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Introduction to the Pharmacology of Psychoactive Drugs

by: Dorris Purdy

Introduction to the Pharmacology of Psychoactive Drugs PSYC 472

Marketplace > University of Idaho > Psychlogy > PSYC 472 > Introduction to the Pharmacology of Psychoactive Drugs
Dorris Purdy
GPA 3.5


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This 56 page Class Notes was uploaded by Dorris Purdy on Friday October 23, 2015. The Class Notes belongs to PSYC 472 at University of Idaho taught by Staff in Fall. Since its upload, it has received 9 views. For similar materials see /class/227926/psyc-472-university-of-idaho in Psychlogy at University of Idaho.


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Date Created: 10/23/15
Learning Physiology and Addiction Sub stance Dependence Tolerance Withdrawal 0 Increased use Unsuccessful efforts to stop drug taking quotith socialoccupational A 5 JllLCl 1c c functions Use continues despite kno edge ofthe problem 0 Lots of time is spent gettin39 the substance Positive Reinforcement Addictive drugs activate positive reinforcement mechanisms 1n bra1n 7 Responses tlat result in activation of reinforcement mechanisms are strengthened Immediacy of drug action is crucial to drug reinforceme t A IDL addictive drugs it the nucleus accumbens 7 Addictive dings either induce releasc om or block reuptake into presynaptic elements dopamine levels Within nucleus accumbens Negative Reinforcement Behaviors that terminate aversive effects are negatively reinforced 7 It feels so good When it stops hurtingquot 7 Negative reinforcement strengthens behaviors that turn off aversive stimuli 7 Negative reinforcement is not punishment Withdrawal Symptoms Are usually aversive e The negative symptoms of Withdrawal can be terminated by taking the dmg again Negative reinforccr maintaining drug use NR is important for acquiring a rug addiction 7 Life hurm to muche take dmg to s p the hurt 39 important in Mechanisms ofTolerance Tolerance desensitization ofdrug action Occurs due to down rnglatjon ofreceptors 7 Overstimulation ofreceptors canproduces fewer receptors or reduced effects ofreceptor activation Begins with Associative Learning Defined as the the relationship between two stimu i S1 becomes associated with 52 1 Key The stimuli n ich associations can develt p can be a thing Classical Conditioning Concepts come from physiology and ralexology Pavlov mum Wm rd a a L gt ummmwus umnmnwm 5 m m Examples UCS UCR Food Salivation a UL UCR Bell Food quotvation CS gt C Bell Sal vation Other Examples of CC Air puff Blink Tone Airpuff Blink Tulle Blink ls General Across Organisms Occurs in Dogs rats human fetuses neurons I I environments Classrooms Resa Woods Emitine NauseaVomiting Alcohn39 Fmitine NIV Alcohol Nausea Vomiting Related Classical Conditioning Concepts Extinction Is a decrease in some response due to repeated exposures of the CS Occurs when the m is not present Spontaneous Recovery After extinction has occurred give a rest period then present the CS again Aaai a CR but it is lower than the original Can do several times Total Extinction When you present the CS after spontaneous recovery but you get no CR Spontaneous Recovery is Important for Relapse Doing ne See acue or stimulus associated with where you used will Causes cravings Generalization When a response is acquired to a CS other CS39s will also evoke the same conditioned response 39eser the new Is to the 39nal Why stimulus t e higher the probability that the resp lnse will occur n 22 Example Contiguity Original cs The cs must precede the ch by only a brieftime period Uses a red light Get CR in general the longerthe delay between the cs Oranm quotM liqht Same CR and ucs the poorertne conditioning Yellow Red Ilg Less CR Yellow light No CR CS Must Act as a Cue The CS trust provide the most reliable inforn39ation about the occurrence of the UCS over other stinulus cuesthat maybe present in the environ lt nust predict the UCS the best s can also prevert or block the f he CR Other cue developn39ent o t Learning Biological Aspects of Drug Craving Craving is an impulse to reinstate drugtaking Robinson and Benidge 1993 account ofcraving 7 Addictive drug activate the mesolimbic dopamine system 7 Stimuli that 39 with dopamine activatim needles mirnrs pipes etc acquire t alience c exciting 7 Exposure to or thinking about the rugrelated stimuli results in craving for the drug Optimal Period for Learning Depends on the response 7 450ms for eyeblink closure re ex r 2 sec for skeletal movements 7 4 sec for salivaryresponse r 20 sec for heart rate response ly Depends u encyfor responding in the particular re ex sy Con itlonln 7 Can be hours e t39on Poison Based Avoltance 9 Strength of the UCS In general the stronger the UCS the faster the conditioning The stronger the UCS the higher the level of the CR it does not always occur for the CS Saliency or Nature ofthe CS 39n39uli will differ in their abilityto become UCS Some conditioned stinuli cannot become associated with the UCS Sal V quota degree ofassociability of a particular OS to a o r Salient stimuli become asses r Nonsalient stimuli do not become lsociated CS Delivery The CS trust precede the the UCS No pairing will occur if the UCS occurs without the CS as often as it occurs with it 5050 ratio of presentations No CR will develop l occurs without the UCS I L39 en me some neutral stinulu Predictiveness Bolles Proposed that contiguity is not enough The everts trust occur together before we get a CR 39Iredict the UCS and not Opponent Process Soloman and Corbit All experiences produce an initial affective reaction called the A State Drinking alcohol Can he Taking an exam Strength depends on tn nsity of the experience 7 The stronger the event the more ntense the A state Can be pleasant B State The A state causes a second reaction 7 B State Is opposite of the Astate 7 HA is positive B is negative and Vice Versa 7 D nation creates a pleasurable relief response Contend biological systems 39ate an opposing response to counter the initial eiiect of all events 7 similar to sympathetic and parasy pathetic systems Variables I B s initially less intense than A I B intensi es more slowly thanA 7 Produces a adaptation effect or reduced quot HM event occurs I B diminishes more sh 39thanA I So B continues a er the A a ite is finished Example Smoking Pleasure A state Arousal of B Withdrawal due to A begins Ultimately B causes the A state to diminish QLOp smoking A A quot 1re declines and you experience the B sic Withdrawal B ultimately decreases over ime Example 2 UCR CS UCS UCR I CS CR I CS acts as a cue Hotel Will take drugs slow system down A state SWquot 39 tn the UCS in Morph Need more dmg to go down effect tolerance reg System compensates for the druL B state Change the one home No AS ate I Same amount ofdrug I Overdose Example 3 Muirquotw quotWW PM i f i m a mlnsum law m bum sugar lave rm sum asmara man mm H1 m MN m w WWW Canvpar salovy Stlmuhd Edam wantons mmnov wlililnlo glutagnn 15E is m Related Issues Conditioned Withdrawal Wikler and Prescor Placed dogs in a distinctive cage CS Gave dog muphine UCS Feel good UCR Dog became addicted Stop MN 39 CS NO UCS uced them in withdrawal stat V Extinction Mmths later Place dogs in distinctive cage S No UCS Dog experience