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Biological Psychology Week 3 Notes

by: Maggie Loy

Biological Psychology Week 3 Notes Psych 383

Marketplace > University of Wisconsin - Oshkosh > Psychology > Psych 383 > Biological Psychology Week 3 Notes
Maggie Loy
GPA 3.3

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About this Document

Exam notes.
Biological Psychology
Dr. James Koch
Class Notes
Biology, Psychology, neuroscience
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This 7 page Class Notes was uploaded by Maggie Loy on Wednesday October 12, 2016. The Class Notes belongs to Psych 383 at University of Wisconsin - Oshkosh taught by Dr. James Koch in Fall 2016. Since its upload, it has received 3 views. For similar materials see Biological Psychology in Psychology at University of Wisconsin - Oshkosh.


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Date Created: 10/12/16
Bio Psych Week 3 Notes Psychopharmacology What we will cover: Drugs Administration and distribution Body membrane (blood­brain barrier) Physiology (e.g. heart rate) Neuroanatomy Specfic receptors Dose/behavior relations and safety Neurotransmitters Families Synthesis and metabolism Synthetic cells and networks of distribution Receptor types Relationship to behavior Targets of drugs Pharmacology Psychopharmacology Drugs of abuse Therapeutic drugs All other drugs E.g. blood pressure medication, antibiotics 4 Components of Pharmacokinetics Absorption Through tissues; depends on method of administration Distribution Throughout body and blood Metabolism Drug changed to inactive form by enzymes (usually in liver) Excretion  In urine, by kidneys Routes of Administration Intravenous (IV) – veins  Fast, higher risk Intraperitoneal (IP) – abdominal cavity Common in animal research Subcutaneous (SC) – under skin E.g. shots Sublingual – under tongue Oral – stomach Metabolism issues Intracerebral – directly into cerebrum Intracerebroventricular (ICV) – into cerebral ventricles Inhaled – smoked or “huffing” Recreational or “mist” delivery (asthma) Snorted – intranasal Topical – through skin Patches Intrarectal – self­explanatory  Drug Distribution Two compartment model rd Distribution equilibrium 3  body membrane Brain­blood barrier Rate of passage of a drug into brain is determined by 2 factors: 1. Size of drug molecule 2. Lipid (fat) solubility Drug Metabolism Intermediate compounds Prolonged action of drug Some are toxic Metabolism of drug in liver Active drug= fat soluble Inactive drug= water soluble Metabolism of NT in neuron Drug Excretion Liver creates inactive excretion products Urine, bile Variation in Effectiveness due to: 1. Site of action 2. Affinity (like magnetism) for receptor/ site of action *After a certain point, increasing the dose does not produce a stronger effect Run higher risk for adverse side effects Effects of Repeated Administration Tolerance Takes more drug to get the same effect Sensitization Takes less drug to get same effect Withdrawal No more (or a lot less) drug produces aversive effects *A drug’s margin of safety is reflected by the difference between the dose­response curve for its  therapeutic effects and that for its adverse side effects Therapeutic index: LD50/ED50 – tested on animals Effective dose 50% Lethal dose 50% Placebo Effect Psychological and physical effects Power of placebo is extremely strong Neurotransmitters (and Drugs) Families of neuroactive compounds Made and released by presynaptic neurons Bind to: Postsynaptic receptors Can affect ion channels Produce EPSPs or IPSPs Presynaptic autoreceptors Affect NT release via negative feedback Heteroreceptors Affect NT release Increase or decrease Drug Effects on Synaptic Transmission – fig. 