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PSYC 30 Chapters 5-7 Notes

by: Stacey Kane

PSYC 30 Chapters 5-7 Notes PSYC 309

Marketplace > Towson University > Psychlogy > PSYC 309 > PSYC 30 Chapters 5 7 Notes
Stacey Kane
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About this Document

These are the notes form chapters 5, 6 and 7.
Paul Pistell
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This 14 page Bundle was uploaded by Stacey Kane on Tuesday March 29, 2016. The Bundle belongs to PSYC 309 at Towson University taught by Paul Pistell in Spring 2015. Since its upload, it has received 28 views. For similar materials see Psychopharmacology in Psychlogy at Towson University.

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Date Created: 03/29/16
 Catecholamines o Dopamine (DA)  Dopaminergic o Norepinephrine (NE)  Noradrenergic o Epinephrine (EPI)  Adrenergic o Monoamines  Synthesis o Multi-step pathway  Regulate NT availability  Precursor: the more the precursor the more the NT  Blockade: NT level are lowered o TH is rate limiting enzyme  Regulated by:  DA and NE levels: if there’s enough the system says to stop production  Rate of cell firing: the faster its firing the more active TH is to help create more NT o Drugs  L-DOPA: drug used to help a psychiatric condition; increases level of dopamine  Alpha-methyl-para-tryosine (AMPT): TH blocker (reverses efficacious antidepressants)  Storage and Release of Catecholamines o Vesicles  Prepackaged amount  Degradation protecting o Vesicular monamine transporter (VMAT)  VMAT1: adrenal medulla  VMAT2: brain  Transport synthesixed NT to vesicle o Drugs  Reserpine: VMAT1 and VMAT2 blocker  Animals- sedation  Humans- depressive symptoms  NE and DA cannot be released from vesicle  L-DOPA reverses: creates precursor for dopamine  Amphetamine  Releases NE and DA independent of cell firing: no action potential has to arrive  Increases locomotion  Stereotyped behaviors: purposeless movements that are repeated over and over  Catecholamines and Autoreceptors o NE and DA: many receptor subtypes o D2 and Alpha2 are autoreceptors  Activation reduces Ca2+ entry  Agonists: even if there isn’t too much it will still stop release of NT  Antagonists: block auto-receptor and doesn’t stop release of NT o Opioid withdrawal  Activated NE system: increased heart rate, blood pressure and diarrhea  To treat: release agonists at auto receptor; symptoms are blocked o Clonidine (alpha2, agonist) o Yohimbine (alpha2 antagonist)  NE and anxiety  Yohmibine: can trigger panic attacks, increases anxiety  Catecholamine Inactivation o Two processes  Reuptake by DA and NE transporters  Drugs (blockers)  Tricyclic antidepressants: NE and 5-HT  Reboxetine: NE  Atomoxetine: NE  Cocaine: DA, NE and 5-HT o Metabolic Breakdown  Enzymes: COMT and MAO  Metabolites  DA: homovanillic acid (HVA)  NE: MHPG; VMA PNS  You can increase or decrease the breakdown  Drugs:  Phenelzine and tranylcypromine: MAO inhibitors (MAOIs): depression  Entacapone and tolcapone: COPT inhibitors – L-DOPA supplementation  Dopaminergic Systems o Catecholamine classification system  A1-A7: noradrenergric  A8-A16: dopaminergic o Nigrostriatal tract  SN to caudate-putamen (striatum)  Control of movement o Mesolimbic: from midbrain to cortex and limbic system o Mesocortical: from midbrain to cerebral cortex and hippocampus  Schizophrenia  Drug abuse  Nigrostriatal Damage o Two toxins:  MPTP: will cause a person to get full blown Parkinson’s in a short time  6-OHDA  Specific for catecholaminergic neurons  Bilateral lesions o Sensory neglect o Motivational deficits: won’t go for food or water, no motivation o Motor impairment: not complete  Unilateral lesion o Postural asymmetry: one side of the body works and the other doesn’t work at all o Will only happen if you have stroke, will not happen on its own  DA Receptor Subtypes o D1-d5 all metabotropic o D1 and D2 in striatum and nucleus accumbens  D2 also postsynaptic receptor