withdrawal symptoms shaking hypothermia increased l Cravings emouona rty Spontaneous Recovgry Implications I Must take CC into account for treatment I Current treatment models 7 Avoid Triggers I However CS can generalize to similar CS 7 Hotel Motel I Recall Spontaneous i r 7 Takes several time of CS 6X before trial I Recall Opponent Process 7 B still there a er no drug is presev Treatment Alternative Childress et al I Exposed cocaine addicts to stimuli they associated With drug taking 7 Videotapes of their cooking procedures 39mg to quot39 7 Handling Paraphernaua Measured Withdrawal and cla 7 responses Over time cravings and Withdraval responses decreased With repeated exposm s KEY Present stimuli under controlled settings Not on the street Use cognitive imagery or similar runqucs Conclusions Classical conditioning is extremely important to addiction Follows classical models V s uraJUl 1 quotans in biological systems models Drug Craving and D3 Receptors PET scan studies oflongterm cocaine users I Exposure to drugrelated stimuli activates the dorsolateral prefrontal cortex amygdala cerebellum I D receptors locatedwithin nucleus accumbens may g mediate drug cravr 7 T1 rww 7 quotall a ercocaine us Cocainerexparrmced n e selfradmrn startheDg receptor agonistiOHrDPAT Whereas cc salve k m o gym not 7 D3 receptor density is increased im leus accumbens of cocaineoverdosed humans 7 Antagonism of brain D3 receptors F 897 can reduce cocaine action in rats trained to self dminister cocaine Habituation A decrease in some response due to repeated exposures to a stimulus eg Walk into a room with a bad odor Sulfur At first you grimace and attempt to avoid the smell Once you habituate it doesn t smell as strongly as it did at first Sensitization An increase in some response due to repeated exposures to a stimulus eg Walk through the woods At first you are alert to the noise sensitized then you habituate Then atwig snaps You immediately become alert and responsive again Signals may be potential dangers Works in Neurons Hebb rule Habituation and Sensitization Often occurs very rapidly Usually is not caused by fatigue Usually is associated with some type f annulus quotan be harmful to the organrsm Discrimination Here the organism differentiates or discriminates between the original stimulus and the new stimulus f2 orgarns resented with the original CS and a CS The organism responds o the original CS and not tot re new CS Drug Craving and D3 Receptors PET scan studies oflongterm cocaine users Exposure to drugrelated stimuli activates the dorsolateral prefrontal cortex amygdala cerebellum D3 receptors located Within nucleus accumbens may mediate drug craving 7 T1 r V 39 quotall a ercocaine use Cocainerexparimced me selfradrmmstarthe D3 receptor agonistiOHrDPAT wheeas cc waive monkeys Willnot 7 D3 receptor density is increased in n leus accumbens of cocaineoverdosed humans 7 Antagonism of brain D3 receptus F 897 can reduce cocaine action in raw trained to self dminister cocaine Classical Conditioning Anabolic Steroids MacGregor Brown amp Bryce Inman Psyc 472 PeIfonnance Enhancing Dlug Statistics o 3 6 ofhlgu school students abuse stemlds RJsenmarlyZVmZEIEIZanlydnlgmhznhmecslasymshnwm 0 Men that abuse seermds have a h 1 meldence ofsome form of oplold abuse 0 Over 3000000 people lu the USA have reponedthe use of stemds 0 19577175000 Women reported stermd use 0 15 ofNCAA athletes use performance enhanclng drugs 0 90 of athletes reponedhave used some form of performance enhanclng drugs dunng there career Testosterone o Producedby Leydig s eellslutestes o Responsible for secondary sex characteristics lumen o Sex glandsJibido from elevatedleve s History of PeIfonnance Drug Abuse Gaels nyonedusmgcextammmhmoms 2mm seedm muse Pex mnce FeduzlAmbolm CmmlAd bussuuueemlas us AsclrlAMe 3 drug EstrogenAromatase lasuuaml esuugeh eplmy Ammanse e uh 2111 m whlch fem sex humane cammls remluy eye In Wmen Estradml ls bemflcul m mus cl gewlh DHT E o Through 5alphareouctase testosterone is convertedto ahormone 4x as poten dihydrotestosterone o DHT binds to receptors much more avidly than testostemne o 5alphareouctase is present in high amounts in tissues ofthe prostate skin scalp liver and central nervous system AnabolicAndrogenic Anabulic e skeletal mus dmsity hemn gnhin nitrn gm retention and prnten synthesis building incrmsed AndrugEmcr sham gens are sex ale mass bune hui39munes that an induce rrale Lmitseg gnwunnrsexnrgans increased budy hair libidu 5km n e o AnabolicAndrogenic steroids AAS seekto rnaxnnize the anabolic e ec s w e mmirmzlng the androgenic effects The ratio ofthese anabolicandrogenic effects is called the Mempeutm index Testosterone is the baseline at 1 Basic modifications of Testosterone e RemuvetheH With amethyl nr enzyrratie ennvesinntn awm a gen What are steroids rat snluhlernnleenlewhiehenntains asystemuM rings madeup om Erbun atnrns E g ehnlesternl estrogentestostenneprngestemne cumsul ete AnahnhesterninDEAeAny hui39mu su ancechEmically and pharmaculugcally relatentn testosterone thatprnrnntes nnisele guWLh a ens Therapeutic index of common AAS Do anabolic steroids work Most research has Fuwier Results rmss steroids produce no Juhnsun g errbul inrngnay Nu inneasein MM lgoseNihal znrnynay Nu intraseinmusde M ii a rDrbul lunrngnay Nninneasein MM AAS Administration Oral preparations 7 17 methyl alklayted to survive acidic gastric secretims short half life e g dianabol winstrol Injectable solutions 7 prepared in wata or oil Longer release times for oil e g Nandrolone Decanoaue o o e g m i a an E l 25 3 g 5 Q7 E E a 8 E S E i 3 57 3 F 0 Aerosol propellant 7 rapid effects very hard to detect in drug tests 0 Sublingual preparations 7 absorbed directly into blood stream so avoid digestive system rapid effecm Positive side effects ofAAS Enhanced muscle massstrength Enhanced blood volume and hemoglobin concentration Enhanced bone density and strength Hastened healing ofmuscular injuries Decreased body fat Increased immune response to Elevated mood Common AAS Practices 0 Cycle 7 period oftime ranging from 1 to 4 months in which AAS user mkes steroids 0 Stacking 7 combining 2 or more steroids 0 Pyramiding 7 a gradual buildup in dosage and then tapering off at the end U Why AAS produce muscle Activation oerNAresulting in protein synthesis Anticatabolic effect 7 block action ofnatural cortisone Increase free testosterone levels Stimulates activity of IGF1 Insulinlike growth factor Clinical Applications v Bone metabolism conditions 7 osteoporosis Testosterone de ciency conditions 7 male hypogonadism andropause Cardiovascular conditions 7 reduces angina pectoris hypertension coronary artery disease AIDS 7 reduces AIDS Wasting Common AAS 0 Illegal In US Testosterone Cypiorrate Testosterone erranthate Nandr ne Decanoate than ostenolone Oxyme sterone Vehe 39na Sher ds eqn poise BoIdenone undeeye1ate Trenbo one Dianabol methandrostenolone h o Easyto useveryeffecuve alk d 0 C17 alph ylate Can sh xlxem effects dte to tts tendeney to e l7alph a nnethylestaadol a form of estrogen that 15 nnueh more aetaye lnLhe body 0 Short half llfe 375 hrs Side Effects Hypertension aene ui intention hypogonadism gynecomastia s eep disturbances increased aggression epistaxis nose bleedswld1drawal depression prostate enlargement hean enlargement ylnuzan39on abnormal blood