Biological Psychology Week 3 Notes
Biological Psychology Week 3 Notes Psych 383
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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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