4.7 AGO= Agonist Mimic/ promote action of NT ANT= Antagonist Decrease/ block action of NT Ach= Acetylcholine Sites and Mechanisms of Drug Action Agonists Facilitate (mimic) action of NT on postsynaptic cell Antagonist Hinder (block) action of NT on postsynaptic cell Effects on: Production Storage and release Receptors Reuptake or destruction Effects on Production Serve as precursor (AGO) L­dopa and DA Attempt to boost dopamine, decrease Park’s symptoms Block synthetic enzyme (ANT) PCPA and 5HT Blocks synthesis of serotonin, reduces release Effects on Storage and Release Prevent storage in synaptic vesicles (ANT) Reserpine and monoamines Blocks neuron Mimic symptoms of depression Directly block release (ANT) Botulinum toxin and Ach Botox muscles relax Directly increase release (AGO) Black widow spider venom and Ach Effects on Postsynaptic Receptors Competitive v. noncompetitive  Competitive binding Drug binds to same site as NT Direct agonist v. direct antagonist Direct stimulation (AGO) Nicotine and Ach Direct blockade (ANT) Chlorpromazine and DA Noncompetitive binding Drug binds to different site than NT Indirect agonist v. indirect antagonist Indirect stimulation (AGO) Valium and GABA Indirect blockade (ANT) Ketamine and GLU Effects on Autoreceptors Stimulation (ANT) Further suppress release of NT Apomorphine and DA Blockade (AGO) Idazoxan & NE Effects on Destruction or Reuptake Block breakdown enzyme (AGO) Leave more NT in tact MAOIs and MAs – monoamines (DA; NE; 5­HT) Block reuptake (AGO) Cocaine and DA SSRIs and 5­HT Neurotransmitter Families and Members Amino acids Glutamate (Glu) & GABA Acetylcholine (Ach) Monoamines (MAs) Catecholamines Dopamine Norepinephrine (NE) Epinephrine Indolamines Serotonin (5­HT) Peptides Endorphins and substance P­ pain signals Gases Nitric oxide (NO) Lipids Anandamine, 2­AG Endocannabinoids Gases & lipids = retrograde messengers Goes backwards Decrease NT release Neurotransmitter receptors Glutamate NMDA, AMPA, Kainate (ionotropic) Metabotropic (8 subtypes) GABA GABAa (ionotropic) GABAb (metabotropic) Acetylcholine  Nicotinic (nicotine) Muscurinic (mushrooms) Dopamine D1 (post) D2 (pre & post) All metabotropic NE Alpha1 & Alpha2 Beta1 & Beta2 All metabotropic Serotonin 5HT1A­F, P, S 5HT2A­C 5HT3 (only ionotropic) Nausea & vomiting 5HT4­7 Peptides Opioids: Mu, kappa, delta, & orphan (subtypes also) Lipids Cannabinoids: CB1 (CNS) CB2 (PNS) Amino Acid Transmitters Glutamate Primary excitatory NT in CNS (produces EPSPs) Widely distributed NMDA receptor and learning GABA Primary inhibitory NT in CNS  Widely distributed Antianxiety drugs (benzodiazepines­ like valium) Synthetic Centers and Distribution Network for Ach Nucleus basalis Releases into cortex Degenerates in Alzheimer’s  Medial septum Hippocampus, amygdala, olfactory bulb, etc. Pons Thalamus, substantia nigra, tectum, etc. Biosynthesis of Ach Precursors Acetyl coenzyme A (Acetyl­CoA) Choline Enzyme Choline acetyltransferase (ChAT) Transfers acetate ions from acetyl­CoA to choline End products Coenzyme A (CoA) Acetylcholine (Ach) Breakdown of Ach Fig 4.13 Acetylcholine­esterase (AchE) Breaks apart acetylcholine molecule in synaptic cleft Recycle choline molecules (reuptake for reuse) Biosynthesis of Catecholamines Precursors Tyrosine L­DOPA Neurotransmitters DA  NE Enzymes Tyrosine hydroxylase DOPA decarboxylase Dopamine B­hydroxylase Metabolized by monoamine oxidase (MAO) DA Synthetic Centers & Distribution Pathways  Substantia nigra Caudate nucleus, putamen, globus pallidus Degeneration  Park’s Ventral tegmental Thalamus, amygdala, hippocampus, cortex Nigrostriatal system Substantia nigra striatum Mesolimbic & mesocortical systems


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