clottinglilyido reduetion appetite stimulation benign prostate enlargement Deca Durabolin Nandrolone deeanoate 7 g e eets Deteetable for over 1 year tn drug screemngs Winstrol stanozolol h 0 Not eapable ofconvemng tnto estrogen dte to modlflcauons at the WC o 3 2 ronn C17 nnet ylataon relatayely few de effects Acne and hair loss gt Sebaceous glands gt Highly androgenic a 1 fquot il sterords that convert to seere on are stimulated by DHTWIII aggravate andro ens baldng gt Bad aene may deye1op gt D 391 hair onthe shoulders back follicle eventually and face killing it Gynecomastia o Female hreasttissue resulting from high levels of estrogen o Estrogen acu upon receptors in the breast and stimulates the gowth of marmnary tissue o Removed only by surgery Stunted Growth 0 Iftaken during adolescence or before AAS m It gro This occurs because they stirrlulate epiphyseal plates on long bones to fuse prematurely Once fused no growing can occur 0 Stunted growth caused not by AAS but the conversion of AAS to estrogen AAS that do not convert to estrogen will actually promote height Cardiovascular disease 0 AAS have a strong effect 0 AAS increase IDL levels on LDL and HDL levels and lower HDL levels D od o Oralcompoun much cholesterol because it more likely to promote this removes cholesterol adverse effect deposits omthe arteries o LDL hasthe opposite effect Permanent SteroidInduced Rage Behavior o Animal studies show alterations to the test receptors inthe brain They ve also shown modi cations to other receptors o The mostbothersome alterations in the brain are the increase these receptors A er cessation ofAAS usethese receptors are thought to be hungy for elevatedandrogen levels Other NT s recogiize this de cit and may remainlow similar to andropause resulting in depression selfesteem problems and a geater tendency to lash out Testosterone and Aggression 0 Testosterone associated AAS monounced effects on With social dominance 39he llmblc system 0 Test exacerbates ght or gt AAS can zeta neurotransmitters lght response gt In supraph ysiologic doses AAS can alter function of n and increase e number of 3918 tted With receptors Pn39son studies situational gt Can also modulate other studies 39 the brain 0 Studies indicate anincrease 15 o Cancer 1 0 AAS are just a Symhem versmn of The only exception to this hormones that are already present in the is the use Of 517 alpha body so the stress on alkylaled C l 0u ds organs is not very high which are llver toxic 0 such cancer They have been known resulting from AAS is to induce liver damage extreme y rare and cancer Sexual Dysfunction Testicular atrophy Impotence Male reproductive system produmon o gst is 6 turn level of androg off along wrtn ho ones Reboun ma equot65 5gt effect occurs alter AA Sumng m a use in Whlch no meab change m androgens are present size othe testicles in the body Body Dysmorphia AAS o en produce addiction and body image disorders that have bee abeled as Megorexia or bigorexia Reverse anorexia Adonis complex Muscle dysmorpliia Women and AAS virilizatio 0 Large amounts oftest n can produce Wumen develup maseuline i o e eliaraetensae sa very noticeable side effects s sueli a tin niee enanges in slon texture aene libido liair less budy liar and enlargement of tlie elitnns AAS amp the Gateway Phenomenon A er AAS over 50 used drugs such as 31 estrogen receptor inhibitors 22 HCG 17 diuretics andor uppers 15 pain klllers Aromatase inhibitorsEstrogen Blockers o Aromataselnhibitors o Estrogen Blockers Blneks the arumatase enzyme Bmds tn See an H L ugenuus test prnduetinn e g Nulvadex Tamuxlfen eiaate suppresses 1191 ennlesternl prevents water retenann e g Anmldex anasanznle Stimulation of Test Production HCG e usedehme ally to treat Hypothalamus GnRH hypergonaddsm Used postr ate endogenous test by thmtary LHFSH mtmie LH ciornrde used eunreauy as a Testes fertility atd ets as an estrogen antagoms opposes negative feedback of estrogens on hypothalmus Testosterone Cutting compunds Clen terol one Betaezsypatnornrnetre Used yroid d s b enodriato de ciency obesrty d 5 as mdmm otner rnet b 1 e dsorders 1r propertresbt Syntheti ofT usedpnmar y as a men stimulates tnyrord thermogem eornpound by glandresut e tly st ting fat eeeieranon ofeellular eeus andbr down dons m ease rn mglyeendes Effects are metabolis temporary e o own eardovasemarrunedons gulatm ebound effect Androstenedione 0 Produced by the adrenal glands 17alphahydroxyprogesterone ampDHEA 0 Once produced it is one step away from testosterone and estrogen 0 Missing the a hydrogen atom in the 173911 position 0 Processed by the liva where the hydrogen atom is added Hypoglycemia one possible outeorne of use Can also result rn immediate death eorna or rnsuirn dependent diabetes Steroid PrecursorsProhormones h 0 Androstenedione 0 Androstenediol o Dehydroepiandrosterone DHEA Steroid Chart Estrogen or Testosterone Estrogen or Testosterone o Testosterone A An ostene ne is converted into testoster by 17betarhydroxysterold dehydrog nase which quot r IS activat d l 1 Zing ho N yp us and pituitary glan o Estrog Androstenedlone may also be converted to the estrogen by the enzyme aromatase Androstenediol Why Androstenediol E 0 Similar to Androstenedione 0 Has higher conversion rates to testosterone o Lacks a 3keto group that enables the o Doesn t convert into estrogen conversion into es o Does not convert into DHT cause of 0 A much more androgenic compound balding produces much more male based etrects Why Take a Steroid Precursor o 2 steps away o Increase lean muscle mass o A precursor to testosterone that is produced 39 adrenal glands o Aids in prod ing Androstenedione which produces testosterone an 0 Increase libido 03 quot Only temporauly increases blood levels of 0 DHEAgtAndrogtTestosteroneEstrogen testosterone does not c body to naturally produce testosterone 7 d H Negative Side Etfects t Enlnigedproitnte t Redinediiennoount t Inorenrednggieiiion t Kidnech Liwrdnning t Dumpt the nienrtiunloyole t DECMSE lewliofHDLohJ eiterol HATUDALI BALANCE H What is Creatine t Ananino unidtaken into thehodythrough meats and animal products What does Creatine do in the body 0 Once ingeitedoientne ii iyntheiinzdinto phUSphDCMilW in the kidneys iwr nnd the panoienr t Crentine u iyntheiizedhythe thiee ninino nerd nrginine glynine nnd methionine 0 Once iyitheiizediito yhoiphooientine itii trnrninrtedto skeletal nuclei the henit nnd the hrninforenergy innge What Does Creatine do inthe Body Cont t Assistsutithheprodue donofATPwhiohii used for short term energy exerti on H What is All E t Adenoiine hiphoiphute ATM t ATP is used during shortterm hdiinteniity energy outnuti n do ADP an W39he ATP is broken down during is produced with the loss ofaphos tensity exerci A w d phosphorous reproduced to provide maximum When this occurs phosphocre its phosphate ions to facilitate ATP How Does Creatine Assist with the Production of ATP exercise energy phate ion se is constantly and energy output atine donates one of the resynthesis of Results of this Process o Reduced msclefatzgue the rate own does not excee at which it can be resynthesized o Decreased Lactic Acid o Faster Recovery at which d the rate There 31 h Possible Risks increased nskf incre sed cancer cause Excessive us prnduce cre Side Effects is no pure evidence that creatine causes actual physic