o Opposite effects on adenylyl cyclase  D1 increases  D2 decreases o Work through different G proteins (G1 and G2) o Changes in cAMP alter excitability of cell  DA Receptor Agonists and Antagonists o Agonists: increases behavior  Apoorphine – D1 and D2 = behavioral activation  SKF 38393 – D1 = elicits self-grooming  Quinpirole – D2 and D3 = increases locomotion and sniffing o Antagonists: decreases behavior  Haloperidol – D2 = catalepsy  SCH 23390 – D1 = catalepsy  D2 antagonists used for schizophrenia  DA Knockout Mice o Mice lack the gene for TH in dopaminergic neurons o DA missing  KO mice lacking the DA transporter o Hyperactivity: DAT mice cannot clear S o Reduced response to cocaine and amphetamine  D1 and D2 KO Mice o D1 receptor  Reduced growth and death without moistened food  Increased locomotor and reduced habituation  Motor coordination deficits  Exhibit cognitive deficits o D2 receptor  Impaired spontaneous movement  Impaired coordination  Impaired postural control  Degree of impairment dependent on background strain o Both rd  Fatality by 3 week  Cannot be rescued by L-DOPA o D1= increase activity level o D2= decrease activity level  D3-5 KO mice o Not studied as extensively o D3- complex behavior changed  Impaired ability to inhibit behavioral response in novel situations  Failure to stop a behavior o D4 and D5- little apparent behavioral effects  D4: differ in response to psychoactive drugs o Physiological effect:  D2: elevated prolactin levels  Any DA receptor: hypertension via dysregulation of salt balance and blood pressure  Ethanol and DA KO mice o Ethanol can produce either locomotion stimulation (low doses) or sedation (higher doses) o D2 and D4- enhanced locomotor stimulation o D2- blunted ethanol-induced sedation o D1 and D2- reduced voluntary ethanol consumption  Reward pathway  Didn’t see ethanol as rewarding so they didn’t take more o A single transmitter, acting through different receptor subtypes  May influence many different behaviors and physiological functions  May play a complicated role in responses to psychoactive drugs  Locus coeruleus (LC) and NE projections o NE also plays a critical role in the PNs  Sympathetic branch of ANS (NT)  Adrenal gland (hormone)  NE in blood cannot enter brain: NE stays in the area in which they are and do not cross into the other  Adrenergic Receptor subtypes o All metabotropic o Mediate both NT (mainly NE) and hormonal (mainly EPI) o Alpha1 A, B, D, L: phospholipase C (PLC) and increase Ca2+ o Alpha2 A, B, C: decrease adenylyl cyclase = decrease cAMP and Ca2+ o Beta1,2,3,4: increases adenylyl cyclase and  Behavioral Implication Arousal o Injection of NE into LC promote arousal o LC neurons fire more rapidly when awake o NE increases time awake o Injections into medial septal area  Phenylephrine (alpha1 agonist)  Isoproterenol (beta agonist)  Behavioral Implication Consolidation of Emotional Memories o One-trial passive avoidance (emotional learning)  Increase EPI, glucocorticoids, CNS NE o Weak shock and EPI 0-10 minutes after but not later increased latencies  Increase in EPI is attached to the emotional memory o Later studies:  Implicated NE, glucocorticoids and other NTs in amygdala  Nonpsychiatirl Conditions o Beta agonist (albuterol): asthma o Alpha1 agonist (phenylephrine): colds and allergies o Alpha2 agonist (clonidine): hypertension o Alpha2 antagonist (yohimbine): impotence o Alpha1 antagonist (porzasin): hypertension o Beta antagonists (propranolol and metaprolol): hypertension and anxiety  Keep heart rate at a steady pace in order to prevent a panic attack  Serotonin (5-HT) o Popular culture o Synthesis (two steps)  Tryptophan: from dietary amino acids  Tryptophan to 5-HT is rate limiting step  Tyrptophan and the BBB o Fernstrom and Wurtman (1970s)  Fasted rates and fed protein rich meal  Typtophan blood levels elevated but not brain levels  Proteins contain more large amino acids  Ratio is critical  Fasted rats and high carbohydrate diet  