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by: Tremayne Beer

Neuropsychopharmacology PSYC 7705

Marketplace > University of Memphis > Psychlogy > PSYC 7705 > Neuropsychopharmacology
Tremayne Beer
University of Memphis
GPA 3.84

Charles Blaha

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Charles Blaha
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This 13 page Class Notes was uploaded by Tremayne Beer on Friday October 23, 2015. The Class Notes belongs to PSYC 7705 at University of Memphis taught by Charles Blaha in Fall. Since its upload, it has received 136 views. For similar materials see /class/228445/psyc-7705-university-of-memphis in Psychlogy at University of Memphis.

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Date Created: 10/23/15
PSYCHOSTIMULANTS COCAINE AND AMPHETAMINES Classification of some CNS stimulants Class Mechanism of action I Examples Behavioral stimulants Augmentation of Cocaine norepinephrine and dopamine Amphetamines Methylphenidate Ritalin Pemoline Cylert Phenmetrazine Preludin Clinical antidepressants Blockade of norepinephrine reuptake Imipramine Tofranil Amitriptyline Elavil Increased norepinephrine Tranylcypromine Parnate secondary to MAO inhibition Blockade of serotonin reuptake Fluoxetine Prozac Legal recreational drugs Caffeine Nicotine Blockade of adenosine receptors Stimulation of acetylcholine receptors Psychostimulant Effects elevated mood euphoria and alertness reduced fatigue increased energy decreased appetite improved task performance relief of boredom increased motor activity Examples of psychostimulants cocaine 2 amphetamines dextroamphetamine and methamphetamine 3 amphetamine derivatives used to treat ADHD methylphenidate pemoline Cylert 4 variety of drugs formerly used to treat obesity fenfluramine Pondimin phentermine under trade names as Ionamin ObeNix AdipeXP ObyTrim and Fastin and phenmetrazine Preludin 5 caffeine and theophylline psychoactive drug in coffee and other caffeinated beverages and nicotine ingredient in tobacco All stimulants subject to compulsive abuse and have limited therapeutic use signi cant side effects and toxicity Common side effects cocaine and amphetamines anxiety insomnia and irritability High doses intense irritability and anxiety and psychotic behaviors Low doses alerting arousing response not unlike normal reaction to an emergency or to stress eg increase blood pressure and heart rate pupils dilate skin to internal organ blood flow shifts and rise in blood oxygen and glucose levels Cocaine Historical Facts Erythroxylon coca leaves Peru and Bolivia Social use religious mystical stimulant and medicinal purposesto increase endurance promote sense of wellbeing and alleviate hunger usual total daily dose 200 mgs 1859 active alkaloid in coca isolated and named cocaine 1884 Freud advocated use of cocaine to treat depression and alleviate chronic fatigue He described cocaine as a magical drugquot and even wrote a quotSong of Praisequot to it 1884 Koller demonstrated cocaine39s local anesthetic properties and for ophthalmologic surgery 1885 cocaine incorporated along with caffeine in popular patent medicine later known as beverage CocaCola until 1903 60 mgs8 ounce serving 1891 at least 200 reports of cocaine intoxication and 13 deaths reported 1914 Harrison Narcotic Act banned cocaine in medicines and beverages 1924 American Medical Association reviewed 43 deaths of patients who had been under local cocaine anesthesia and attributed 26 of those deaths to cocaine toxicity 19205 Use of cocaine rose then decreased during 1930s when amphetamines became available presumably because cost less and produced longerlasting effects 19605 cocaine not used much until federal restrictions on amphetamine distribution raised cost of amphetamines making cocaine attractive once again Net effects indistinguishable as euphoriants availability price and sociocultural considerations now largely determine comparative popularity of the two 19705 cocaine again became popular in mid19805 smoking of concentrated preparations of cocaine free base and crack cocaine opened new era in cocaine abuse characterized by high dose rapidonset effects with rapid development of dependence 2030 million in US have used cocaine 4 million people use it regularly and 2 million are quothard corequot cocaine users At peak use 800000 Americans had cocaine daily today a number closer to 300000 is likely result of intensive antidrug campaignnumber of users has not decreased Cocaine addicts typically young 12 to 39 yrs poly drugdependent and male 75 tend to have coexisting psychopathology 30 anxiety disorders 67 clinical depression and 25 paranoia 8590 are alcohol dependent Associated with violent premature deaths including homicides suicides and accidents Cocaine Chemistry Extracted as coca paste 6080 cocaine each leaf contains 0510 C Coca paste converted to hydrochloride salt before exportation and sold as cocaine hydrochloride quotcrystalquot or quotsnowquot Inhaled cocaine hydrochloride provides 1025 mgs into each nostril Hydrochloride salt form not suitable for smoking because it decomposes at temperatures required to vaporize itthus Hydrochloride form altered to base