arm Weigit gain uf erkgs due tn the increase uf tiuid stores Dr rnuscie ciarnps and tears du water retenann cancer ernay de reas the bodies natural ability tn aane etuthe ax How is Creatine Taken 0 Powder form 0 Pill Typical Dosage o 5g daily A regular usage o 20g daily 7 During lo creatine supply in the ading period to build up body U Growth Hormone GH 0 Anaturally occurring hormone in the body 0 Signaledrelease from the hypothalamus 0 Release from the pituitary gland regulated by two hormones omatostatin SS 7 decreases GHoutput Growth HonnoneReleasing Hormone GHR 7 Increase GH output I Can also be regulated by the amount of GH and Insulin Like Growth Factor 1 JLGF 1 that is circulated back through the body U Other Factors that Increase GH E 0 Decreased blood glucose during exercise and sleep trigger the release of GH 0 High protein increase small amounts GH release 0 Some amino acids such as Larginine can increase GH by decreasing the release SS from the hypothalamus 0 Niacin has been shown to increase exercise induced GH release by 300 600 Murray 1995 U Theory 2 ual Effector Theory Similar to the Somatomedin hypothesis except itis believed that GH alone has anabolic elfects without ILGF Studies inmice have shown that mice injected with GH are signi cantly larger than those that were solely injected with ILGF U GH in the Body 12 U Theories about GH E Somatomedin hypothesis Daughaday 1972 GH is released from the pituitary gland O N Travels to the liver where it is converted into ILGF ILGF enters the blood stream and stimulates muscle growth 5 How does GH Cause Muscle Growth Once converted into ILGF ILGF stimulates the production of and the conversion of satellite cells into muscle cells Satellite cells Cells that lie dormant around muscle tissue until stimulated by ILGF Have the ability to replicate the genetic makeup of muscle cells Side Effects 0 One of the most common side effects of GH abuse is acromegaly overgrowth ofbone and connective tissue which leads to achange in physical appearance suchas a protrudingj aw and eyebrow bones 0 Metabolic dysfunction Glucose intolerance U Beta Blockers E 0 Medically used to Reduce blood pressure Migraine headaches Heart arrhythmia Alcohol withdrawals Antianxiety Physiological Effects During heightened arousal adrenaline is produced Heart rate increases and blood pressure is increased Beta Blockers block the beta receptor on the muscles ofthe heart which reduces these effects How is GH Administered 0 Must have a prescription 0 M injections 0 Dosage Aweekly dosage of 030 mgkg of body weight 0 Very expensive Can be over 20000 for an annual supply of Growth Hormone U Athletic Uses Reduces anxiety jitters and slows the heart rate Commonly used in sports that require a steady d Golf Archer Rifle shooting Side Effects v 0 Impotence 0 Low Blood Pressure 0 Insomnia 0 Cardiac failure 0 Poor circulation 0 May reduce performance capacity Diuretics Increase the amount ofurine formation and the rate at which it is excreted Usedin sports that require reduced Weight such as Wrestling Huse racing Bodybuilding Boxing Also used to maskthe use ofother performance enhancing drugs U Blood DopingErythropoietin E 0 Blood Doping Adding additional blood to the system to increase the amount ofred blood cells in the system Increased red blood cells increases the amount of oxygen that the body can carry 0 Thus increasing the perfumance during endurance rm spo Illegal but hard to detect Side Effects I Can be very dangerous Bacterial infection Induce shock Hypertension troke May receive the Wrong blood type Increased blood viscosity Increasedworkload Increased risk for blood clom Increased risk for heart amck 9999999 In Side Effects 0 Dehydration 0 Decreased circulation of blood volume 0 Muscle cramps 0 Renal disorders 0 Dizziness 0 Disrupted Heart rhythm U Erythropoietin 0 A naturally occurring hormone released from the kidneys 0 Causes increased production of red blood cells Increased oxygen capacity Increased tolerance to lactic acid Additional Performance Enhancing Drugs 0 GHB Enables athlete to reach deeper state When sleeping 0 Body produces more growth hormone Highly abused among athletic community as a recreational drug because it produces similar intoxication to alcohol Without the caloric intake and hangover Additional Performance Enhancing Drugs 0 GHB Enables athlete to reach deeper state when sleeping 0 Body produces more growth humme Highlyabused among athletic community as a recreational drug because it produces similar intoxication to alcohol Without the caloric intake d over Hallucinogens BY Kasey And rews Kelly McDowell Statistics at 1965 1971 Hallucinogen use rose tenfold from 90000 to 900000 new users at 1990 2000 Use again rose nearly 3 fold from 600000 to 15 million new users at 2001 2002 LSD use decreased dramatically while MDMA and others rose De nitions Substances that create gross distortions in perception without causing loss ofconsciousness when administered in low doses Substances that alter sensory processing in the brain causing perceptual disturbances changes in thought processing and depersonalization Hallucinogens also called I Psychedelics substances that expand or heighten perception and consciousness I Psychotomimetic substances that mimic psychosis I Psychotogenic substances that produce psychosis Hallucinogens Are found naturally in plants and can be produced synthetically Are used by Native American tribes for use during religious ceremonies Resemble 1 of 4 neurotransmitters gt Aoetyhholine gt Catecholamines Norepinephrine amp Dopam39ne gt Serotonin Common Hallucinogenic Effects Alterations in time and 4 Visualdisturbances tion 39 Space Pe39FeP Le ashes of light 2 Changes 39quot se39f39 or kaleidoscopelike awareness patterns 3 Increase sensitivity to mums shap l tastes 5 Hallucmatlons and sounds 5 Feelings of enlightenment or spiritual awakening 4 Categories of Hallucinogens i Anticholinergic Catecholamine Iike SerotoninIi ke Psychedelic Anesthetics J J J J 4 Anticholinergic Hallucinogens 0 Attach to Acetylcholine receptors and blockthe site so Acetylcholine cannot attach y impaiis ieamind and memniv as iesult o Fomd in Belladonna Nighlshade Jirrsonweed and Mand39ake plants 0 mouth decreased sweating dry skin increased body temperature blured vision increased heart rate dilated pupils d39owsiness decreased attention 39 Hallucinatiors paralysis of respiratory system coma and death 0 Examples Scopolamine Mand39ake Hyoscine Hyoscyamine and Atropine Scopolamne y used as DDlSDH and aDhiDdisia in Renaissance Times untamed in Datdva piant Mixed With diinks td ieate m in W s dtehiets m Wamms befuie v were bulied alive 0 Mandake used td tieat anxiety and acute Dairi um Catecholamine Like Hallucinogens I Also tallied Phenethylamine PSYCI39EdEIllS I Structurally similar to Calecholamins Norepinephn39ne amp Dopamine and Explans why these dug have stimulant and hallmriogenic ettece I Are mixed Dopam39ne and Serotonin agonists EXAMPLES Mesoahne Mwsnn E emcm Symmeuc A rrphetam ne Derwau ves M lstm amp Elemlcm Symhe c Amhe am ne Der a es oDOM emermmwmmumm e e 3 1 5 oPMA Panmelhul PNVEhmrE uCause mease ufserutumn m synapuc den amp week we reuptake u tfmm cb same furDuparmne unueasea Sevutumn effetts sensu w mfuvmatmn VEEEDUuH and Kansas mamas m s eeD Daltems and emuums