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week 6 notes

by: Emma Notetaker

week 6 notes NSCI 4530

Emma Notetaker
GPA 3.975

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week 6 notes
Dr. Donhanich
Class Notes
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Popular in Psychopharmacology

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This 8 page Class Notes was uploaded by Emma Notetaker on Thursday October 6, 2016. The Class Notes belongs to NSCI 4530 at Tulane University taught by Dr. Donhanich in Fall 2016. Since its upload, it has received 20 views. For similar materials see Psychopharmacology in NSCI at Tulane University.

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Date Created: 10/06/16
Tuesday, October 4, 2016 Week 6 Exam 1 Review • epidural administration IS NOT the same as intrathecal • **sublingual administration of nitroglycerin is the preferred route for immediate relief from chest pain caused by constriction of the coronary artery because: nitroglycerin undergoes extensive first-pass administration • NOT poorly absorbed by the GI tract, NOT water soluble • nitroglycerin is the classic drug administered sublingually • intranasal drug administration bypasses BBB, 1st pass, gastric degradation and allows peptides to access the brain • intestinal surface area promotes more rapid absorption of most drugs neutral pH of plasma hinders return of aspirin from blood into stomach • • **nicotine (weak base) can be absorbed from cigar smoke my lining of the mouth (pH 7) unlike cigarette smoke because cigar smoke has a more basic pH compared to cigarette smoke • (more basic, so more molecules are unionized) • won’t get pH high above 7 in most living beings • when in a water-soluble state, most drug molecules enter and exit general capillaries following administration via intercellular clefts • plasma protein binding is NOT irreversible • movement of most drugs from brain capillaries into brain substance usually occurs via lipid soluble diffusion • —> no pinocytosis, intercellular clefts or fenestra • movement of charged compounds (NOT lipid soluble) like glucose or amino acids get into the brain via carrier-mediated transport (ex: glucose channel) • area postrema is located IN the medulla (CAN be accessed by polar molecules) • in order to facilitate excretion, biotransformation produces a form of a drug that will be ionized in renal tubules • increasing the pH of the renal tubule fluid would promote excretion of a weak acid • people may smoke more when they’re stressed because they’re eliminating more nicotine (stress makes renal tubules more acidic) • metabolic rate is NOT affected by drug concentration in zero-order metabolism • ADH increases aquaporins in collecting tubules • synthesized by hypothalamus • higher T = lower risk of side effects • decreased eliminateon unlikely to shift dose-response curve for an agonist to the right partial receptor agonist fails to fully activate effector mechanisms • • affinity and accessibility ARE NOT NECESSARILY LESS than those of full agonist • DECREASES effect of full agonist when administered simultaneously • radioligand doesn’t necessarily have to exert intrinsic activity when bound to receptors (could be an antagonist) • intrinsic activity examples: induces dissociation of G protein • • activates effector enzymes • activates protein kinase • opens ion channel • epinephrine accounts for 80% of the adrenal output of catecholamines 1 Tuesday, October 4, 2016 • product and secretion of adrenal medulla (NOT cortex) • NOT induced by activation of noradrenergic receptors (nicotinic receptors) • on competition plot, y axis is % specific binding of radioligand • x axis: increasing concentration of competitors • compete occupancy of competitors at the far right • intrinsic activity cannot be determined via competition experiment Psychostimulants • main psychostimulants: cocaine and amphetamine mainly affect catecholamines • • catecholamines • catechol nucleus • benzene ring + 2 adjacent OH groups • amine group (NH ) 2 • basic • catecholamine synthesis: • process: tyrosine, DOPA, dopamine, norepinephrine, epinephrine • all are metabolites of each other • tyrosine is an amino acid (NOT catecholamine bc no adjacent hydroxyl groups) • tyrosine —> DOPA via tyrosine hydroxylase (TH) • • TH adds adjacent OH group onto the benzene ring • DOPA is a catecholamine • TH is rate limiting enzyme • DOPA —> dopamine • via aromatic amino acid decarboxylase (AADC) • gets rid of COOH from alpha carbon • dopamine —> norepinephrine • via dopamine beta-hydroxylase (DBH) • this adds an OH to the center carbon • norepinephrine —> epinephrine via phenyethanolamine N-methyltransferase • • adds methyl group to nitrogen (makes NH-CH ) 3 • synthesis can be increased by L-DOPA (precursor) • high catecholamine levels inhibit TH - negative feedback effect • storage: • catecholamines stored in synaptic vesicles inside presynaptic membrane • vesicularization - vesicular monoamine transporter (VMAT2) • protein channel takes up dopamine after synthesis and packs them into vesicles • H+ ions pumped into vesicle to maintain low pH (this is so they do not diffuse out of the vesicular membrane - at a high pH, they would become unionized and lipid soluble) • stops enzymes from breaking down neurotransmitter controls rate of release, controls quantum nature of release • • reserpine • reserpine blocks vesicularization of monoamines • free monoamines degraded by MAO (monoamine oxidase) • ultimately depletes brain of monoamines 2 Tuesday, October 4, 2016 • induces sedation, reduces blood pressure, implicated in mental disorder theories • has been shown to reduce schizophrenia symptoms, increase depression’s symptoms release • • controlled by calcium influx • regulates enzymes that control moving towards membrane, docking, fusing, etc • calcium enters via voltage-gated ion channels • cluster of proteins in synaptic vesicle • budding filing with neurotransmitter • • packing of nt prevents it from being degraded by enzymes • docking and priming • exocytosis - fusion with membrane caused by calcium • release inhibited by auto receptors (these open K+ channels) • removal from synapse via reuptake (via transporters) OR degradation catecholamine transporters act in reuptake: in membrane of presynaptic membrane • • DAT - reuptake of dopamine • NET - reuptake of norepinephrine • dopamine degradation (2 methods) into homovanillic acid • mainly broken down via catechol-O-methyltransferase (COMT) or monoamine oxidase (MAO) 1. dopamine —> 3-methoxytyramine (3-MT) • • via COMT • 3-MT —> homovanillic acid (HVA) • via: MAO and aldehyde dehydrogenase • 2. dopamine —> 3, 4 dihydroxyphenyl-acetic acid (DOPAC) • via: MAO and aldehyde dehydrogenase • DOPAC —> HVA cia COMT • **measuring levels of HVA can tell you how much dopamine was there in general • norepinephrine degradation (2 methods) • 1. norepinephrine —> normetanephrine • via COMT • normetanephrine —> vanillylmandelic acid (VMA) • via MAO • 2. norepinephrine —> dihyroxymandelic acid • via MAO • dihyroxymandelic acid —> vanillylmandelic acid (VMA) • via COMT • epinephrine degradation (2 methods) • 1. epinephrine —> dihyroxymandelic acid • via MAO • dihyroxymandelic acid —> vanillylmandelic acid (VMA) • via COMT • 2. epinephrine —> metanephrine • via COMT • metanephrine —> vanillylmandelic acid (VMA) • via MAO • metabotropic receptors: • D1 • D2 3 Tuesday, October 4, 2016 • D3 • D4 norepinephrine: can work through different types of receptors that link to separate 2nd • messenger systems (gives flexibility) • a1 • activates PLC • contest pip3 to DAG and ip3 • IP3 causes calcium to stimulate smooth muscle contraction —> phosphoinositide stimulated • • a2 • inhibition • Gi protein • decreases cAMP activation • B1 activation increases cyclic AMP • • Gs protein • contracts heart muscle • B2 • B3 • release regulated by autoreceptors located in presynaptic membrane • • NOT the same as reuptake!!! • bind neurotransmitters onto presynaptic membrane • inhibit transmitter release (like “brakes” for the system) - inhibits calcium entry into the cell • D2 - for dopamine • ????2 - for