form by extraction in ether quotfree basequot Cocaine base or quotcrackquot from cracking sound it makes when heated Absorbed from mucous membranes gastrointestinal tract and lungs Detoxified in plasma and liveronly small amounts excreted unchanged Cocaine Absorption Routes oral chewing intranasal snorting intravenous mainlining and inhalation smoking or freebasing Orally absorption over I hour with 75 metabolized in liver on first passthus only 25 reaches brain eliminating feeling ofquotrushquot that follows other routes lntranasally poorly absorbed as hydrochloride salt poorly crosses mucosal membranesvasoconstriction limits absorption2030 absorbed with peak levels in 3060 mIn Inhalation smoked base particles trapped in nose while others pass into trachea and lung from which absorption is rapid and completeonset of effects seconds and persist for 510 minutes632 of initial amount reaches plasma remainder undergoes pyrolysis before inhalation Intravenous injection bypasses all barriers to absorption placing drug immediately into the bloodstream3060 second delay in onset of action Cocaine Distribution and Elimination lnto brain rapidly brain concentrations far exceed plasma concentrations After brain penetration cocaine redistributed to other tissues Freely crosses placental barrier achieving levels in unborn equal to mother Halflife of 3090 min and almost completely metabolized by liver enzymes Major metabolite is inactive benzoylecgonine detected in urine for 3 days and much longer 1522 days in chronic users Small amounts metabolized to an active intermediate norcocaine Urinary detection of benzoylecgonine forms basis of drug testing Persistence of metabolite in urine implies longterm users accumulate drug in body tissues from which it is later absorbed into plasma metabolized and excretedcocaine metabolites toxic to liver Cocaine Pharmacodynamics Three prominent actions local anesthetic blood vessels constrictor and psychostimulant with strong reinforcing qualitiescompulsive drug abuse Potentiates synaptic actions of dopamine norepinephrine and serotonin via ability to block transmitter reuptake into presynaptic terminals Dopaminergic action crucial to behaviorreinforcing and psychostimulant propertiesboth dopamine and cocaine decrease discharge rate of ventral tegmental area and nucleus accumbens neurons Dopamine exerts inhibitory effects on postsynaptic receptors mechanistically cocaine potentiates dopamine postsynapticinduced decrease in ring rate Cocaine binding to transporter induces a change in dopaminebinding site that decreases affinity of dopamine Two of five D1 and D2 dopamine receptors involved in cocaine action D2 receptors underlie positive effects on behavior reinforcing and locomotor effects and stereotypical behavioral effects Serotonin depletion increases efficacy of cocaine as a positive reinforcer thus cocaine actions on serotonin contribute aversive effect limiting its selfadministration Serotonin uptake inhibitor fluoxetine enhances discriminative stimulus effects of cocaine Chronic exposure of postsynaptic receptors to high dopamine levels leads to decrease in postsynaptic dopamine receptors downregulation subsensitivity and increase dopamine transporter Cocaine Side Effects of ShortTerm LowDose Use Nontoxic physiological responses increases in alertness motor hyperactivity tachycardia vasoconstriction hypertension bronchodilatation body temperature pupillary dilatation glucose availability and blood ow Enjoyable psychological effects low doses of cocaine 25150 mgs depending on tolerance and route of administration Major psychological changes mood giddiness enhanced selfconsciousness and boastfulness cognition drive states hunger sex thirst talkative garrulous with tangential incoherent speech Mild euphoria with anxiety 6090min then protracted anxious state hrs Major physiological and behavioural changes suppressed appetite with later rebound delayed sleep increased motor activity and restlessness After quothighquot anxiety depression and paranoia followrapid shift causes user to crave more drug Drug craving becomes intense and forms a part of withdrawal syndrome Higher doses loss of coordination tremors and eventually seizures followed by depression dysphoria anxiety somnolence and drug craving Medical complications snorted chronic rhinitis nasal septum perforations and loss of sense of smellintravenous diseases transmitted by needle hepatitis and AIDS and infectious endocarditis infections of heart valvessmoking crack pulmonary dif culties and black sputum Cocaine Side Effects of LongTerm HighDose Use Toxic symptoms anxiety sleep deprivation hypervigilance suspiciousness paranoia toxic paranoid psychosis Other highdose longterm effects sexual dysfunction interpersonal con icts severe depressive conditions dysphoria and bizarre and violent psychotic disorders that last days or weeks after quitting Acute toxic dose 12 mgskgthus 70150mgs of cocaine is a toxic onetime dose for a 150 pound personphysiologica toxicity follows higher doses f quot 39 and sequelae strokes in healthy young individuals persistent alterations in blood perfusion of brain heart oxygen deprivation cardiac arrhythmias and seizures