DOM n 175 mg duses pmduoe euphu a and haHuunatuns fur era hum m duratun n HaHuunugemc effects uverpuwer me amwetarmne effecs s summantat uw D At 1 my duses can pruduoe tremurs cunvumuns and deem Meubc e Wm Uxed m mm 2pm Quad mm my beau men mm enuhn wmem Wm WM M quotan e W m mmuam m mm 9 m mum men muka 2ndde2lh MDMA I m Adam Ecstasy X E XTC Bbe K sses E bombs Happy Pill Hpg Drpg Smurfs Wafers 8t others I Moe psychedel c than MDA Synthes zed in 1912 I Schedule 1Drugh1985 I Effects similar to MDA MDMA Combos o Candy Flipping LSD MDMA o Diamonds Amphetamines MDMA o Disco Biscuits Depressants MDMA o Flower Flipping MLshrooms MDMA o HBomb Heroin MDMA o Gum Opium MDMA o Kitty Flipping Ketamine MDMA o Sextasy Viaga MDMA I Pharmacokinetics I orally injected or snorted I Effects last 36 hous I Dose is 12 tablets 60120 mg each I Readily absorbed in GI tract I Pharmacodynamics I Increases levels of Norepineptrine dopamine amp serotonin released MDMA Effects 9 Hallucinogenic Effects distortions in time ampperception e Stimulant Effects Euphoria amp hyperactirity increase blood pressure amp heart rate MDMAThe Negative Effects o Psychobg cal depressbn seyere anxiety paranoia and sleep dsturbances o Phys cal muscle tensbn teeth clenchhg nausea blurred ysim rapid eye movements chilb ampfantness a High doses sharp hcrease hbody temperature muscle beakdoym and ichey 8t wrdoyascular system failure 9 Tneseeffectalso happenatlgwdjses in coirbinanon Withintmse exegseoiagnyity o LongTerm lyer damage 8t brah damage eBaindama e eto mrtimofsecmjnnpiodicin mums Sel bet picblems inglatirg irmd pain sleep and aggression l5 i MDMA effect on Serotonin producing neurom 2 weeks caudal nucleus 2wks 839 reduction in serotonin axon density lyrs somerecoyeiy occursbutsigniticant loss of serotonin neurons has occurred vvvvvv PMA that of MDMA but more toxls Is extremely potent and lethal ed le 1973 Effects slmllar to old talslet sap l or powder form A lnlstered orally Inhaled or Injected o m a LETH g L sauslnd sardlas arrhythrrua renal fallurE vornltlnd hypertherrrua eath Mltsublshl Doublenstack PMA Cont gt 1973 produlted In Canada In Iandestine labs 1391 deaths attrlbuted to ts use n ths year gt 2000 7 d at ue to PMA ue vstrns lseleved they were taklhg esstasy so they assdentally overdosed Serotonin like Hallucinogens n a b l 39 2324 5 5 M j vl ExamQ es LSD Psilocybin PS 0 n MT Bufotenine Harmlne LSD Lysergxlt Agxd Diethylamxde Street Names Acid Battery Acid Pane Brown Bombers Pearly Gates Pink Panther Rainbow Superman White Ligwtening Window Glass Yin Yang Zen Yellow Sunshine Sugar Cubes amp others X Deried from ergot akabrds of the rye fungus X Coia39Ess odorless bttertrastzei X Most potent moo peroeptm aterng d39ug known to man can ca e effects at 25 pg n Weight to a few g39alre of salt X Can be synthesized n 1 week x Was used to weatacoholsm paranoia SCl ilZOpl39TEl iB and aurtsmi History at 1938 Abert Hofmam synthesizes LSD 25 1943 Hofmam dscovers halidclnogenc effects 13 hand Wen re acctentrall n st to lngests 025mg ufltthlnkrng lt is a mlrilmal dase When in actuality it is 10 times the duse needed to pruduce an effett ieid wavered and everything appeared deformed as h a faulty mlrrur Space ah time became more and more d lsurganlzed and i was uyercume by fear that i was gulrig aut at my mind it was particularly striking huw amustic perceptiuns such as the noise ufvvater ushlng from a tap at the spukeri word Were transformed hta Eptlcal illusions quot History Cont 19501963 LSD used experimentally n mental faclltes as treatment fo39 rrental dsordersi e 1950s CIAampArrry cmcLlctsecret experiments on human suerecls us LSD at 1953 Frark Chen a bocl39emst his himself after unh39towngl cmsurm rk ontanlng LSDi e 1966 Tlmo 39ly Leary an fo39mer professo39 at aryard fo39ms a relrglon caled League of Sprtual Dscoveryquot n an attemptto use LSD and o 39er halLlc nogere Egaly History Cont 1976 truth about the CIA ampArmy experiments are uncovered revealing that nearly 585 soldiers and 900 dviliam were given LSD without theirknowledge for research purposes March 31 2003 DEA bists the biggest LSD lab in history seizing 413 kg or91 lbs of LSD LSD in Popular Culture I Timothy Leary was a psyclnobgst in the 1960 s r 39 awareressi He began ruming H l ml 398 tt39el39nfLence ofLSDi Jerry I After beng remoed from his further LSD sturdy LSD In popular culture cant I Lewis Carroll39s Throug we Looi mass written about an LSD experience I Popular rrusiciars of i H nced yLSD Ex Beatles Grateful Dead etc Pharmacokinetics y Administered orallv smoked snorted or iniecred ses 253nm pd ietnai dpse 14EIEIE p y Micrpdpts tapiet form Window pares LSD in deiatin matter acid iiddid added to paper Sugar cdpes LSD in sugar cdpes Few it anv Witndrawai svmptoms raierance ard crossrtolerance to atner naiidcinpdens does occur is last Witnin davs after cessation ofuse Pharm acodynamics gt Binds to 5HT2 serotonin receptors gt Effecls the to disruption ofraphe nuclei pensmedulla which lters incoming sensory stimuli creating uge ofsersory information overload of brain circu39ls gt Effecls cerebral cortex involved in mood cognition and perception amp locus ceruleus receives sersory in o gt LSD in high concentratiors in iris of eye Effects 1 Dilation of pupils dczness deem depcned teeings cnanges in time perception cobrsmellssomds intersted increase heartrate amp bbod pressue ng mo inatioe d At High doses causes nausea tremors ampconfu5m u Moods typcaw depends on mood pro to use cadsng dnose to become ntensted D However moods can change qdckly from ecpnoe to terro and panc 2 Types of Emotional Responses to Q o Ecsta cTrarscendental Reactiors Lsers become talkative eLphoric ideas seem to have geat importance Panic ampPsychoticlike Reactions users experience interse anxie amp fear lose control of thoung ampemotiors become paniced n a d rig Can result in accidents or accidental sdicides duE to individual attempting to ee panic and terror thev are experiencing Long Term Effects Ps ch is dramatic mood swings sensory distortions seeing false motions or trails etc DMT Dimethyltryptamine Short acting serotonin agonist 30 min called busrnessman39s lunch break drugquot Produces LS like effects snorted or smoked can39t be taken orally because acrd In stomach destroys drug before absorptron can occur Metabolized by MAO monoa mine oxidase Found in Leguminous trees ampshrubs in West Indies and South America Dose 60 150 mg Bufotenine 0 Found in toad Skins 0 Metabolized by MAO o o o o PsilocybinPsilocin 4 phosph oryl DMT4 hydroxy DMT Found in psiaycbe maxcans mushroom Peak effects within 2 hours and last 6 10 hours Psilocybin broken down into psilocin active psychedelic agen Eaten dried or fresh Hallucinogenic effects at doses gt 4 mg a Drled mushroom contarns 0204 psllocybln W mushro ms magic mushrooms shrooms Musk Silly Putty Simple Simon o 1955 identified by n Wasson PsilocybinPsilocin History Gordo 1958 extracted by Albert Hofmann o Ate 32 mushrooms to d39scover effect Ololiuqui Found 39n morn39ng gbry seeds Used by tribes in Central amp South America s cre s halluclnations d39storted nfusio fecls na 5 I ng headache amp ess Harmine gt Found in plants amp shrubs in Middle East amp South America gt Side Effects intoxication hallucinations 9 sleep nausea and vomltln Psychede c Anesthetics Phencyclidi ne 