a 12 month period 1. tolerance 2. withdrawal 3. substance is taken in larger amounts over a longer period of time than intended 4. there is a desire/unsuccessful effort to cut down drug use 5. a great deal of time is spent in activities necessary to obtain and use the substance or recover from its effects 6. important social, occupational or recreational activities are given up or reduced because of use 7. the substance use is continued despite knowledge of having a persistent or recurrent physical or psychological problem caused/exacerbated by the substance REVIEW: when aaron started college he needed one cocktail to relax but now he needs many drinks. when he cant drink he feels really bad. he’s been trying to decrease drinking. his behavior reflects: substance dependence when he drinks he drinks more than he should (short term). gets dui, mip, getting in trouble with law. violent when he drinks. conflicts with classes. substance abuse September 30th REVIEW: What is sensitization? =increase in effect of drug with repeated use ▯ -how is it different from tolerance? ▯ =in tolerance, effect goes down, sensitization effect goes up. reverse tolerance. ▯ -give an example of sensitization to a drug’s effect. ▯ =you need to smoke less weed to get high. the high gets greater and you need ▯ less drug. How can we explain addiction scientifically? Explaining drug self- administration: ▯ Three models of drug addiction (-models are inclusive, you don't have to reject one model to accept another) 1. Disease Model-important for drug treatment problems. addiction is a disease. 2. negative reinforcement model ▯ -aka physical dependence model. using drug to escape feeling bad ▯ -Koob and Lemoal’s Hedonic Dysregulation model 3. Positive REinforcement model Disease Model Moral model--> disease model -it was a move away from moral model which said a person with a problem with addiction has a moral failing and that explains addiction. if they cleaned up and got on track it wouldn’t be a problem. it’s their own fault. -addiction similar to any other disease -strengths: ▯ ▯ -not “normal”, some afflicted and others aren’t, user can’t control ▯ ▯ -can explain an abnormal behavior ▯ -obligation to provide treatment! -weaknesses: ▯ ▯ -pathogen/cause. how does it contribute to taking drug? the cause isn’t ▯ ▯ clear. ▯ ▯ -why would disease make person take drugs? Learning models: Concepts -behaviorism -concepts and principles from operant learning (Watson and Skinner) to explain drug taking behavior. ▯ -drug taking behavior follows normal rules of behavior ▯ -stimulus--> response-->outcome learning ▯ S.R.O. (-according to behaviorism, it makes sense people take drugs! you learn to like it and expect it. ) SRO example: skinner box. stimulus=light/sound etc. response follows stimulus-light on or off responding-lever being pressed a lot or not appetitive outcome-pellet dispenser. sometimes gets a pellet, sometimes not. aversive outcome-shock Appetitive positive=Positive reinforcement up responding appetitive negative=negative punishment down responding aversive positive= positive punishment down responding aversive negative=negative reinforcement up responding y axis outcome x axis contingency positive/neg reinforcement is relationship between response and outcome positive contingency=response is made and you get outcome. rat presses gets sweet treat or gets shock negative contingency=presses lever and doesn’t get pellet, or doesn’t get shock. real life examples: positive reinforcement: get an A on test and you get cookie positive punishment: child misbehaves and you spank them negative punishment/omission training: do something bad and parents take away car negative reinforcement: use drug to escape withdrawal symptoms review: Raj uses cocaine because it makes him feel good =positive reinforcement howard drinks alcohol, experiences a bad headache, and never uses alcohol again =positive punishment when sheldon uses heroin, the legal system takes away his cherished freedom =negative punishment/omission training leonard starts his day with three beers to escape from a bad headache and nausea =negative reinforcement Negative Reinforcement Model -use drugs to escape/avoid “feeling bad” ▯ -therapeutics and self medication (based off negative reinforcement) ▯ (take drugs to avoid pain/depression) ▯ -prolonged, compulsive use ▯ (howard drinks beer every day to avoid bad feeling) -withdrawal/abstinence syndrome ▯ -physiological/physical dependence(use drug to escape or avoid nausea, ▯ headache, vomiting, something med doctor would observe) ▯ -psychological dependence (“craving”) ▯ (=if you don’t get drug you have to have it. if you don’t have it you NEED it. CNS) sometimes you can have physiological and psychological, or no physiological but psychological. September 26th REVIEW Chin ho says “my brother is addicted to heroin because he is weak. if he would ‘shape up’ he wouldn't have trouble.” he supports what model? -moral model danno says “i drink a lot of coffee. when i cant drink coffee i get a bad headache. so i drink more to get rid of headache. “ -negative reinforcement Negative Reinforcement Model =psychological dependence “craving” ▯ -Koob and leMoal based on Solomon and Corbit’s Opponent Process Theory -”you pay for stuff in the end. no free ride” 0 is neutral, not feeling good or bad. A side is feeling good. from zero to A you feel really good B side is feeling bad. from zero to B you feel worse feeling good/bad are opponent