PSYC 3458 Midterm: BIO PSYCH- Exam 3 Study Guide
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Department
Psychology
Course
PSYC 3458
Professor
Jennifer Honeycutt
Semester
Fall

Description
BIO PSYCH: Exam 3 Study Guide Acetylcholine (ACh): At neuromuscular junction Only NT in motor division (somatic) Alzheimer's pathology 2 regions of ACh origination: 1) Basal Nucleus 2) Pedunculopontine Nucleus/ lateral tegmental nucleus Dopamine (DA): Regulates motor and motivational behaviors Target of many drugs: -antipsychotic drugs—> antagonists, increase reuptake, increase breakdown degeneration of DA neurons leads to Parkinson's: neurons can't make enough dopamine 2 regions of DA origination: 1) Substantia Nigra- those are the ones that project to accumbens and striatum for motor behavior 2) Ventral Tegmental Area (VTA) Serotonin (5-HT): Modulatory—> increases plasticity (aids in learning) Implicated in Depression/Anxiety SSRIs stop the breakdown/reuptake of serotonin—> more is left in the synapse—> make more receptors to bind all the serotonin 2 regions of 5-HT origination: 1) Dorsal Raphe Nuclei 2) Caudal Raphe Nuclei Norepinephrine (NE): Arousal-inducing NT Synthesized from Dopamine Interacts with adrenergic receptors: -amphetamines increase release of norepinephrine Region of NE origination: Locus Coeruleus Monoamines: Monoamine NTs share a common structure and cell bodies originate in the brainstem and send projections throughout the brain Catecholamines: -Dopamine (DA) -Norepinephrine (NE) -Epinephrine (EPI) Indolamines: Serotonin (5-HT) Tyrosine, L-Dopa, Dopamine, Norepinephrine: all have similar structure simple step-by-step structure to get from tyrosine to norepinephrine since they share this base structure, they act in similar ways What is Pharmacology? studying the actions of drugs on living organisms Neuropharmacology drug-induced changes in the functioning of neurons Psychopharmacology drug-induced changes in behavior Neuropsychopharmacology drug-induced changes in the functions of select neurons that influence specific behaviors Drug Actions V. Effects Drug Actions: molecular changes that are produced by drug binding at a receptor; what happens at a molecular level when a drug binds? what is the cascade of events in the cell? Drug Effects: molecular changes that alter physiological/psychological function Drug Effects: multiple effects on function due to actions at a variety of sites oral ingestion: no specificity--> if it's getting to the brain, it's going everywhere Therapeutic Effects: drug/receptor interactions that produce desired effect Side Effects: misc. (i.e. downstream) and varying drug effects tremors, weight gain, etc. Agonist Versus Antagonist Agonist: -Mimic MT -Drug molecule works like NT (e.g. nicotine binds to ACh receptor and acts like ACh) Antagonist: -Block receptor complex -drug molecules block receptor, preventing endogenous NT from acting/binding Agonist: actions -promote synthesis in pre-synaptic neuron -stimulate pre-synaptic release -activate post-synaptic receptor -inhibit reuptake of NT -inhibit enzymatic degradation -block pre-synaptic autoreceptors Antagonist: actions -prevent synthesis in pre-synaptic neuron -block pre-synaptic release -block post-synaptic receptor -active pre-synaptic autoreceptors Autoreceptors: regulate the amount of NT released from the axon terminal into the synaptic cleft drugs that activate presynaptic auto receptors reduce amount of NT released (antagonist action) drugs that inactivate presynaptic auto receptors increase amount of NT released (agonist action) Depressants: -decrease in cognitive/behavioral activity -alcohol, barbiturates (sedatives), benzodiazepines (tranquilizers), marijuana Stimulants: -general increase in alertness and elevated mood -nicotine, caffeine, amphetamine, cocaine Hallucinogens: -alter sensory perception -marijuana, LSD, PCP, ketamine Opiates: -produce analgesia and euphoria -pain-reducing effect -morphine, codeine, heroin, opium Factors that influence drug action in CNS: -chemical structure -dose -bioavailability (amount in blood that is free to bind to target) Factors that contribute to pharmacokinetic component of drug action: -route of administration -absorption and distribution -binding characteristics -inactivation -elimination/excretion -Drug administration—> absorption and distribution—> binding—> inactivation—> excretion (see PPT image) Administration: Determine how