39 7 4 Street Nams An el Dust Black Dust Blue d ee lefhanger Crazy Coke CrystalT D39pper Devls Fh39d Rocket Fuel Tic Tac Wobble Weed Yelbw Weed H isto ry Developed in 1956 as intravenous anesthetic 1965 Use was discontinued due to delirium and mania experienced after coming off drug effects lasted up to 18 hours 1967 1st appeared on streets Pharmacokinetics gt Administered orally smoked snorted or injected gtOften applied to parsby oregano or marjuana gt Stimulates brain reward areas thus creating psychological dependence gt Withdrawal symptoms sometimes occur Dose Effects W lt 5 mgj increased respiration heart beat and bloo pressure pro use sweatin numbness of extremities muscular incoordination hallucinations feelings of increased strength and invulnerability lzllQthQSis gt 10 mg decreased respiration heart rate and blood pressure nausea vomiting blurred vision ickering eyes Drooling dizziness seizures coma death memory loss speech difficulties depression weight loss I Pharmacodynamics NMDA N methyl D aspartate or Glutamate receptors Blocks open channel on NMDA receptor preventing glutamate from attaching and creating its effect oGlutamate phys rob in pa39n perception memory cognition and emot39on PCP Therapy 1 Minimize sensory input by placing them in quiet environment Administer acitvated charcoal orally it binds to in the stomach amp intestines preventing it from being reabsorbed Physically restrain user to protect them an thers 4 Sedation with Benzodiazepine i3 Ketamine Ketalar ale Jet llta if Special K v n gt Developed n 1953 to replace PCP nesihetc V1 menu gt Injected snorued oraly 3 lngested quotquotquotr odorless teteless so 39 often Lsed as dam rape drug v Ketamine Cont gt Blocls NMDA receptor channel or decreases outside of receptor Effects similar to pcv with bad trip called Kchole Other Hallucinogens Kinikinik Also called Bearberry rockberry beargrape or Samah Found n shubs or red WIllOW Inner red bark and dred leaves can be mixed wlh tobacco andor various herbal m xmes and smoked r es side Effects rash nausea vomtng abdomnal cramps gastrlts blsters n moulh and throat Conclusion n Hallucinogens are relatively safe a Hallucinogens are extremely potent a Hallucinogen39s effects are unpredictable thus can be dangerous to user and others a cause hallucinations and hallucinogenic eFFecls when taken in high doses 5 Alcohol Ethyl Alcohol Ethanol Types 6 Over 100 different types as Ethanol C2 H5 OH a Methanol CH3 OH in lsopropyl Ch32 CH2 OH E E E E E E E Background 6 Fermentation to make alcohol dates back to 4200 BC 6 Second most used drug in the world caffeine 1 6 Luxembourg tops list for legal purchase and consumption 126 litersperson 6 Latvia tops listfor legal illegal and homemade purchase and consumption 1620 litersperson a Whites have highest alcohol consumption rates 3 Americans consumed twice as much alcohol in 1830 as they do now College and University Use a Students drink 4 billion cans of beer arly a 360000 of 12 million undergraduates will die from alcoholrelated causes while in school 6 Nearly 12 of college students are binge drinkers 8 Average student spends 900 per year on alcohol books 450year Other Social Problems Associated with Alcohol Consumption 3 Correlated with crime in general Domestic violence 0 Rape 0 WI 15 Economic costs are huge gt82 Bllllol l ll l lostbroductiyity o 18 8 bllllOl l toralcohol problems ngllllonfol39othel39drug problems Economic burden of alcohol and drug problems falls on the population that do not abuse alcohol or rugs Other Comments Can have therapeutic effects when consuned in moderation 1 drink per day 0 Does not depend on the beverage Causes body damage when consumed in greater amounts Minimum age drinking laws have mixed effects Most laws related to drinking and driving have minimal impac nging ehavior Get short term reductions and the behavior goes back to rmal Ross studies Ethanol Background Information a Is a simple molecule a Is classified as a CNS depressant 3 Contains no vitamins minerals etc a Only contains 210 caloriesoz 9 Requires no digestion 6 Once in the system it stays until metabolized amp Makes it unique Distribution 49 After absorption goes evenly throughout the body a Easily crosses the bloodbrain barrier Also crosses the placenta and erters the blood stream of a developing fetus a Essentially goes to all cells a Impacts all cells Hun III Behavioral Effects 01 Decreased lnhibitions 0102 Vision Changes 03 Changes in inhibition 05 Buzz Beginning to decrease motor coordination 08 10 Decreased motor coordination legal limit 15 20 Severe loss of judgment and muscle coordination 30 Passing out coma 40 5 Death Factors that In uence BACs 3 1 Concentrationthat is ingested S 2 Proof of the beverage 3 3 Speed of consumption a 4 Carbon Dioxide a 5 Sex ofthe individual a 6 Tolerance a 7 Altitude 8 Circadian Variation 3 9 Ascending vs Descending BACs 3 10 Fructose 11 RO15 4513 and others Concentration that is onsumed E Generally the greater the concentration the faster it enters the bloodstream Dnthe rocks is betterthan not on the rocks a if concentration becomes to great can decrease bloodstream entry I Can shut down the system Proof of the Beverage 8 Amount of alcoholvolume of water 0 100 Ethanol 0 Water 200 Proof Oniyexists il i airless environmenE UsuaiiyiQO Proofis as good as you can get 0 50 Ethanol 50 Water 100 Proof 0 40 Ethanol 60 Water 80 Proof a Is not the same as concentration amp The greater the proof the faster the entry into the blood stream a To high gt100 proof it can inhibitentry unth ed the concentration Is red uc Speed of Consum ption a The faster you drink the faster the BAC rises Carbon Dioxide a Carbon Dioxide makes ethanol cross the mucosal membranes faster than straight ethanol 6 Makes you drunk faster is Scotch and Soda gets you faster than Scotch and water Sex of the Individual 6 If a male and female are the same body weight the female will get drunk faster than the male Reasons Women have less alcohol dehydrogenase than men Metabolizes alcohol slower in 6 Men have more muscle to fat than women More muscle more blood in solution dilutes the ethanol and lowers the BAC is Women have more body fat than men Fat contains little blood in solution Less solution the higher the BAC Tolerance aThe greaterthe tolerance the betterthe person will function when under the influence a Note BAC is still the same Altitude eThe greaterthe altitude the fasterthe ethanol crosses the mucosal membranes Get drunk faster Circadian Variation 3 Circadian Rhythms will influence how drunk you will get Ascending vs Descending BACs You are drunker on the ascending side of the BAC curve than at the same level on the Descending side of the BAC curve Gibw Time Why s Neurons have adapted somewhat 6 Beginning Tolerance Fructose a lncreasesthe metabolism ofthe liver 6 Slightly decreasesthe BAC R0154513 and others a Block the effects of alcohol on receptor binding sites 6 Have the same BAC but no behavioral effects Effects of Ethanol on Body Structures Mouth 6 Trace amounts absorbed here 9 Causes Irritation lesions o ulcers oral cancer a Is a tube surrounded by muscles and blood vessels 3 Has a mucosal lining 6 Causes Damage to mucosal lining Esophageal ulcers Esophageal Cancer Esophageal Varices stomach Pylorlc Valve a 1520 absorbed here 5 Stimulates