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Chapter 1

by: Stacey Kane

Chapter 1 PSYC 309

Stacey Kane
GPA 3.4
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Chapter 1 class notes
Paul Pistell
Class Notes




Popular in Psychopharmacology

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This 9 page Class Notes was uploaded by Stacey Kane on Monday February 8, 2016. The Class Notes belongs to PSYC 309 at Towson University taught by Paul Pistell in Spring 2015. Since its upload, it has received 42 views. For similar materials see Psychopharmacology in Psychlogy at Towson University.

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Date Created: 02/08/16
 What is psychopharmacology? o Systematic study of drug­induced changes in mood, thinking and behavior o Classic view: drugs­> behavior o Enlightened view: drugs­>brain­>behavior  Drug­>Brain­>Behavior o Drug:  A chemical that is not made in our body  Is not essential for normal biological processes  Affects normal biological processes o Behavior:  The measurable reaction of an organism to some internal or external  stimulation  Measure the unobservable  Psychoactive drugs: chemicals that induce psychological effects by altering the normal  biochemical reactions that take place in the nervous system o Key factors:  Chemical structure  Dose: bigger the dose the bigger the reaction  Time: morning vs. afternoon; before or after food  Frequency: once a day vs. multiple times a day o 3 other ingredients:  Set: psychological makeup and expectations of individual  What do I expect this drug to do to me?  If you expect a drug at a certain level to make you react a way it  just might make you act that way  Setting: social and physical environments  Environmental cues can have a huge influence over our behavior  Individual biochemical makeup: genes and environment  Humans are not unique o Self­administration in rodents & nonhuman primates o Preference for alcohol o Birds & fermented berries o Bees & stupefying nectar o Llamas & coca leaves o Ant & beetle herds  Modern Psychopharmacology o Extracts from flora and fauna  Opium  Morphine  Cocaine  Heroin o Amphetamines: first major synthetic drug o Popularity of psychedelics in 1960s  LSD & PCP: not naturally occurring, have to be made in lab o First forays into relationships between drug variables and psychological  processes, e.g. mental illness  Jacques­Joseph Moreau de Tours “Hashish and Mental Illness”  Role of context  Charvel & Opium in animals  Individual’s history, dose, tolerance route of administration  Freud “Uber Coca”  Mental stimulant  Digestive disorders  Appetite stimulant  Morphine and alcohol addiction treatment  Asthma treatment  Aphrodisiac  Local anesthetic  Albert Hoffman & LSD o However still no concerted effort to study their influence on cognition, emotion & behavior o Pharmacological revolution  Development of first antihistamine  Promethazine o Surgery: given before to keep calm o Schizophrenia  4560 RP­ chlorpromazine (thorazine)  Reserpine: antipsychotic  Meprobamate: anxiolytic  Iproniazide: antidepressant (MAOI)  Imipramine: antidepressant (tricyclic) o Understanding Drug Use  3 Important reasons  Recreational use and abuse are persistent phenomenon  Use of drugs as treatment for psychiatric disorders has become  extremely common  Drugs are tools for unlocking the mysteries of the brain  The Science of Drug Action o Drug action: specific molecular changes that are brought about by the result of a  drug  Change neurotransmitter action etc. o Drug effect: alterations in physiological/psychological function  Ex. Relieves depressions relieving anxiety o Site of action may be very different from drug effect  Atropine vs. morphine in pupil dilation  Where it is delivered doesn’t always mean that’s where the reaction is  There has to be some type of domino effect to change the effect of the  drug o Drugs act at a variety of target sites  Therapeutic effects vs. side effect (amphetamine­like drugs, narcolepsy vs. weight loss)  Drugs can help in one area and cause a side effect, and in another  situation be reversed  We take a drug for a specific reason but the drug can have a many target  sites and effect/change many things  Goal: trying to reduce side effects and have more selective target sites o Specific drug effects  Biochemical effects o Nonspecific drug effects: not based on chemical effects  Placebo effect  Double­blind studies  When you trial a new drug the experimenter might give off clues  and end up treating participants differently  Drug Names o A company develops a drug and submit it for patent and therefore gets a code  name o It will also have a chemical name for the chemical makeup  o Generic name: the general drug name o Brand name: after patent is up anyone can buy drug and therefore you can get the  same drug that is different in appearance but is same in the makeup o Street name: for drugs that can get abused  Haramacokinetics o Bioavailability: amount of drug free to bind at target sites  5 important factors:  Drug administration: pill, injection, patch­ will determine how  much drug is left and how it will get to target site  Absorption and distribution: Drug has to get from site of  administration to blood stream (may need to go through intestines)  Binding: Binding at target sites (neuron receptors, hormones or  neurotransmitters) or