Carbs trigger insulin and stimulate diet o Carbs trigger insulin and stimulate uptake of most amino acids from blood except tryptophan o Ratio is increases o Increased brain levels  Humans show similar results, but not as large  Rapid tryptophan depletion and depression relapse o PCPA  Irreversibly inhibits tryptophan hydroxylase  80-90% of 5-HT reduction for up to two weeks o Humans can be given a cocktail of amino acids without tryptophan o Leads to return of depressive symptoms  5-HT storage, release and inactivation o VMAT2- transports 5-HT into vesicles  Reserpine: VMA blocker o 5-HT1B or 5-HT1D terminal autoreceptors  Inhibit 5-HT release o 5-HT agonists  Para-chloramphetamine  Fenfluramine  MDMA o Inactivation  5-HTtransporter (SERT) and SSRIs  Metabolized by MAO into 5-hydroxyindoleacetic acid (5-HIAA)  SERT KO mice  MDMA o More potent effect on 5-HT o Initially used therapeutically o High doses deplete forebrain 5-ht and loss of serotonergic axons o Effective for severe treatment-resistant PTSD at low, controlled doses in therapeutic setting  Anatomy of the Serotonergic System o Dorsal and median raphe nuclei o Innervate virtually all forebrain areas  Serotonin Receptor Subtypes o 14 subtypes o M-HT1A: metabotropic (decreases adenylyl cyclase: decreases cell activity) o M-HT2A: Metabotropic (increases PLC: increases cell activity) o All are metabotropic except for 5-HT3 which is ionotropic  5-HT1A o Many brain areas  Hippocampus, septum, amygdala, and dorsal raphe o Located postsynaptically  Inhibit adenylyl cyclase and therefor decreases cAMP  Open K+ channels  Decreasing second messengers and takes it father away from an action potential o Agonists  Buspirone, ispapirone, 8-OH-DPAT o Antagonist  WAY 100635  5-HT2A Receptors o Cerebral cortex  Striatum, nucleus accumbers, and others o Located postsynaptically  Phosphoinositide (increases Ca++ and increases PKC) o Agonist  DOI: “head twitch” response and hallucinations  LSD: appears to stimulates receptors o Antagonist  Ketansein and ritanserin  Clozapine and risperidone (also effect DA; antipsychotics with reduced motor disturbances)  Other Receptor Subtypes o Widespread expression in nervous system and non-neural tissues o 5-HTaB and 5-HT1D and migraines  Abnormal dilation of blood vessels = migraines  Agonists (triptans) constrict blood vessels to treat migraines o 5-HT3 nausea and vomiting  Located on peripheral terminals of vagus nerve  Transmits sensory info from GI tract to brain  Chemotherapy drugs and radiation release f-HT in gut, stimulate 5-HT3 receptors and cause vomiting  Makes you not want to eat  Antagonists counteract: taken before chemo, will reduce vomiting  Behavioral and Physiological functions of 5-HT o In humans  Correlate CSF 5-HIAA or post-mortem regional 5-ht and 5-HIAA concentrations with behavior or disorders  Assess behavioral, subjective and physiological responses to 5- HT challenges (agonist, antagonists, SSRIs)  Can be injected into system and then observe how behavior is effected  Association between psychiatric disorders and polymorphisms in SERT or other receptors  Do people have mutations in these receptors? Do these mutations effect behavior?  Animal Studies o Mice born missing serotonergic neurons: do not create any serotonin  Will survive, but significant mortality  If they make it past 30 days, they will survive  Thermoregulation difficulties (when placed in the cold)  Long episodes of apnea: if given DOI, it comes back just not in the same way o Hunger and eating  Hypophagia: not eating enough, appetite depressants  H-HT1B of 5-HT2C agonists, 5-HT6 antagonists  Hyperphagia: increased appetite  5-HT1A agonists o Anxiety  5-HT1A agonists decrease anxiety  5-HT1A KO mice exhibit increased anxiety  5-HT2A and 5-HT2C agonists increases anxiety  5-HT2A or 5-HT2c KO mice exhibit decreases anxiety o Pain  Implicated in pain processing at level of spinal cord  Hypoalgesia mediated by 5-HT1B and 5-HT3: reduces pain  However, under