Chronic cocaineinduced psychiatric syndrome affective disorders schizophrenia syndromes personality disorders etc Cocaine addicts personality profiles reckless rebellious and low tolerance for frustration and craving for excitement Cocaine addicts typically abuse opiates and alcohol either to enhance effects of cocaine or to medicate themselves for unwanted side effects calming jitters dulling perceptions and reducing paranoia Intravenous drug users often take cocaine and heroin together in mixture speedball Cocaine Fetal Effects Fetal cocaine syndrome jittery baby syndrome and infants known as quotcrack babiesquot Not well defined since most fetal effects related to vasoconstriction hypertension and infarcts at any time during gestation and in any structure To determine possible effects on fetus must examine not only indirect maternal effects on fetal development but also direct teratogenic effects Indirect effects on fetus result from vasoconstrictive action in mother which decreases blood ow to uterus and reduces fetal oxygenation Results of fetal hypoxia placental detachment placental insuf ciency preterm or precipitous labour fetal death stillbirths and low birth weightand can lead to intrauterine growth retardation small head size microcephaly and aberrations in brain development Unborn is exposed to cocaine even before fertilization because cocaine can bind to sperm Cocaine promotes destructive lesions leading to Neonatal Neurological Syndrome typi ed by abnormal sleep patterns tremors poor feeding irritability seizures and increased riskincidence of sudden infant death syndrome SIDS 50000100000 babies born each year to mothers who have used cocaine during pregnancy Crack babies show dif culty with unstructured play and low tolerance for frustration also structure input and information poorlyand show high incidence of ADHD Treatment Problems of Cocaine Abuse Variety of psychological behavioral and pharmacological approaches tried with major complications to overcome 1 Intensity of both drug effect and behaviorreinforcing action of cocaine 2 Pronounced tendency toward relapse with cocaine acting as cue to increase craving for drug 3 Virtually all cocaine addicts have additional drug dependencies andor psychiatric disorders including affective disorders bipolar disorder borderline personality disorder antisocial personality disorder and eating disorders Given these complications needs of cocaine addict are at least 5fold 1 immediate abstinence 2 diagnosis of any coexisting disorders 3 determination if addiction is primary disorder or secondary to other disorders 4 maintenance of abstinence long enough to diagnose and begin treatment of coexisting disorders 5 prevention of relapse Treatment Approaches of Cocaine Abuse Treatment approaches are many from classical quot12stepquot recovery programs AA to psychopharmacotherapy psychotherapy or cognitivebehavioral approaches Abstinence essential and must be monitored by frequent unannounced urine tests to screen for drugs 3phase cocaine abstinence model phases called crash withdrawal and extinction Crash 9 hrs4 days user is uninterested in using cocaine appearing quite depressed and somnolent Withdrawal 110 wks max relapse potentialdrug craving Extinction continued monitoring required since conditioned cues can trigger craving and result in relapse Psychopharmacotherapy to treat cocaine abuse 1 antagonize the effects of cocaine at its receptors 2 produce an aversive Antabuselike reaction 3 treat the coexisting psychiatric disorder 4 reduce cocaine craving and withdrawal To date no successful antagonists are available nor are any aversive drugs thus psychopharmacotherapy aimed at utilizing drugs to attenuate drug craving Most popular drug for reducing craving is antidepressant desipramine Desipiramine relieves craving and withdrawal effect is not predictable positive effects shortlived Other agents include antiparkinsonian dopamine receptor agonist bromocriptine the amino acid tyrosine phenothiazines antipsychoticsantidopaminergics other antidepressants the mood stabilizer lithium and the anticonvulsant carbamazepine AMPHETAMINES AND RELATED DRUGS Amphetamine Historical Facts Amphetamines methyl derivative methamphetamine and several other derivatives methylphenidate fenfluramine pemoline exert stimulant effects resembling cocaine 1888 synthesized but not used for medicinal purposes until 1930s when found to increase blood pressure and stimulate CNS and cause bronchodilatation 1935 treat narcolepsy thought not to pose threat to health 19351946 list of 39 conditions for which drug could be used schizophrenia morphine addiction tobacco smoking heart block head injury radiation sickness hypotension seasickness severe hiccups and caffeine dependence World War II to ght fatigue and enhance battle performance 1940s largescale abuse usually oral ingestion and continued to be used and abused as diet aid 1960s abuse pattern changed with advent of injectable forms Amphetamine Mechanism of Action Indirectacting catecholamine agonists CNS effects exerted by causing release of newly synthesized catecholamines especially dopamine from nerve terminals Behavioral stimulation and increased