quickly/much is liberated and absorbed into blood, how quickly it reaches target, and how quickly the drug effect occurs Liberation: release of drugs into a system from an administered form -drugs mixed with excipients (chemicals) so drug can exist in different forms—> drug formulation (e.g. sustained release Routes of Administration: Oral/per os (PO) -Most common; difficult route- must survive stomach Intravenous (IV) Subcutaneous (SC) -under the skin Intramuscular (IM) -flu shot Rectal Intraperitoneal (IP) -into the cavity in the abdomen and is absorbed from there Gaseous/Inhalation Narcan: Used to combat an opiate overdose Competitive antagonist Knocks off the opiates from opiate receptors and reverses the overdose Very safe drug Give it inter-nasally —> gets to the brain much faster Absorption and Distribution: Movement of drug from site of admin to blood circulation—> influenced by route of admin PO- Oral Administration: Popular- safe, economic, comfortable Capsules, pills, liquids Must dissolve and pass through stomach wall to reach capillaries -must be resistant to strong acid/enzymes -not fully absorbed until they reach small intestines PO absorption influenced by: Amount/type of food First Pass Effect -absorbed into blood; go to liver (reduces amount of drug available) -rise slowly and produce irregular/unpredictable levels IV- Intravenous Administration: Most rapid/accurate -circumvents stomach and first pass effect Hazardous Quick onset—> reaches brain almost instantly -little room for corrective measures in event of dose problem Sterility of injection; could lead to infection Dissolving of drugs in fillers may pose hazards (e.g. allergies) Route of Admin and Absorption: Route of administration alters rate of absorption Identical doses of drug administered by different routes can yield different concentrations of drug in the blood over time Elimination: Elimination: duration of effectiveness before drug is broken down/inactivated Half-life: amount of time it takes to eliminate 50% of the drug drug metabolism: biotransformation -typically occurs in liver; broken down into metabolites Biotransformation:
 Inactivates drugs and makes them more water soluble Phase I: -modification of parent structure (oxidation or hydrolysis) produces a polar [charged] metabolite -can be eliminated from body via urine Phase II: -conjugation with salt or amino acid -produces ionized biologically inactive molecules Toleranc e: Repeated admin—> diminished effect Requires increased dosage to maintain effect Withdrawal are opposite of drug effect (accompanies tolerance) Can result from decreased binding or reduced action Can lead to addiction (physiological and psychological need) Tolerance DOES NOT mean addiction Sensitization: Repeated admin—> heightened effectiveness Actions of Psychoactive Drugs: Either act directly on the receptors like the neurotransmitter (agonist; e.g. nicotine) Block endogenous neurotransmitter action (antagonist; e.g. claritin is an anti-histamine that blocks histamine receptors; scopolamine is an anti-cholinergic that blocks muscarinic ACh receptors) Increase release of neurotransmitter (e.g. amphetamine increases dopamine and norepinephrine release through a myriad of reactions at the actual synapse) Block reuptake (e.g. cocaine blocks dopamine reuptake; Prozac blocks serotonin reuptake)—> more in the synapse leads to more binding Addiction: physiological and psychological need for the drug Withdrawal: physical and psychological symptoms opposite from drug actions Opponent-Process Theory of Addiction: Overstimulation—> opposite compensation Body strives to maintain homeostasis -Drug produces changes ("A-Process") -Body tries to reduce the change by producing opposite effects (B-Process) Opponent-Process Theory: Tolerance As drug is continuously used, the strength of the B-Process increases (body's response to drug) Body becomes tolerant to the drug, and it is therefore less effective Tolerance fuels addiction: enjoy the drug—> take it often—> same dose becomes less effective—> take even more to get the same effect—> take even more as tolerance increases—> addiction Opponent-Process Theory: Addiction Need more A-Process "high" to counteract strengthened B-Process "low" Therefore, use more and more of the drug Overdose (brain/body is too saturated with the drug and can no longer compensate) Addiction is cyclical Opponent-Process Theory: Withdrawal When drug is removed (A-Process) body only has strengthened opposing B-Process Effects opposite to those induced by a drug Psychoactive drug releases an unnaturally high volumes of a particular chemical into the brain—> the brain compensates by limiting its natural production of the surging neurotransmitter—> when the drug usage stops the brain finds itself with a shortage—> the shortage causes the experience of observable withdrawal symptoms Most commonly abused drugs: nicotine, cocaine, heroin, prescription drugs, amphetamines, weed, alcohol, LSD, painkillers, caffeine Caffeine: Most widely used drug (~80% of adults drink 3 cups of coffee per day) Absorbed within 30 minutes, effects peak after 2 hours (half life of 3-5 hours) Adenosine receptor antagonist (role in sedation) -increase alertness, decreases fatigue, eases breathing -high doses can cause irritability, insomnia, nervousness Nicotine: CNS stimulant drug found in cigarettes and tobacco Stimulant effects: feelings of alertness/irritability, hunger suppressant; increased blood pressure/heart rate ACh agonist that binds to 'nicotinic' receptors Endogenous neurotransmitter for nicotinic receptor is ACh; nicotine mimics effects First it moves to the lungs where it is absorbed into the bloodstream—> the heart pumps it through the body, including the brain—> nicotine easily moves from the bloodstream into the brain Alcohol: CNS depressant (w/ stimulant effects) Enhances effects of GABA (increases Cl- influx) Global inhibition (inc. reduced action of glutamate) Increase dopamine and serotonin release Biphasic Marijuana: Hallucinogenic Drug Most commonly used illegal drug Active ingredient: THC Acts at cannabinoid receptors in the brain -endogenous neurotransmitter: anandamide Alters perception; impair memory and attention Amphetamines: Stimulant drugs including methamphetamine and methylphenidate (ritalin) Produce feeling of alertness and euphoria Increase the release and activity of dopamine and norepinephrine neurons—> make us focused and/or hyperactive Requiem for a Dream -amphetamine abuse (diet pills) Opiates: Any drug with properties similar to opium -Morphine CNS effects include analgesia, euphoria, sedation, respiratory depression -Heroin Synthetic and dangerous derivate of morphine (10x more powerful) Highly conductive to abuse and addiction Using needles—> disease transmission Opiates: Mechanisms of Action: 4 opiate receptors -Mu opioid receptor (pain analgesia) -Kappa (bind enkephalins in spinal cord) -delta (alter affect and euphoria) -sigma (dysphoria; feelings of discomfort) Endogenous Opiates -enkephalins, beta-endorphins, dynorphins Reversing an opiate overdose: Naloxone (Narcan)- competitive antagonist Drugs and Context: Siegel et al (1982) -individuals taking their "typical" dose in normal environment tolerate the drug better than same dose in a novel context Pavlovian Conditioning Agonist Substitution: Safer drug with similar chemical composition [methadone for heroin addiction; nicotine gum/patch] Antagonist Treatment: drugs that block or counteracts the effects of a substance [naloxone (mu-opioid receptor blocker for opiate overdose)] Aversive Treatment drugs that make ingestion of abused substances very unpleasant [antabuse for alcoholism; silver nitrate for nicotine addiction] Neuroscience of Addiction: Cycle: Drug euphoria (positive reinforcement- activated reward pathways)—> neuroadaptations (withdrawal and tolerance- protracted hedonic dysregulation)—> drug craving (negative reinforcement- dysregulated reward pathways)—> loss of control (denial/poor decision- making, hypofrontality/low D2 + reduced gray matter density)—> drug administration + drug-seeking behavior (failed impulse suppression What is "Normal"? -"typical" is a better word -there is no "normal": there is "typical development" -"neurodiversity": everyone is very different, even at the neurological level What is “Abnormal"? -deviations that are maladaptive -negatively hindering -subjective -culturally-based -'abnormal' does not necessarily mean 'disordered' -however, some individuals meet a specific criteria (e.g. DSM-5) identifying them as having a psychological disorder -now disorders are considered on a spectrum What Causes Psychological Disorders? There is no known singular cause; could be a cause of many different underlying issues Many different perspectives of how they come about: Medical Psychodynami
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