inactive storage depots (bone and fat and in  here it has no action)  Inactivation: breaking down so they are no longer active (liver)  Excretion: Intestines, kidneys, lungs sweat glands etc. (excretion  products: feces, urine, water vapor, sweat, saliva) o Pharmacokinetics: dynamic factors that contribute to bioavailability  Routes of Administration o Entoral  Oral (PO): most popular; variable in how much actually becomes  bioavailable  Rectal o IV: Straight into blood vessel o Intramuscular (IM): right into muscle o Intraperitoneal (IP): not common in humans; into the stomach cavity and around  that general area o Subcutaneous (SC): right under layer of skin o Inhalation: asthma inhalers, right into lungs and capillaries o Transdermal: Patch on the skin o Infusion pump  Introcerebroventricular: doesn’t matter entry point, but it cannot enter  brain so it has to be administered through a needle to the brain  Intracerebral: directly to one specific area in the brain o Gene therapy: attaching drug to virus and virus go into the DNA of cells and  changes the way the DNA functions  Drug Absorption o Factors that modify:  Route of administration  Transport across membranes  Delivered in IV this does not matter  Lipid solubility  Passive diffusion & concentration gradient  Dissolves in fat and can move across membranes easily  Ionization  Acidity/alkalinity (pH) (1­7  basic, 7­14 acidic)  Intrinsic property of molecule (pK) o At what level is 50% ionized  o A weak acid in a strong acid doesn’t become ionized  The more ionized the less lipid soluble   A weak acid in a weak acid cannot enter stomach and once it  makes it into intestines, it cannot reenter blood stream  Most drugs don’t dissolve in water, so they become ionized but not completely  Others  Intestinal area: intestines are longer and therefore drug will stay in  intestines longer o Less may make it in initially, but with time the same  amount may be able to enter intestines  Fluid volume: size, gender, children o Drugs tend to be more potent in women than men o Children need much smaller doses of drugs  Drugs Distribution and Selective Barriers o In general, distribution dependent on blood flow o Blood­Brain Barrier  Semi­permeable not impermeable  Reduced ionized (water­soluble) but not non­ionized (lipid­soluble molecules) can get through  Not complete  Area postrema in medulla – very sensitive to toxins and allows  toxins to be identified o Once detected brain will cause vomiting  Medan eminence of hypothalamus – feedback that helps determine levels of hormones o Placental Barrier  Allows exchange of nutrients from digested foor, O2, CO2, fetal waste  products and drugs  Similar properties to other cellular barriers  Critical implications for developing fetus (fetus is not fully developed yet  and exposure to certain toxins ca cause damage)  Acute toxicity: drugs reach fetus but are not completely  metabolized  Teratogens: agents that induce developmental abnormalities; if  ingested by mother the fetus can develop developmental problems  Depot Binding o Takes drug in and makes it inactive but does not change drug  When drug seeps out, it is still the same and has all the same effects o Occurs at inactive sites (albumin, muscle and fat) o Drugs taken orally will not 100% reach blood stream because of these spots o Significant impact on magnitude and duration  Reduced concentration  Competition for sites: alcohol gets taken up by depot binding spots and if  there is Xanax in these spots, the effects of the alcohol will speed up and  can change  Cannot be altered by liver enzymes  Can be responsible for rapid action/inactivation  Biotransformation, Elimination & Bioavailability o Drug clearance: usually exponential  First­order kinetics and half­life  Half­life: amount of time that has to pass in order for drug to be  reduce for half after initial dose  Dependent on concentration  Determines dosing regimen  Zero­order kinetics (alcohol)  Alcohol doesn’t matter how much you drink it will always go out  at a steady pace  Biotransformation and Liver Enzymes o Two Phases  Phase 1: nonsynthetic modification due to oxidation, reduction or  hydrolysis  Drug doesn’t go through a major alteration  Usually metabolite less liquid soluble and often less active  Compound that is less biologically active but still active  Phase 2: Modifications are synthetic reactions requiring combination with  another molecule  Metabolite of drug is very not lipid soluble (less likely to move  across membrane)  Getting out of system becomes an issue  Metabolite less lipid soluble due to high ionization and almost  always biologically inactive o Some drugs go through phase one and/or phase two  Can repeat phases after it becomes a different metabolite o Microsomal enzymes (cytochrome P450)  Usually nonspecific  Can be responsible for metabolizing many metabolite  Enzymes can change over time  Factors influencing drug metabolism o Enzyme induction repeated drug use increases liver enzymes  Carbamazepine and oral contraceptives  Cigarette smoke and antidepressants or caffeine o Enzyme inhibition: direct inhibition of enzyme action  Monoamine oxidase inhibitors (MAOIs) & tryamine o Drug competition: limited number of enzyme molecules  Limited pool of enzymes  Some drugs compete for the same enzymes  Alcohol and other sedative­hypnotics (barbiturates or valium)  Combination