factors working against each other. first time we use drug, B is generally weak. A incline stays same but B gets stronger to work against it. Hedonic dysregulation model best way to get out of B is substitution, counter conditioning to bring out of B manage anxiety/depression to get out of B hole=best! review: why might heroin cause an overdose in users with a long history of heroin use? =environment acts as stimulus to prepare body for drug. body cant compensate without it and overdose. Positive Reinforcement Model -early animal research (1950s) ▯ -self administration procedure drugs are pleasurable because of frontal cortex. helps think/plan ahead. -intravenous self administration animals don't like to self administer lsd or psychedelics september 28th REVIEW: Dr smith has trained a monkey to self administer cocaine (.03 mg/kg/inf) on a fixed ratio 5 (FR 5) schedule what is the monkey doing in her experiment? =every 5 responses the monkey gets cocaine. looking at positively reinforcing properties of coke. how many times it responds is dependent measure. now Dr smith’s monkey is responding on a progressive ratio schedule -what’s the monkey doing and what is Dr smith trying to learn? =number of responses gets greater each time. looking for break point. break point tells us how reinforcing it is. tells us expected value of drug. (what it’s worth to you) CNS what is happening in the brain? Biology of motivation: -Olds and Milner did research on animal learning -used open field (big box) where rat could go wherever it wanted. -what would make an animal not go to a certain location? -they are anesthetized and an electrode is put into amygdala -they could control how active/inactive amygdala was -when rat went to certain corner they activated electrode and fear was learned and they’d stop going to that side of box. -18/20 wandered randomly while 2 would stay in that corner where brain was activated for 18 electrode placed correctly. for 2 electrode was improperly placed and stimulated the mesolimbic dopamine pathway ▯ =go from ventral tegmental area to nucleus accumbens -when that pathway was stimulated they wanted to approach Biology of Motivation: -brain stimulation reward assay -intentionally put electrode in pathway then put in skinner box. when lever pressed their mesolimbic dopamine pathway was stimulated -animals will respond at high rates and high breaking point for that pathway drugs: indirectly or directly activates mesolimbic in some way -increase dopamine release in nucleus accumbens cocaine directly affects nucleus accumbens cannabinoids, meth, alcohol, downers, etc indirectly work to get dopamine neurons going. Biology of motivation: homeostatic input-->hypothalamus-->ventral tegmental area sensory input--> thalamus-->ventral tegmental area ventral tegmental-->hippocampus amygdala ventral tegmental-->nucleus accumbens-->cortex-->motor output -incentive sensitization theory of addiction ▯ -the more the mesolimbic is activated, they fire at higher rate/become sensitized/ ▯ release more dopamine -go from using drug because we like it to using it because we need it ▯ -goes from positive reinforcement to negative reinforcement ▯ -long term potentiation (neural plasticity) based on the neural model of addiction discussed what is the role of the... hypothalamus- thalamus- hippocampus and amygdala- mesolimbic dopamine pathway- October 1st Alcohol and sedative hypnotics drugs used to decrease distress and anxiety and to induce sleep (anxiolitic) ▯ -alcohol ▯ -patent meds (Mickey Finn) ▯ -barbiturates (pentobarbital) ▯ -benzodiazepines (xanaz and valium) ▯ -2nd generation drugs (ambien) ▯ -opiates (morphine and heroin) sleep disorders: -insomnia▯ ▯ -symptom of /comorbid with psychiatric disorders (depression) ▯ -transient insomnia ▯ ▯ -because of specific event (most common) ▯ ▯ -once stimulus passes you go back to normal ▯ -learned insomnia ▯ ▯ -bad sleep behavior ▯ ▯ -can go from transient to long term Sleep stages: -stages 1,2,3-4 (slow wave) and REM sleep 1- between awake and asleep 10-15 mins 2-brain transitions from being awake and going to sleep. desensitization 3-4 slow wave sleep you start to have dreams but are boring REM- 60-70 mins in, muscles paralyzed with eyeballs moving. weird dreams back to slow wave, then REM, back and forth background: -manage anxiety (anxiolytic) and stress ▯ -acute stress and anxiety ▯ -phobias (ex social phobia) ▯ -panic disorder and agoraphobia ▯ -generalized anxiety disorder ▯ -post traumatic stress disorder relatively high abuse liability ▯ -positive reinforcement ▯ -negative reinforcement ▯ ▯ -withdrawal symptoms -date rape ▯ -alone and or in combination with alcohol▯ ▯ -dissociative properties (information doesn’t get consolidated or put in storage, ▯ you don’t remember) Alcohol: Kinetics-how it moves thru body mouth-stomach-small intestine-blood stream-liver-brain -we have poor absorption of alcohol through stomach -alcohol gets metabolized in the stomach oxidation- liver changes alcohol to water, co2 and energy main metabolic pathway: gets into blood, if it binds to alcohol dehydrogenase it becomes acetaldehyde (toxic) -acetaldehyde explains hangover acetaldehyde dehydrogenase metabolizes acetaldehyde into acetic acid bad headache due to lack of acetaldehyde dehydrogenase because high levels of acetaldehyde meos system- if we drink a lot and get enzyme induction then we will recruit the MEOS s
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