psychomotor activity due to stimulation of dopamine receptors in mesolimbic system including nucleus accumbens Highdose stereotypical behavior constant repetition of meaningless acts involves dopamine neurons in caudate nucleus and putamen of basal ganglia Increase in aggressive behavior complexseen primarily in adults in children they reduce aggressive behavior and activities characteristic ofADHD Potent anorectics decrease appetite but tolerance to satiating effects develop rapidly Involves lateral hypothalamus but may also involve serotonin neurons which when activated produce satiety Amphetamine Pharmacology Psychomotor stimulant in the CNS increased alertness euphoria excitement wakefulness reduced fatigue loss of appetite mood elevation increased motor and speech activity and improved task performance dexterity loss Excreted in urine and detectable up to 48 hrs after use Low oral doses 2520 mgs increase in blood pressure with reflex slowing of heart rate relaxation of bronchial muscle Moderate doses 2050 mgs stimulation of respiration slight tremors restlessness a greater increase in motor activity insomnia agitation appetite suppression wakefulness and causes sleep deprivation recovery takes many weeks High dose gt50 mgs stereotypical behaviors continual purposeless repetitive acts aggression and violence paranoid delusions severe anorexia and state of amphetamine psychosis indistinguishable from acute schizophrenia attack Chronic amphetamine in animals associated with persistent depletion of both dopamine and enzyme tyrosine hvdroxylase synthesis of dopaminethus toxic to dopaminereleasing neurons Loss of responsiveness to quotnatural reinforcersquot develops dopamine neurons lose their sensitivity to dopamine Other harmful highdose effects psychosis and abnormal mental conditions weight loss skin sores infections resulting from neglected health care poor eating habits and lack of sleepincuding deterioration in social and occupational affairs Toxic doses vary widelysevere reactions can occur from low doses 2030 mgs whereas persons who do not have tolerance have survived doses of400500 mgs Amphetamine Dependence and Tolerance Prone to compulsive abuse induces psychological dependence Dependence follows classical positive conditioning model positive reward leads to further use Tolerance rapidly develops and accompanied by dysphoria sedation lassitude and drug cravingsoution to this state is taking more drug in higher and higher doses which starts a vicious cycle ofdrug use and withdrawal At this point tolerance to euphoriant effects develop and periods of quotbingingquot begin Tolerance leads to further drug intake social withdrawal and a focus on procuring drugs Amphetamine Therapeutic Uses and Status Medical uses are restricted and often controversial and include treatment of 1 narcolepsy application is now rare 2 attention deficit hyperactivity disorder 3 obesity Note amphetamines are not of much value in treating major depression because of great potential for addiction and general lack of therapeutic ef cacy Amphetamines and Attention Deficit Hyperactivity Disorder Since 1936 started with amphetamine and has progressed to use of methylphenidate Ritalin pemoline Cylert and more recently the antidepressant nortriptyline Evolution of terminology for the disorder quotminimal brain dysfunctionquot to quotminimal brain disorderquot to quothyperactivity syndromequot to quotattention de cit disorderquot to present ADH D No definitive CNS pathology has been demonstrated however a dopamine hypothesis of ADHD has evolved invoking a disorder of polysynaptic dopaminergic circuits between prefrontal and striate centers Affects 6 of schoolage children characterized by inattentiveness impulsivity and hyperactivity that are persistent and severe to cause functional impairment at school home and with peersevidence that disorder may be inherited Symptoms may persist into adulthood Effective intervention early in childhood may alter course of ADHD decreasing conduct disorder as an adolescent and antisocial personality disorder with its various complications eg alcohol and drug abuse criminality as an adult Pharmacological treatment usually discontinued when a child reaches puberty because adolescents presumably are more prone to abuse amphetaminelike drugs Growthreducing effects blunt adolescent growth spurt even with quotsummer holidayquot from drug Drugs improve behavior and learning ability in 5075 ofADHD children Methylphenidate has rapid onset and short duration thus must be administered at both breakfast and lunchtime Pemoline has longer but variable halflife disadvantages slow onset and reduced level of therapeutic ef cacy Dextroamphetamine rarely used for ADHDhowever can be useful in nonrespondents to methylphenidate or pemoline Antidepressants not widely used for ADHD but one nortriptyiine has been studied Amphetamines and Obesity lmpediments side effects dependency addiction and rapid tolerance Small amounts of weight loss lt1 pndwk accompany use effects lost after only few weeks Anorexics benzphetamine Didrex phendimetrazine Anorex Oblan Phendiet Wehless diethylpropion Tenuate Tepanol mazindol Mazenor Sanorex phentermine