some conditions 5-HT3 activation leads to hyperalgesia o Learning and Memory o Powerfully influenced by various agonists and antagonists  Pre-training 5-HT1A agonist (8-OH-DPAT) impair contextual fear conditioning and memory  Similar effects with 8-OH-DPAT into hippocampus  Blocked by prior infusion of 5-HT1A antagonist (WAY 100635)  5-HT4 partial agonists enhance learning and memory  5-HT5 antagonists facilitate memory on several tasks o Serotonin relates to learning and memory  5-HT and Aggression o Human aggression: intent is important  Premeditated: planned  Impulsive: frustration or threat o Animals: must operationalize o Neural circuitry has been outlined in humans and animals o All of the brains areas receive substantial serotonergic innervation  Correlate CSF 5-hIAA with aggression  Increase 5-HT via SSRI administration or SERT KO mice  Decrease 5-HT via tryptophan hydroxylase inhibition or 5-HT neurotoxin o Overall, relatively higher levels of serotonin is associated with less aggression and lower levels of serotonin are associated with higher levels of aggression  5-HT1A and 5-HT1B agonists decreases aggression  5-HT1B KO mice exhibit increased aggression o Might be working on other NT systems o Could be influences impulsivity  Prefrontal cortex balance 5-HT2A (high activity increases impulsivity) and 5-HT2C (high activity decreases impulsivity) o Rhesus monkeys and 5-HIAA  Taken four years previously  Measured levels of 5-HIAA, and then four years later saw who was dead and who was alive  Those with lower levels were much more likely to get in fights and be aggressive and more were dead, those with high levels were much more likely to be alive o Human violence and aggression are serious social problems o Low levels of 5-HIAA in the CSF  Aggression and antisocial behavior (assault, arson, murder, and child abuse) o Aggression and 5-HT agonists  Fluoxetine (SERT antagonist (boosted levels of serotonin) : decreased irritability and aggressiveness  Behavioral Effects of 5-HT (serotonin syndrome) o If endogenous tome of 5-HT is increases (either by providing pre- cursor, blocking MAO or with some agonists) a characteristic behavioral syndrome is produced. That syndrome includes:  Rats:  Fore par treading (piano playing)  Straub tail  Hind limb abduction  Rigidity  Head shaking  Resting tremor  Salivation o Human Serotonin Syndrome  Hyperserotonergic state  Can be fatal  Death can be rapid  Increased incidence since 1960s o If serotonin is only available below the raphe nuclei, you can still get serotonin syndrome o There are 5-HT terminals on motor neurons o If we record from a motor nucleus from a rat and apply glutamate, we observe an increase in unit firing o If we then apply 5-HT alone, we see no effect on unit firing o If we apply both 5-HT and glutamate we see a marked increase in unit firing o 5-HT modulates firing at motor neurons  Acetylcholine (ACh) o Curare o ACh: life sustaining, but deadly  If you don’t have enough you die, but if you have too much you die o Only synthesized by a small number of neurons (cholinergic)  Synthesis of ACh o Formed in a single step  Choline: in diet and liver  Acetyl CoA: metabolism of sugar and fats in cells  ChAT only found in ACh neurons  Choline + Acetyl CoA = ACh o Rate of synthesis  Availability of precursors: more precursors means more ACh  Rate of cell firing: more firing means more ACh  o Decreased ChAT??? o Increased choline and Alzheimer’s disease gave no improvement  Cholinergic Synapse o Couple thousand per vesicle o Vesicular ACh transporter (VAChT) o Drugs  Vesamicol – VAChT blocker  Black widow venom increases PNS ACh release: more is released into  synapse  Leads to sweating, nausea, pain, salivation, tremors  Botulism decreases/prevents ACh release  Paralysis  ACh Metabolism o AChE carefully controls ACh levels  Presynaptic: excess ACh levels  Postsynaptic: released ACh levels  Muscle cells secrete AChE o Choline undergoes reuptake o Choline transporter KO