production of HCL 4 Irritates and damages mucosal lining 6 Changes the electrical properties ofthe stomach lining a Gastritis s Ulcers a Achlorhydria 6 Spasms in the presence of large amounts of ethanol Intestinal Wall I O O Blood Vessel 0 Small Intestlne i a Majority of Ethanol absorbed here 0 L a Damages Mucosal Cells Villi and I c 0 IL Microvilli l 6 Decreases absorption of nutrients O and vitamins 00 OO O a lncreasesTriglyceral and Cholesterol 0 O i 0 production Intestinal Wall Pancreas 9 Increased concentration of Pancreatic enzymes a Decreased volume of enzyme secretion is Pancreatitis a Decreased insulin production Secondary Diabetes Pancreatic Duct Pancreatic Duct Gall Bladder Large Intestlne a Decreased amounts of Bile Secretion a Decreased water and vitamin absorption 3 Diarrhea RBC s Decreased Production Effects on Blood Cells Anemia WBC Decreased production Decreased response time Get more infections Increased risk for STD sIHIV f r Platelets a Decreased production 6 Decreased clotting time E More bumps and bruises Nervous System Neurons ha Alters neuronal membrane Lipid Bilayer a Decreases amounts of Na that enters the ax 3 Decreased height of the action potential 396 Alters Ca influx Decreases the amount of NT that is released 3 Decreases transmission speed gt8 Increases tolerance a Demyelination More a Inhibits the function of NMDA subtype of Glutamate Receptor Decreases the responsiveness of NMDA receptors to glutamate a Binds on BZ subunit of GABA receptor Inh bits other neurons by increasing CI into post synaptic element a May impact Serotonin receptors 5HT2 5HT3 located in Dopamine Post Synaptic Elements in Nucleus Accumbens Brain Structures Alters newer evolutionary structures first then older structures a Damages Frontal Temporal lobes hippocampus etc a Decreases the numbers of dendrites and axons 6 Increases Ventricle Size 9 Decreases blood flow Related Brain Damage Blackouts Sleep Changes WernickeKorsakoffs Syndrome Other Psychological and Psychiatric problems 6626 WernickeKorsakofl39s Syndrome 3 Due to a lack of B vitamins 49 Results from damage to cortex peripheral nerve cells 6 Key symptom is corrfabulation Get holes in memory so you fill them in a Usually STM is the most affected a Poor Prognosis Visual System a Decreased accommodation time a Decreases tracking ability 6 Double vision 6 Decreased recovery time Endocrine Effects 6 Inhibits Vasopressin release a Decreases thyroid hormones progesterone testosterone Luteinizing hormone and others s Damages or kills Leydig Cells 6 Increases feminine characteristics 3 Decreased sexual drive reproductive failure impotence Females 6 Early Menopause 6 Premenstrual discomfort a Increased menstrual Flows 6 Infertility Muscle Tissue Skeletal Muscle a Disrupts internal structure of the muscle 6 Cramps pain weakness Alcoholic Myopathy Cardiac Increased Weight of the heart Dilation of heart chambers Scar tissue Card iomyopathy 662626 Rem oval of Ethanol Methods s Trace amounts through respiration and sweat a Some through fecal material a Most is metabolized by the liver via two systems Alcohol Dehydrogenase System Substance Degrading Enzyme amp Ethanol Alcohol Dehydrogenase 3 Acetaldehyde Aldehyde Dehydrogenase a Acetic Acid a 002 H20 9 Respiration a Urination Microsomal Ethanol Oxidase System MEGS 3 Substance Degrading Enzyme a Ethanol MEOS 8 Acetaldehyde Aldehyde Dehydrogenase i Acetic Acid a 002 H20 3 Respiration i Urination Ethanol Effects on the Liver Fatty Liver Cirrhosis Portal Hypertension Decreased vitamin production Decreased hormones and other products important for body functioning w Other Issues Genetic Differences a Decreased ADH metabolic Rates for Europeans s6 Increased ALDH metabolic rate for Europeans FAS s Increased numbers of spontaneous abortions Endocrine Changes a BAC 6v Drugs Additive effects Benzodiazepines Synergistic effects Barbiturates Decreased effectiveness Antibiotics Conclusion 6 Most damaging drug there is 19 Influence every system 6 Causes major socialeconomic problems 33 Highly correlated with aggression Membrane Neurophysiology Overview of the Neuronal Membrane Associated Ions and Ion Channels Measuring the Difference Betweenthe Inside and Outside of a Neuron I A axon from a Voltmeter giant squid is placed in seawater in a recording chamber Microelectrode I Glass microelectrode is inserted into axon El Voltage rreasures inside with respect to outside Chamber Concept I In ux Material Ions moving to the inside ofa membrane I Efflux Material Ions moving from the inside to the outside of a membrane I Equilibrium Where material ions concentrations etc are equal on both sides ofa membrane Structure of a Neuron at Rest Na CI K Anions Resting Membrane Potential I Is the difference in voltage between the inside and outside of the axon membrane Why do Ion s Move I Concentration Differences Compounds move from hi h concentrations to lower concentrations I Electrostatic Pressure Like charges repel each other Opposite cha rges attract each other Sta I Can be explained by the Nernst Equation in nonrliving organisms and GoldmanrHodgkinr Kat equation in living organisms Why is There a Resting te The neuron membrane is selectively permeable to certain ions I m I Pomssium K Resting State I At rst K ions can lave the axon while I Causes the exterior of the nerve cell be more positive than the inside of the axon w Na ions can enter the axon I Chloride Cl 7 I Calcium Ca rad39 Result I Have high conoentrations of Na and Cl Ion Concentrations at Rest on the oulside of the axon Hign Na Hign Cir Low x High conoentrau39ons of K and Anions on the inside of the axon Hign w Arllorls 7 Low Na Relative Ion Concentrations concept Across the Axon Membrane Mllllll lllllllllllllllllllllllllllllllllllllllllb i gs 39 39 I Depolarizamn Beoomes more posi ive I Hyperpolarization Becoms more Channels I Axons have two types of channels or pores for different ions Passive Channels I Are open al of the time and allow ions to pass through the membrane Voltage Gated Channels I Are activated by changes in voltage I Eg voltagegated Na channeb Passive I Are open all the time Channel Outside Cell Membrane In side Passive I Many K passive channels are open I Some Na passive channels are also open I Channels are ion selective Na channeb are only selective for Na K dosn39t get through K channels are only selective for K Na dos not get through Ions abo go through channeb at different rats l 12 Kto 1 Na Some ions are moving but not many Ifth of movement you get equilibrium VoltageGated Channels I Are needed for the action potential I Several types Na K Ca I Channels are ion speci c I Open at some level of depolarizaton then inactive gate closes a bit later I After inactive gate closes active gate closes inactive gate then reopens I Repeat Sodium Voltage Gated Channel o Inactive Active Gates are Usually Closed With Depolariztion Active Gaes open Steps I Get Depolarization I If depolarize 15mV Active gate 0 ens Sodium enters Get an action potential I If does not depolarize 15mV Nothing So all or nothing is happening at the Axon Hillock Side Note I If you provide a substance that causes Na to bind to the inactive gate and bloch it shut get lack of pain from receptors Mechanism of action by Lidocaine Procaine Cocaine Potassium Voltage Gated Channel Inactive 0 0 Q Active