Fastin lonamin Phentrol AdipeXP ObyTrim phenylpropanolamine Dexatrim and d amphetamineamphetamine combination Obcontrol Search continues for amphetaminerelated derivatives that suppress appetite without potential for drug abuse and without concomitant development of tolerance New drugs fenfluramine uoxetine and sertraline related to amphetamine but act to potentiate serotonin neurotransmission rather than dopamine Fenfluramine Pondimin partially inhibit serotonin reuptake and facilitate its release Fenfluramine combined with phentermine dopamine releaser enhanced weight loss over what could be achieved with behavior modification exercise and nutrition program and effect sustained over 4 yrs discontinued Fluoxetine and sertraline are serotonin reuptake inhibitors that are clinical antidepressantsboth drugs produce satiety and reduce food intake tolerance to anorectic effect after several weeks Nasal Decongestants ND Structurally related to amphetamine they alter synaptic actions of norepinephrine both in brain minor effects and in peripheral nervous system more potent in PNS ephedrine tetrahydrozoline Tyzine metaraminol Aramine phenylephrine NeoSynephrine pseudoephedrine Sudafed xylometazoline Otrivin nylidrin Arlidin propylhexedrine Benzedrex phenmetrazine Preludin naphazoline Privine oxymetazoline Afrin After use compensatory rebound increases nasal stuf ness similar to cocaine stuffy nose Ephedrine is active ingredient in illicit preparations alleged to be amphetamine quotICEquot a Free Base Form of Methamphetamine crank crystal and speed More potent than amphetamine and easily synthesized in clandestine labs from inexpensive chemicals ephedrine making large amounts available at low cost In animals implicated as a neurotoxic agent such toxicity not yet demonstrated in humans When converted to base form ICE methamphetamine can be vaporized and inhaled in smoke Abuse of ICE began in Hawaii spread to Japan where it is called shabu then to California and dispersed everywhere Since not injected smoking removes guilt feelings needle marks infection risk evidence ofdrug use and heavy drug impressions associated with injection of illegal drugs Methamphetamine Pharmacokinetics Rapid absorption into plasma which abates over 4 hrs and then progressively declines in plasma levels thereafter90 eventually reaches plasma Biological halflife over 11 hrsafter distribution 60 slowly metabolized in liver and excreted through kidneys along with unmetabolized methamphetamine 40 excreted unchanged Thus long action follows from slow and incomplete metabolism in contrast cocaine is rapidly and completely detoxi ed by enzymes found in both plasma and liver Methamphetamine Effects and Toxicity Indistinguishable from cocainepotent psychomotor stimulant and positive reinforcer Repeated high doses associated with violent behavior and paranoid psychosissuch doses cause longlasting decreases in brain dopamine and serotonin Changes are irreversible since chemical effects persist for gtyear Permanent neurochemical changes alterations in sleep sexual function depression movement andor schizophrenia Acute delusional and psychotic behavior occurs after smoking lCEhowever unlike cocaine ICE induced psychosis persists for days or weeks Fatalities result from cardiac toxicity manifested as pulmonary edema or heart failure HALLUCINOGENS Psychedelic drugs PD s group of compounds that induce visual and auditory hallucinations Disturb cognition and perception and behavior similar to that in psychotics Naturally occurring PD s used for thousands of years for effects on sensory perception Prior to 60s PD s were restricted to religious rituals During late 60s 70s psychedelic agents used to enhance perception expand reality promote personal awareness and induce comprehension of spiritual or supernatural Structures resemble acetylcholine two catecholamines norepinephrine and dopamine and serotonin Structural similarities lead to 3 classes of psychedelics Anticholinergic psychedelics intoxication amnesia and delirium by blocking postsynaptic acetylcholine receptors Catecholamine like act by in uencing a subset of catecholamine and serotonin receptors Serotonin like psychedelics act by in uencing a subset of serotonin receptors 4 I 39 J quot block 39 NMDA receptor calcium ion conductance p t MN u A LSD Dimethyltryptamine DMT Psilocybin psilocin bufotenine Ololiuqui morning glory seeds Phencyclidine Angel Dust Semyl Ketamine Ketalar Anticholinergic Psychedelic Drugs A PD s Historical Background Scopolamine and atropine block muscarinic acetylcholine receptor sites and have no intrinsic activity Distributed widely in nature in plant Atropa belladonna as belladonna or deadly nightshade in Datura stramonium Jamestown weed jimsonweed stinkweed thorn apple or devil39s apple and Mandragora officinarum mandrake Used in Middle Ages as source of poison nightshade Atropa belladonna derived from Atropos Greek goddess who cut the thread of life Belladonna means quotbeautiful womanquot which refers to ability to dilate pupils when it is applied topically to eyes Delirium caused by these substances may have persuaded certain persons that they could flythat they were witches Used