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PSY 245 Lecture Notes (2/2 & 2/4)

by: Kristi Dorsey

PSY 245 Lecture Notes (2/2 & 2/4) PSY 245

Kristi Dorsey
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Hello, Here are the rest of the lecture notes so far. I will post the last set of lecture notes by tomorrow night. Enjoy!
Drugs and Behavior
Mark Galizio
Class Notes
PSY 245; Drugs and Behavior; Galizio; UNCW




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This 11 page Class Notes was uploaded by Kristi Dorsey on Monday February 8, 2016. The Class Notes belongs to PSY 245 at University of North Carolina - Wilmington taught by Mark Galizio in Spring 2016. Since its upload, it has received 40 views. For similar materials see Drugs and Behavior in Psychlogy at University of North Carolina - Wilmington.

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Date Created: 02/08/16
2/4/2016 The Brain  Billions of neurons  Cerebral cortex; exterior of the brain; recently evolved part of the brain/uniquely human Recently Evolved Part of the Human Brain  Cerebral cortex  Know less about this part of the brain (can’t study it in nonhumans)  Much of it learned by accidents  Neuro imaging techniques have allowed us to study Orange Region  Where spinal cord is ascending into skull  7 = medulla  8 = reticular formation Evolutionarily Conserved Part of the Brain  Hind and midbrain structures are well conserved  Virtually same structures performing same functions in other nonhuman mammals and birds  “reptilian brain” (midbrain/hindbrain) o Communicating with/connected to higher brain structures  Serve basic functions; any vertebrate needs to survive  9 = thalamus  10 = hypothalamus o Dead center of brain o Primitive/reptilian brain o Composed of various nuclei (as opposed to single structure) Revolution in Brain Research 1. 1950s and 60s; scientists began to study the hypothalamus by lesioning (damaging a structure) to see what’s wrong after surgery 2. Minute filament-like electrode into structure o Produces 120 mV activity that simulates neural firing of neurons in that region of the brain Phil Teitelbaum  Mapped out hypothalamus  Lesion/remove structure then study animals for difference in behaviors  Damage in ventromedial hypothalamus nucleus = if animal given free access to food it would eat excessively; stimulation = will not eat  Damage in lateral hypothalamus = unless animal is given intravenous feeding it will starve to death in front of palpable food; stimulation = eats excessively  Hunger Center; pathway that initiates hunger  Satiety; pathway that depresses hunger  Different cues in your body communicate to different regions of brain to initiate hunger o Blood sugar low = hunger center (cues from stomach)  Many psychological functions seem to have a dual control Jose Delgado  Excitatory center for aggression and inhibitory center in region slightly outside of hypothalamus (amygdala/limbic structure)  Implanted electrode in inhibitory aggression center in pull’s brain  When bull charged at him he pushed a button that sent an electric signal to receiver planed in bull’s brain and activated inhibitory center  Stimulation in certain pathways in the reptilian brain structures can initiate biologically significant behavior (eating, thirst, sex, etc.) James Olds  Tried to map out rat brain  Implant electrodes in different regions; stimulate it; observe animal’s behavior  Most of the time nothing will happen when stimulated  Pleasure center is stimulation in this region of the brain o Mesolimbic dopaminergic pathway o Anywhere you stimulate along there seems to be a powerfully rewarding event o Region important in experience of pleasure/motivation o At heart of modern theories of drug addiction o Pathway runs along the limbic system o Dopamine is key neurotransmitter here o When drug produces activity in this pathway it produces pleasure that make certain drugs addictive (cocaine; dopaminergic; rewarding when administered there) o One of the first clue of how drugs might affect the experience of pleasure  Opiates not typically dopamine agonists (action on endorphins indirectly increase dopamine levels; starts chain that results in increases in dopamine) Wilder Penfield  Neurosurgeon  Stimulated areas of brain around where surgery was being done while patient was conscious; tried to observe what patient would say  Could affect memory, language, etc.; use information to figure out what regions he shouldn’t touch (if operating on a tumor for example) Prefrontal Cortex  Know less about this; outside of reptilian brain o Judgement region of brain involving impulse control  Phineas Gage; railroad worker o Tamping iron went through his eyeball and came out the back of his head (prefrontal cortex) o Didn’t lose consciousness o “complete recovery” o Inability to control impulses  Reason to think that addicts and alcoholics impulsive/inability to make good decision Henry Molaisin (HM)  Uncontrollable epilepsy early in life  Removed brain region expected to innate seizures  Free of seizures