of two drugs may not be what is expected o Individual differences (genetics, age, gender)  Genetic polymorphisms for drug metabolizing enzymes  Some have more and some have less  Doesn’t always line up with eating metabolism  Age: liver and kidney function  Gender and alcohol  Females have less enzymes that break down alcohol  Kidney and ionization  Kidney is main way to get rid of drugs  Can kick back ionized drugs back into system  Pharmocodynamics: Drug­Receptor Interactions o Study of physiological and biochemical interaction of drug molecules and target  issue o Receptor: large protein molecule and initial site of action for ligands  Where drug attaches to o Ligand: molecule that binds to a receptor with some selectivity  Extracellular receptors: coupled to ion channel or a G protein and alter cell activity  Located outside cell wall and drug does not have to enter cell  Changes the weather or not a cell sends a signal onto another cell  Intracellular receptor: found in cytoplasm or nucleus and alter gene  expression  Drug has to get through membrane  Almost always primarily change gene expression o Gene expression can change many things (number of  receptors, wiring etc.)  Extra and Intra Cellular: Common Features o Ability to recognize specific molecular shapes  Lock and key analogy  Agonist (high affinity and high efficacy; bind to receptor and cause something to happen) vs. antagonist (has high affinity but low  efficacy; binds to receptor but doesn’t change anything except  agonist cannot attach)  Affinity vs efficacy (potency)  Partial agonists (bind well but don’t cause as much change)  Inverse agonists (can be partial or full, but cause opposite effect;  ex. something that would normally go into cell is now coming out  of cell) o Ligand binding is temporary  Very rarely doesn’t detach from cell o Binding produces physical changes  Opening channel, changing DNA, causes new connections in neurons etc. o Receptors are not permanent   Changes in sensitivity (more or less of an effect)  Changes in number (slower)  Up­regulation or down­regulation o Changes in number of receptors available o Receptor subtypes (therapeutic vs. side effects)  When drug hits a receptor it was not made to hit will cause a side effect  Dose­Response Curves and Receptor Activity o Dose­Response curve  Threshold dose  ED50 (1/2 maximal effect)  Dose that relives 50% of symptom (ex. Pain)  ED100 (maximum effect)  Dose that relieves 100% of symptom  Potency (same effect= smaller dose) o Dose response curves can be used to calculate the therapeutic index (TI)  TI= TD(toxic dose)50/ED50 o Antagonism  Competitive Antagonists  Compete for same receptor as drug  Drug can outcompete o If more drug is in system than antagonist, it won’t be  effected as much  Maximum potency still possible  Important tool o Drugs are invented and now we are better at knowing  where they are attaching  o Antagonists known to attach at certain point will be  released to see if drug reacts/attaches somewhere else  Non­competitive antagonists  Does not compete for receptor  Maximum potency usually not possible  (Biobehavioral interactions):  Physiological antagonism: two drugs act in distinct ways to counteract  each other  Drug A – Drug B   Additive effect: outcome equals sum of each individual effect  Drug A + Drug B  Potentiation: combined effects greater than the sum of their two parts  Drug A + Drug B ( reaction is much higher than in an additive  effect)  Chronical Drug Use and Tolerance o Tolerance: diminished response after repeated administration  The dosage you need to cure symptom will increase over time   Reversible when drug use is stopped  Dependable on dose and frequency: lower dose and frequency means  slower tolerance reaction  Not all drugs develop the same type of tolerance   Don’t develop tolerance to side effects  Cross­tolerance: when tolerance to one drug diminished effects of another  drug (alcohol and phenobarbital)  Acute tolerance: tolerance in a single session (alcohol)  Types of Tolerance o Metabolic Tolerance (drug disposition tolerance): repeated use of the drug  reduces amount available at target tissue o Pharmacodynamic tolerance: most dramatic; nerve cell function compensates in  repeated presence of drug. Not due to altered drug concentration or metabolism o Behavioral tolerance:   Involves learning and adaptation  Body recognizes environment and gears up to alter body in anticipation of  drug  Tolerance only observed in same environment where the drug was taken  Pavlovian or classical conditioning:   “anticipatory” compensation  Can be in both directions  Subtle chances may be similar to pharmacodynamics tolerance  Operant conditioning: alcohol and motor tasks o State­dependent learning  Drug effect may become part of the environment o Sensitization  Enhancement of drug effects following repeated administration o Cocaine & stereotypic behavior o Dose­dependent o Conditioning important o Cross­sensitization can occur o Persist after long abstinence  Pharmacogenetics and Personalized Medicine o Study of genetic basis for drug variability  Identify genetic factors conferring susceptibility to specific side effects  Predict therapeutic response  Adjust dose levels  Pharmacokinetics  Genetic polymorphisms and target sites  Expensive and limited facilities


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