in World War II as truth serum Cigarettes made from Datura stramonium and Atropa belladonna sold in pharmacies until the 70s to treat asthma A PD Pharmacology Act on PNS to depress salivation and sweating increase temperature dilate pupils blur vision and increase heart rate Atropine poorly crosses bloodbrain barrier thus scopolamine is primary CNS active intoxicant Low doses drowsiness mild euphoria profound amnesia fatigue delirium mental confusion dreamless sleep attention loss clouds consciousness and produces amnesia it does not expand sensory perception High doses behavioral state resembles toxic psychosis CNS effects delirium mental confusion sedation and amnesia PNS effects tachycardia blurred Vision urinary retention and dry mouth Catecholamine like Psychedelic Drugs C PD s o Methoxylated amphetamine derivatives mescaline DOM also as STP TMA MDA MDMA ecstasy MMDA DMA and drugs from nutmeg myristin and elemicin 0 Compared to amphetaminescocaine more intense psychedelic action and less intense behavioral stimulant action 0 C PD s produce similar effects sensory perceptual time distortion altered color perception sounds shapes complex hallucinations and synesthesia dreamlike feelings depersonalization altered affect depression or elation and somatic effects tingling skin weakness tremor etc Mescaline o Peyote Lophophora williamsii common plant in southwestern Us and Mexico spineless cactus with small crown or quotbuttonquot and long root When used for psychedelic purposes crown is cut from cactus and dried into hard brown discs mescal button active compound is mescaline Mescaline Historical Background 0 Pre Columbian times when cactus was used in religious rites of Aztecs and other Mexican Indians 0 Legally available for religious practice of Native American Church of North Americaan organization that claims some 250000 members from Indian tribes throughout North America 1896 mescaline identified as active ingredient in peyote Variety of mescaline derivatives synthesized all have methoxy OCH3 groups or additions on benzene r1ng Methoxylation results in high af nity for presynaptic serotonin receptors and exert LSDlike psychedelic effects Mescaline Pharmacology 0 Orally Transport to brain in 30 90 minseffects persist for 10 hrsnot metabolized before it is excreted 0 Low doses 23 mgskg produce amphetamine like behavioral effects and include pupil dilatation increased blood pressure and heart rate increase body temperature EEG and behavioral stimulation Usual oral dose 5 mgkg causes anxiety sympathomimetic effects hyperre exia of limbs static tremors and Vivid hallucinations of brightly colored lights geometric designs Synthetic Amphetamine Derivatives o DOM MDA TMA MDMA MMDA and DMA structurally related to mescaline and methamphetamine and more potent and toxic than mescaline 0 Produce similar effects low doses amphetaminelike effects high doses LSDlike serotoninmediated effects DOM or STP for quotserenity tranquillity and peacequot 0 Effects similar to mescaline doses 16 mgs produce euphoria followed by 68 hr period of hallucinations o 100x more potent than mescaline but less potent than LSD 0 High incidence of overdose acute toxic reactions tremors leading to convulsive movements followed by death MDA MMDA TMA 0 Effects resemble mescaline and LSD re ect mix of catecholamine and serotonin interactions 0 MDMA quotecstasyquot resembles MDA but less hallucinogenic with less sense of disembodiment and Visual distortion 0 MDMA releases serotonin and cause acute depletion of forebrain serotonin and destruction of serotonin neuronsserotonergic systems are implicated in control of sleep food intake sexual behavior anxiety and mood disruption due to cell loss could have major consequences Myristin and Elemicin 0 Active ligand in nutmeg and mace related to mescaline 0 From dried seed and seed coat of East Indian nutmeg tree Myristica fragrans o Ingestion of large amounts I2 teaspoons usually brewed in tea after 25 hr delay induce euphoria and changes in sensory perception visual hallucinations acute psychotic reactions and feelings of depersonalization and unreality o Unpleasant side effects vomiting nausea and tremors Serotonin like Psychedelic Drugs S PD s o S PD s include 1 lysergic acid diethylamide LSD 2 psilocybin and psilocin mushroom Psilocybe mexicana 3 dimethyltryptamine DMT and 4 bufotenine LSD is partial serotoninZ 5 HT2 receptor agonist triggers responses involving other neurotransmitter systems hence overlap between serotonin and catecholamine psychedelics SPD s alter mood and perception via activation of serotonin cells in pontine raphe a neuronal lter for sensations and perceptions eliminating those that are unimportant irrelevant or commonplace Adverse reactions paranoid ideation depression undesirable hallucinations and or a confusional state resembling a druginduced dementia Serotonin receptor blockers are useful in antagonizing psychedelic effects quotbad tripquot Antipsychotic drugs with antiserotonergic properties used to treat LSDinduced psychosishowever not routinely used because neuroleptics evoke motoric side effects LSD Historical Background 0 1938 synthesized by Albert Hoffman Swiss chemist as part