most of his life afterwards  Experienced extensive memory problems; long-term memory intact; short-term memory fine; reduced ability to go from short-term to long-term memory (couldn’t store new memories) Hippocampus  Hippocampus; small structure; Greek (named by shape)  Curvy shape (looks like seahorse)  Basic memory processes  Reward pathway  Mesolimbic dopaminergic Pharmacokinetics  How drugs get to site of action  How they’re eliminated from sites of action  EX: drugs administered (orally, IV, etc.)  drug absorbed at different rates  drug distributed once it hits blood stream; psychoactive drugs always pass blood-brain barrier  drug metabolized by enzymes/eliminated from body Pharmacodynamics  Mechanism of drug action  Happens at receptor sites at synapse Drug Development  Chemical substances accidentally found  Chemists analyzed plants for biological/psychoactive properties  Early tests are in vitro (test tube) o Today we have the technology to clone receptors o Determine what compounds bind to those receptors in test tubes o Can predict what chemical structures would bind to receptor o Chemists can then design drugs that fit into the receptor lock Institutional Animal Care & Use Committee  Animal Welfare Act; 1985; federal law o Establishes requirement that any research with lab animals must be reviewed by an (Animal Care and Use Committee) o Must include at least one veterinarian; expert in bioethics o Before research occurs a proposal/protocol must be accepted by ACUC  Can refuse protocol or require changes (EX: reduce number of animals used; require 2 weeks of anesthesia after surgery)  Weigh medical/scientific benefits against risk to animals o If it’s not clear that the human condition will be enhanced by research the risk tolerance is not as great  Classroom demonstrations and bio/psych lab work has to be approved by ACUC  Research with apes more strict; research with chimpanzees not possible in US or Europe  More strict with mammals than fish  Requirement that before a drug is tested on humans it must be evaluated in animals first  Unannounced site inspections from ACUC every 2 years to ensure compliance with protocol Drug Development  Drug must be tested in at least 2 species of animals (commonly rats and mice)  Drug company might spend $20 million to do preliminary testing  Evaluate toxicity, efficacy, and abuse potential of drugs Dose Effect Curve  Visually graphing effects of a drug  Effect of drug/response to drug on vertical axis  Dose on horizontal axis  Dose expressed in terms of unit of drug per unit of body weight o Used to translate dose across species  Gram weighs as much as a dollar bill o Most drugs measured in mg (cut $100 bill into 1,000 pieces); thousandths of a gram o Microgram = one thousandth of a mg (slice mg paper into 1,000 more pieces); LSD effective in microgram level doses  If you take a drug that’s 20 mg (orally) some will break down in gut; absorbed into bloodstream; broken down in liver; maybe 5mg left to be distribute; small amount gets to brain  Some drugs so powerful we don’t measure them in mg doses Continuation of 1-28 How does vision work?  What is vision? Light of varying wave lengths impinges on the retina inside your eye  Retina composed of specialized cells that convert light energy into an electrical signal  Electrical signal transmitted through the optic nerve then synapses into regions of the brain  Chemicals released that trigger electrical signals that will eventually reach the occipital lobe  Occipital lobe; chemical/electrical activity in this region; perceive that as vision How can a drug produce a hallucination?  Induce activity in occipital lobe  Chemical activity in occipital lobe is vision  Hallucinations understood as alteration of chemistry in occipital field Lock-Key Metaphor  Neurotransmitter molecules = keys  Postsynaptic neuron = locked; won’t fire unless it’s unlocked; delivering chemical keys that are locked neurons  Neurotransmitter “keys” open the lock and those postsynaptic neurons can fire  EX: dopamine o Cell fires; sends signal to axon terminal; releases dopamine molecules into synapse; postsynaptic receptors; axon terminals = keys that fit into dendrite receptors; once these locks are open the neuron will fire How to Study Neural Transmission  Tag a chemical so that they’re radioactive  Figure out in a vitro preparation of rodent brain what receptors they bind to  Led us to understanding of chemical code  Can clone and produce these receptors so they can be studied Mammals  Mammals have similar neurotransmitters to humans  Earthworks and insects don’t have as many as we do; if you look at ancient/simple nervous system they have same key neurotransmitters Pleasure Center  Pleasure center not currently activated  What if you inject heroin right now?  