mice  Die within one hour  Choline pulled back into cell is very critical for body to know levels of  ACh o Drugs  Hemicholinium­3 (HC­3): choline transporter blocker: reduces amount of  ACh where levels of other NT would increase  Physostigmine (isolated from Calabar beans): blocks AChE: levels of ACh increase  Slurred speech, mental confusion, hallucinations, loss of reflexes,  convulsions, even coma and death  Botulinum Toxin – Deadly poison, Therapeutic Remedy, and Cosmetic Aid o Human lethal dose: 0.3 micrograms o Interferes with ACh release at neuromuscular junctions o Therapeutics  Strabismus: cross eyes  Blepharospasm: eye spasms  Hemi facial spasm: half the face spasms  Spastic cerebral palsy  Dystonias o Botox  Myasthenia Gravis o Autoimmune disorder  Antibodies for muscle ACh receptor  Receptor down­regulation (less sensitivity) o Muscle weakness and fatigue o Neostigmine and pyridostigmine  Synthetic physostihmine analogs (do not cross blood brain barrier)  Less AChE (enzyme that metabolizes ACh) increases ACh activity  Stress, pyridostigmine and the brain o Sarin and Soman  Irreversible AChE inhibitors  Nerve gas o Pyridostigmine bromide (PB)  Reversible AChE inhibitor protects AChE from permanent inactivation by nerve gas  Low blood brain barrier penetration o Stress and the blood brain barrier  Mice given forced swim test  Ten minutes later various doses of PB  Stress temporarily unblocks the blood brain barrier  Found that PB was getting into the unblocked BBB  o Gulf War Syndrome  ACh Synapses in the Parasympathetic and sympathetic ANS o ACh is widely involved in neuromuscular and autonomic systems o Drugs that interfere with ACh extremely powerful and can be toxic  Brain cholinergic Pathways o Basal forebrain cholinergic system (BFCS)­ cognition o Balance between ACh and DA in striatum contributes to PD motor symptoms o Dorsolateral pons­ substantia nigra (nicotinic receptors)  Brainstems and thalamic areas (arousal, sensory processing, and initiation  of REM  Cholinergic Interference o Atropine and scopolamine: ACh muscarinic receptor and antagonist o 192­lgG­saporin: neurotoxin specific for BFCS ACh neurons o Signal detection task o May be more attentional  ACh Receptor Subtypes o Two families: stimulated by alkaloids  Nicotinic   Muscarinic  Nicotinic o Neuromuscular junctions in ANS and certain neurons o Ionotropic o Na+ and Ca++ enter (increase excitability) o Fast excitatory response in CNS and PNS o Located pre and postsynaptically o 5 subunits (variations produce subtypes)  Both alpha units must be activated o Desensitization  Continuous stimulation = desensitization  Channels remain closed  Depolarization block: if long enough, resting membrane potential  lost and only restored when agonist removed  Succinylcholine (ACh agonist): powerful muscle relaxant resistant to  AChE  D­tubocurarine (peripheral nicotinic receptor antagonist): blocks  Active ingredient in curare  Muscarinic o Five subtypes (m1­M5) o All metabotropic  Some activate phosphoinositide  Some inhibit cAMP  Some stimulate K+ channels o Widely distributed  Brain  Neocortex and hippocampus (cognition)  Striatum (motor function)  M5 KO mice and opiate reward: didn’t show conditioned place  preference unless it was a high enough dose; mice who are  addicted do not go through withdrawal  PNS  M2 Cardiac heart muscle decreases heart rate  M3 smooth muscle of organs increases  Secretory responses: regulating glucose and insulin o Compounds:  Agonists: parasympathomimetic agents  Muscarine from Amanite muscaria  Pilocarpin from Pilocarpus jaborandi  Arecoline seeds of the betel nut palm o Ingestion leads to salivation, sweating, pinpoint pupils,  severe abdominal pain, strong smooth muscle contraction  and painful diarrhea  Antagonists: parasympatholytic agents  Atropine from deadly nightshade  Scopolamine from henbane o “twilight sleep” you’re awake but you don’t remember  anything


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