of an organized research program to investigate therapeutic uses of compounds obtained from ergot Ergot natural product from fungus Claviceps purpurea which grows on rye in grain fields of Europe and North Americaactive agents are derivatives of lysergic acid 0 Pharmacological actions of ergots constriction of blood vessels and increased contractions of uterus at least at low doses Ergot alkaloids used for migraine headaches and control postpartum hemorrhaging From 1938 until 1943 LSD remained on laboratory shelf unnoticed when Doctor Hoffman had an unusual experience In the afternoon of 16 April l943I was seized by a peculiar sensation of vertigo and restlessness Objects as well as the shape of my associates appeared to undergo optical changes I was unable to concentrate on my work In a dreamlike state I left for home where an irresistible urge to lie down overcame me I drew the curtains and immediately fell into a peculiar state similar to drunkenness characterized by an exaggerated imagination With my eyes closed fantastic pictures of extraordinary plasticity and intensive color seemed to surge toward me After 2 hours this state gradually wore off quot Hoffman ingested compound under controlled conditions and described experience with a dose now known as N10x the dose required to induce psychedelic effectsas a result After 40 minutes I noted the following symptoms slight giddiness restlessness difficulty in concentration visual disturbances laughing Later I lost all count of time I noticed with dismay that my environment was undergoing progressive changes My visual field wavered and everything appeared deformed as in a faulty mirror Space and time became more and more disorganized and I was overcome by a fear that I was going out of my mind The worst part of it being that I was clearly aware of my condition My power of observation was unimpaired Occasionally I felt as if I were out of my body I thoughtI had died My ego seemed suspended somewhere in space from where I saw my dead body lying on the sofa It was particularly striking how acoustic perceptions such as the noise of water gushing from a tap or the spoken word were transform ed into optical illusions I then fell asleep and awakened the next morning somewhat tired but otherwise feeling perfectly well 0 1949 first study of LSD in humans conducted in US and during 50s large quantities of LSD distributed to pharmacologists and physicians worldwide for research 0 LSD tried as adjunct to psychotherapy to help patients verbalize problems this has not proven to be effective 0 Early work on human volunteers introduced LSD to college campuses from there to a wider audiencereached peak in popularity in late 60s after which use has decreased LSD Pharmacokinetics o LSD often added to other substances such as squares of paper backs of stamps or sugar cubes and taken orallyusual doses range 25 300 micrograms and absorbed in 1hr reaching peak in 3hrs and subsiding in 6 8 hrs 0 Distributed rapidly in body brain and crosses placenta liver metabolized detected in urine by radioimmunoassay LSD Physiological Effects 0 Slight increase in body temperature pupil dilatation increased heart rate and blood pressure increased blood glucose levels dizziness drowsiness and nausea 0 Low level of toxicityeffective dose 50 microgms and lethal dose of 14 miligmstherapeutic ratio of 280 LSD Psychological Effects 0 Unpredictable and in uenced by variety of factors personality expectations previous experience with LSD and other psychoactive drugs motivations for using drug drug setting and persons with whom user interacts o Predictable responses alterations in mood and emotion laughter or sorrow evoked easily euphoria and dysphoria 0 Principal psychological effects perceptual changes especially visual hallucinations and perceptual distortionstrue auditory hallucinations rare 0 Psychedelic experience can be divided into three phases 1 Somatic phase consists of CNS stimulation and autonomic changes predominantly sympathomimetic Sensory phase characterized by sensory distortions and pseudohallucinations effects desired by user Psychic phase signals maximum drug effect where changes in mood disruption of thought processes altered perception of time depersonalization true hallucinations and psychotic episodes bad trip occur 54 quot LSD Tolerance and Dependence o Tolerance develops rapidly and cross tolerance occurs between LSD and other CPD s and SPD s 0 Physical dependence does not develop even when drug is used repeatedly or for prolonged period of timeno withdrawal signs exhibitedanimals do not selfadminister LSD Adverse Reactions and Toxicity 0 Fall into four categories 1 effects on the psychological state of the user 2 possibility of permanent damage to the brain 3 possible effects on the fetus when the drug is taken by a pregnant woman and 4 deleterious effects on society if use of drug were widespread LSD eliminates normal defence mechanisms and thus precipitates psychotic episodes Persistent ashbacks occur weeksmonths after last drug usemechanism unknown 15 of usersprecipitated by use of marihuana anxiety fatigue or movement into a dark environment ashbacks persist intermittently for several