Heroin molecules penetrate blood-brain barrier  Float around synapse; don’t belong there  Receptor sites don’t know they should open to heroin because it mimics endorphins (key fits)  Cell fires and releases heroin molecules  Pathway might also be activated by some of the endorphin molecules in the synapse  User experiences intense flash/rush (orgasmic) Agonist  When a drug mimics a neurotransmitter  Binds to receptor and activates it  A lot of drugs produce their actions by binding to receptor sites that evolved to fit a natural neurotransmitter  Nicotine and LSD do that with a different receptor Antagonist  Drugs bind to receptor (key fits) but jams the lock instead of unlocking it  Lock can’t open while the drug is in the receptor site  EX: naloxone; chemical structure similar to morphine and heroin o Animal testing found no addiction effect o Thought they discovered an opiate with less addiction o When they tested naloxone it didn’t relieve pain o When given with other opiate drugs it cancels out the effects of the opiate (antagonizes) Naloxone  Opiates produce respiratory depression  If person injects a lethal dose of heroin you can quickly give them naloxone  Person will feel withdrawal symptoms because it has blocked the heroin molecules from binding to the receptor sites  Drugs differ in their affinity to receptor sites (some more strongly attracted than others)  Naloxone has a stronger affinity to endorphin receptor sites than endorphin/heroin molecules; naloxone  heroin  endorphins  As long as the naloxone is in the system, it out competes the heroin and you’re safe; when the naloxone wears off, it’s metabolized very quickly then the heroin molecules are still there and can now get into the receptor sites and do their thing Naloxone wears off in about 20 minutes so you must administer the dose several times until the person’s life is no longer threatened (heroin effects last around 4 hours)  Every ER & ambulance carries it  Freely distributed at many clinics Ionotropic Receptors  Serve as gate in cell membrane  Action potential; a neuron fires once enough ion channels open up and allow charged particles (ions) to enter the neuron  Some agonists bind to receptors an open ion channels/trigger cell firing  Some agonists bind to receptors and prevent ions from penetrating channels/prevent cell firing  When some agonists bind to some receptors they open the ion channels and let ions trigger cell firing Metabotropic Receptors  When agonist binds it releases a different chemical (second messenger)  Second messenger can open channel (delay it), can close a channel, or change genetic material/structure of neuron  Study them in research on learning and memory; long-term brain effects; second messengers are how the brain changes when learn learn/remember something How Neurotransmitters Discard Neurotransmitters 1. Metabolized by enzyme o Enzyme breaks down neurotransmitter and deactivates it by breaking it into smaller parts or changing it so that the neurotransmitter key no longer fits the lock 2. Reuptake o Recycling of neurons o Neurotransmitter in synapse taken back into axon terminal o Reuptake transports; grab neurotransmitter and shovel it back into axon terminal 2-2-16 Neural Transmission Review  Brain is chemically coded in terms of receptor sites that lock up neurons for neuron to activate another; sends a chemical key (neurotransmitters)  Drug alter neurotransmitter at synapse; direct action (mimic neurotransmitters – agonist) or bind to receptor site/block it (antagonist)  2 ways to get rid of neurotransmitter; enzyme/eliminated; reuptake (transport molecule grab neurotransmitters/bring back to synapse  Antidepressants block reuptake of neurotransmitters; act by blocking reuptake of a brain neurotransmitter Acetylcholine  First important neurotransmitter found (outside the brain)  Key chemical in how nerves communicate with muscles  Muscle Dystrophy/Myasthenia Gravis = acetylcholine dysregulation  Found in axon terminals of every neuron that communicates with muscles  Neuromuscular junction; gap between neurons that activate muscle cells where nerve releases acetylcholine  Korari (Claude Bernard) comes from skins off frogs o When animal hit by chemical it was paralyzed o Thought to put people to sleep (used to induce surgical anesthesia) o Binds to acetylcholine receptors o Agonist (inhibits muscle movement); person paralyzed but conscious/aware  Critical in movement when outside of the brain  Critical in regulation of thirst/memory when inside of the brain Monoamines  3 neurotransmitters that all share a chemical structure (amine group) st  Among 1 to be discovered and drugs that revolutionized modern psychology/mental illness  Released by adrenal gland during sympathetic arousal  Norepinephrine, dopamine, and serotonin  All 3 taken together critical in regulating human mood and emotion Norepinephrine  Identified in brain as likely neurotransmitter (1960)  Same as noradrenaline  Outside brain = regulates hunger/eating  Dopamine; precursor for norepinephrine (dopamine + chemical changes = norepinephrine) Parkinson’s Disease  Lack of dopamine in substantia nigra (“black stuff”)  Primarily found in elderly  Degenerative  Beings with difficulty in controlling fine-tuned motor movements (writing)  Hands shake  Legs gradually affected  No cure; first