Gates are Usually Closed With Depolariztion Active Gaes open Points I Like the Na Channel the inactive gate is sluggish I It takes awhile for them to close Na KATPase or Na K Pumps I Exports Na to the outside of the cell I Imports K to inside of cell I Exchanges 3Na 2K I Usually occurs in the axon Neurophysiology Electrotonic Potentials Electrotonic Potentials I Also Called Passlve Potentlals I Are decremental they decay Rate of decay depends on I D39stanoe measured from point of stimubh39on I Amount of Myelin I Length of the axon I Diameter of the axon I Other Decremental Changes Point of Stimulation ll it Q Q Charges Decrease in Both Directions from the Point of Stimulation I Begin to stimulate get depolarization becomes more positive I K begins to move against the membrane and tries to leave by passive diffusion If the membrane is thick the length of dissipation also increases Length Constant I Distance along the membrane from the point of stimulation where the change in the resting potential has dissipated to 37 of the original Length Constant Point of Stinulation 100 mV 37 Dissipation 37mV SHIP Length Constant 100 37 Point of Stim ulati on L LHJ u Temporal Summation I Present a stimulus every milliseconds I Observe depolarization Time Resistance I If membiane is resistant to K leaving it becomes more dif cult for K to leave I Speed is the same I All is done by passive channels I Decrease resistance by increasing the diameter of the axon Thus length constant will also dictate temporal 39 How do you get an Action Potential Answer I Add and Subtiact Charges I Geneially must depolarize the membiane 15mV to get voltage gated channels to open and get an action potential Action Potential Action Potential 5 Action Potential Influences I Distance away Length constant I Temporal summation I Inhibitory neurons Cause hyperpolarization at the hillock becomes more negative I Combination of depolarization and hyperpolarization determines if Voltage Gated channels open I A alone Get Nothing I B alone Get Nothing I D alone Get Nothing I C alone Voltage channels open get AP I A B D Voltage channels open get AP Alcohol I Alters the lipid bilayer I Causes less Na to enter I Less depolarization fewer action potentials to begin Action Potential General Overview I Occurs because voltage gated channels open I Results in rapid and large Na in ux I Get iapid depolarization and hyperpolarizaton mszmgmz p o T E N T I A L s Process of an Action Potential Stimulation Begins K begins to leave by passive channels Na enters by passive channels El Get a change in concentration gradients El Amount that leaves depends on the strength ofthe stimulus tem oral summation etc El Begins depolarization lfdepolarization is reaches 15mV voltage gated Na channe s open El Get Na in ux Na K ATPases start El Removes Na and brings in K El Three Na per Two K El K also leaves through passive channels El K voltage gated channel begins to open about 12 39 39 Na vultage gated channels open Process of an Action Potential cont 5 Na voltage gated inactive channel finally closes El Action Potential begins to fall K inactive gate finally closes El K is still leaving by passive channels El Na is leaving by K pump El Action potential continues to fal El Get a negative undershoot 39om resting state Ca voltage gated channel begins to open Still do not have enough K so get Ca influx Finally enough K so Ca inactive channel egins to close 10 Ca channel finally closes Process Repeats As 9 mung Review I When a stimulus enters a receptor on a dendnte It causes change In polanty I Causes a change in the chemical concentration gradients I Allows sodium to enter in small mounts and depolarizes the neuron I The depolarization travels to the axon hillock If the charge depolarizes hillock 15mv get an action potential I If the charge is not strong enough the signal stops x Review ICausessudiurtLgatesintheaxonto o n pe I Get Na Influx I Result the axon goes from negative on the inside to positive on the inside I This change goes down the axon like a wave I After the sodium enters the sodium potassium pumps turn on and begin removing sodium I Also goes down like a wave Review I So we have two waves going down the axon The sodium entering the axon The sodium being pumped out I Ultimately the result is a negative undershoot Saltatory Conduction I Asaction39rrotentlarsh39averdown me axoni 1 it depolanzes tine ri ltt Na voltage gated enannel 2 Process of each channel slows down conduction speed I Deuer s on size of the axon Myelin Allows the action potential to jump from one ode of Ranvier to ano er no e 7 AP depolanzes next Na voltage gated enannel at Node of Rarlvler 7 Less work 7 increases speed otdne actori ootenual even ll l small axons When the Axon Potential Reaches the Presynaptic Element I It causes calcium Ca to enter the presynaptic element I Calcium causs the synaptic vesicles to move down protein laments and bind with the prsynaptic membrane I No Ca no ef ux of NT 7 Botulinum Toxin blocks Ca in ux 7 Mg also interferes with Ca in ux rad39 NT Release Result I The neurotransmi er is then relmsed into the synaptic c e I The neurotransmitter crosses the cleft an binds on receptors in the post synaptic element I Causes a Rust Synaptic Fbtential Alcohol Again I Decrmses the amount of Na in ux I Decrmses the amount of K ef ux I Decrmses Ca in ux I Less NT release Postsynaptic Potentials Ps I Areeither 1 EgtltcitatoryEPSP 2 Inhibitory IPSP Receptors I Two Major Typs Ionoh39opic Metaboh39opic Ionotropic Receptors Receptor and lon eg Nicotimc Beta and Delta subunits are concerned with regulatory functioning Characteris ics I Are very rapid to respond I put on some NTand the channel opers Take of the NT and the channel closes I Is a simple system I Ion channel is part of the reoeptor Most are not J Metabotropic Receptors Metabolism ion Channeland receptor ion Channel sites are rn different Uses lnlracellularMessEnuers 0 Vrumlhe ammo site lulhe inn 0 a manner Called second a a D Cam Error 9 Site I a common Messenger Characteristics I 39lhe chamel is not part of the receptor I 39Ihere are intermedia 5 ps that occur pu a te group on the on chamel Called Phoepl39prlaton I Are slow to respond corrpared to ionoh39opic receptors I Are slow to shut down Remove NT but have a delay to remove the Phosphate go thus the system 5 ill works for aw Ie I Rovides more rngIation of the system Metabotropic Receptors How to Shut Down the System I Remove the phosphate group on the channel closes the ion channel I Remove the seoond messenger 7 Pump out the Ca Remove the NT How I Degrade r Simplest method 7 Eg Acetylcholinesterase AChE is on the surface of the Poseynapuc n Degrades Ach is also ll l the synaptic Cleft Sequence Second Way I Reupbake e Reabsorb m into the Presyriaptlc Element I Lashachle Theorm Remove NT from the cleft and the NT on the receptors comes 0 Based orr concentration gradlel lB How Do You Degrade and Bind on Receptors Simultaneously I Receptors have more af nity I Binds tighter Several Types of Voltage Gated K Channels Delayed classic type A Shakerrrelated or Kv Anomalous Recti ers Inward Recti ers 7 Have 5 so types Kr Mir 5 c anne s Each have different roles 7 Some important for Cardiac tuncuorrrrg e have a role rr diabetes


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