years Psychedelics can precipitate serious depressions paranoid behavior or prolonged psychotic episodes LSD like Tryptamine Derivatives Dimethyltryptamine DMT Naturally occurring psychedelic related to serotonin Binds to 5HT2 receptors and active ingredient of South American snuff such as cohoba prepared from beans of Piptadenia peregrina and epena prepared from bark of trees found in upper Amazon River valley as well as vopo 0 Presence of bufotenine from the frog Bufo containing 5hydroxyDMT in its skin also contributes to effect 0 DMT not absorbed orally must be smoked or sniffed Duration of action short 1 hr quotbusiness man39s LSDquot Psilocybin 4 phosphoryl DMT psilocin 4 hydroxy DMT o Psychedelic agents found in 15 species of mushrooms that belong to the genera Psilocybe Panaeolus and Conocybe that grow throughout world including Central America and northwestern portion of US Psilocybe mexicana teonanacatl or quotGod39s eshquot long history as sacramental in Central America 1200 as potent as LSD effects last 6 10 hrs 0 Psilocybe intoxication described in 1955 by Gordon Wasson New York banker when he traveled through Mexico to participate in a Psilocybe ceremonyWasson said It permits you to travel backwards and forward in time to enter other planes of existence even to know GodYour body lies in the darkness heavy as lead but your spirit seems to soar and leave the hut and with the speed of thought to travel where it listeth in time and space accompanied by the shaman s singingat least you know what the ineffable is and what ecstasy means Ecstasy The mind harks back to the origin of that word For the Greeks ekstasis meant ight of the soul from the body Can you find a better word to describe this state Ololiuqui morning glory seeds 0 Naturally occurring used by Central and South American Indians as intoxicant and hallucinogenseeds contain lysergic acid amide not lysergic acid diethylamide LSD Lysergic acid amide identified as 01 as active as LSD Side effects nausea vomiting headache increased blood pressure dilated pupils sleepiness etc Ingestion of gt100 seeds sleepiness distorted perception hallucinations and confusion ashbacks reported Harmine 0 Seeds of Peganut harmala plant native to the Middle East Seeds used as intoxicants for centuries and evokes hallucinations accompanied by nausea vomiting sedation and finally sleep Psychedelic Anesthetic Drugs Phencyclidine and Ketamine o Structurally unrelated to other psychedelic and psychoactive drugs and do not act on serotonin neurotransmission o PCP receptor activation amnesia analgesia and psychedelic dissociation o 1956 developed as potent analgesic amnestic anesthetic Used brie y as anesthetic in humans high incidence of serious psychiatric reactions including agitation excitement delirium disorientation and hallucinatory phenomena 0 Ketamine related to PCP induces anaesthetic state in low doses with moderate incidence of psychiatric side effectsoccasionally in in patients who cannot tolerate cardiovascular depressant effects of other anesthetics 0 Early 70s referred to as quotpeace pillquot PCPappeared on illicit market in form of powder tablets leaf mixtures and quotrockquot crystals and sold as quotcrystalquot quotangel dustquot quothogquot quotPCPquot quotTHCquot quotcannabinolquot or quotmescalinequot PCP Pharmacokinetics and Mechanism of Action 0 Absorbed orally or smoked peak effects in 15 min metabolized in liverelimination halflife 18 hrs but


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Bentley McCaw University of Florida

"I was shooting for a perfect 4.0 GPA this semester. Having StudySoup as a study aid was critical to helping me achieve my goal...and I nailed it!"

Parker Thompson 500 Startups

"It's a great way for students to improve their educational experience and it seemed like a product that everybody wants, so all the people participating are winning."

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Refund Policy


All subscriptions to StudySoup are paid in full at the time of subscribing. To change your credit card information or to cancel your subscription, go to "Edit Settings". All credit card information will be available there. If you should decide to cancel your subscription, it will continue to be valid until the next payment period, as all payments for the current period were made in advance. For special circumstances, please email


StudySoup has more than 1 million course-specific study resources to help students study smarter. If you’re having trouble finding what you’re looking for, our customer support team can help you find what you need! Feel free to contact them here:

Recurring Subscriptions: If you have canceled your recurring subscription on the day of renewal and have not downloaded any documents, you may request a refund by submitting an email to

Satisfaction Guarantee: If you’re not satisfied with your subscription, you can contact us for further help. Contact must be made within 3 business days of your subscription purchase and your refund request will be subject for review.

Please Note: Refunds can never be provided more than 30 days after the initial purchase date regardless of your activity on the site.