treatment didn’t work at all  Too much dopamine = schizophrenic symptoms  Large molecules (such as dopamine) don’t penetrate the blood-brain barrier  Those with brain injuries vulnerable to developing Parkinson’s (boxers; Muhamad Ali)  People who die from Parkinson’s had no dopamine in substantia nigra El Dopa  Precursor to dopamine  Penetrates blood-brain barrier  Converts into dopamine in the brain  Helps you gain control of motor movements within 15 minutes Serotonin  Sleep/pain  Widely distributed in brain  When released in raphe nucleus you fall asleep  Found in “pain center”  Chemical activity that produces pain involves serotonin Monoamine Theory of Mood  Depression poorly understood  Reserpine; first clue that there might be a chemical basis to depression o First drug to treat blood pressure (1940s) o Although it cures blood pressure, people quit taking it o Produces symptoms of depression (self-blame, little interest, less self-worth, suicidal ideation) o Penetrates blood-brain barrier (modern blood pressure medicine doesn’t) o Depletes brain levels of norepinephrine, serotonin, and dopamine (broken down by enzymes); induce symptoms of depression Antidepressants  First antidepressant used in clinical trials as treatment for tuberculosis (1950s) o Before antibiotics, people with TB were put in asylums (contagious; no treatment) o Medical staff reported that it wasn’t improving TB symptoms, but they were much happier o Stimulant drugs (cocaine; amphetamines); learned how they worked in 1970s; produce mood elevation; work by increasing monoamine levels o Lead to Monoamine Theory of Mood Monoamine Theory of Mood Continued  Monoamine oxidase (MAO) breaks down all monoamines  Enzymes always have –ase suffix  Stem of enzyme named in honor of what enzyme breaks down or build  Transmitters as adjectives use –ergic  First antidepressants were MAO inhibitors (inhibit body’s production of MAO)  Substantia nigra critical pathway involving dopamine; take neurotransmitter stem + –ergic = dopaminergic neurotransmitter  A lot of drugs named in terms of neurotransmitter they affect; cocaine (dopaminergic drug) MAO Inhibitors  Inhibit body’s production of MAO  Monoamines broken down gradually  Gradually build up brain levels of the 3 monoamines (stay in the synapse)  Produce a lot of negative side-effects  Modern antidepressants (SSRIS/Selective Serotonin Reuptake Inhibitor); Prozac o Blocking reuptake of serotonin  Elevation of monoamines by antidepressants treats depression Antipsychotic Drugs  Chemical (Thorazine) studied as possible dye had tranquilizing effects  Physician gave drug to people on back ward of his Schizophrenia hospital  Many cases seemed to have cleared up symptoms (early 1950s)  By mid-1950’s these drugs were being administered around the world (no one knew how they worked)  First antipsychotic drug was an antagonist that blocks the monoamines Drug Names  Chemical; named after chemicals in the drug; a o EX: acetylsalicylic acid o Found in bark of willow tree and can be isolated o Medicinal properties o Given scientific/generic name  Scientific/Generic; chemical community agrees on o EX: Aspirin o Never capitalized  Brand/slang name (patent name/bring to market it) o EX: Bayer, Excedrin o Always capitalized Thorazine/Chlorpromazine  Parkinson’s side-effects  Too much dopamine = schizophrenia  Too little dopamine = Parkinson’s; blocking dopamine receptors in motor pathways  Depression side effect  Pharmaceutical companies began to experiment with drugs that block norepinephrine and serotonin but not dopamine o Depression side effects o No longer have Parkinsonian symptoms Dopamine Hypothesis  If you have a compound that blocks monoamines but not dopamine they fail to treat symptoms of schizophrenia  Antipsychotic medicine that blocks dopamine; most potent/effective treatment for Schizophrenia  If it blocks dopamine, it treats Schizophrenia; if it doesn’t block dopamine it doesn’t treat Schizophrenia  Not all symptoms of Schizophrenia are treated; get better w/dopamine blocker; still symptoms they don’t treat Stimulant Drugs  Elevate mood (cocaine/amphetamine)  Overdose = symptoms of Schizophrenia (paranoid delusions) Endorphins  When we discovered that heroin binds to endorphin receptors and heroin blocks the receptors  Led neuroscientists to ask why the receptors are there?  Wasn’t until late 1970s that the brain’s natural heroin chemicals were found (endorphins/”internally occurring morphine”)  Action on these receptors through that pathway is how opiate drugs work GABA  Gamma Amino Butyric Acid  Brain’s principle inhibitory neurotransmitter  Found throughout brain  Critical in regulating lots of neural actions  Inhibitory neurotransmission o Making a neuron harder to fire  Excitatory Neurotransmitter o A drug that opens the channel and makes a neuron more likely to fire  GABA agonist drugs; depressants (drug would activate GABA, inhibit neural activity, and produce depressant action)  Alcohol acts through alcohol system


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