norepinephrine • most cell bodies of catecholaminergic neurons found in mesencephalon (project from mesencephalon to higher areas) • nigrostriatal pathway (dopamine) • substantia nigra (A9) to striatum (caudate-putamen) • mediates movement, coordination • mesolimbic pathway (dopamine) • VTA (A10) to nucleus accumbens • reward, reinforcement (mediation of drug dependency, addiction) • mesocortical pathway (dopamine) • VTA (A10) to cortex • coherent thinking, concentration, etc. • tuberoinfundiblar (A12) pathway (dopamine) • more of a hormonal pathway • arcuate nucleus —> median eminence • median eminence —> anterior pituitary • dopamine dumped into portal vessels • DA inhibits prolactin release • milk synthesis • noradrenergic pathway (norepinephrine) • locus coeruleus (A6) to higher brain regions • arousal, attention, focus • neurotransmitters do not interact directly with drugs • typical drug targets 4 Tuesday, October 4, 2016 • receptors • transporters autoreceptors • • enzymes • reuptake blockers: increase transmitter in synapse • autoreceptor agonists: decrease transmitter release • enzyme inhibitors: increase transmitter levels • amphetamine/meth can cause release of catecholamines without nerve cell firing cocaine: erythroxylon coca • • plant derivatives: bases containing nitrogen (nitrogenous bases) • Peru, Bolivia, Columbia • preparations: • leaves • cocaine HCL (salt) cocaine base (free base) • • pressed to purify, get rid of the liquid • leaves softened, toxic things added (gasoline) • created LOTS of waste • processing: • coca leaves chewed to absorb buccal (free-base form) • • some chew something with it to make mouth more basic to unionize more cocaine • doesn't cause dependency • coca paste made from leaves (still in basic form) • toxic chemicals added to be able to snort and make cocaine HCl • cocaine HCl • stable salt, most purified • best for export due to stability (won’t break down for a while) • CANNOT be inhaled • water-soluble • degraded before vaporizing (vaporization point higher than degradation point) • this causes little effect because much is destroyed before absorption • used to only be used in this state • cocaine base: • free base • water insoluble • process: • mix cocaine HCl with ammonia • extract precipitate with ether (ether very flammable and explosive) • evaporate ether - vaporizes • now free base that can be inhaled for absorption (put in pipe) • crack cocaine • mix cocaine HCl with baking soda (sodium bicarbonate) • heat • filter precipitate • wash precipitate and dry - now can be smoked • can be made without dangerous ether • administration • leaves - buccal 5 Tuesday, October 4, 2016 • HCL - intranasal, intravenous • base (free base or crack) - inhalation absorption and distribution • • weak base • increasing GI absorption with increasing pH • rapid absorption intranasally • very rapid absorption via inhalation (almost like injection) • onset and duration of action intranasal: onset in minutes, duration of 60 minutes • • inhalation: onset in seconds, duration of 15 minutes • distribution: • crosses blood brain barrier • plasma cocaine concentrations: • IV and smoking are very rapid, shorter duration cocaine biotransformation: • • metabolism: • via liver • first order • major metabolites (ecgonines) • benzoylegonine cocaethylene • • half-life • after around 4 hours, drug eliminated from plasma • metabolite persist up to 3-5 days after last administration, much longer in heavy users • detection depends on sensitivity of procedure • mechanisms: • cocaine action at synapse: • blocks reuptake of dopamine (blocks DAT) • increases dopamine concentration in synapse, which activates reward system • could also block uptake of serotonin (SERT) and norepinephrine (NET) • need both dopamine and serotonin for cocaine to have effect? • cognitive and behavioral effects: • arousal • alertness • wakefullness • energy • decreased distractibility • increased concentration • confidence • well-being • euphoria • body weight effects • increased general activity/physical performance • suppressed appetite • decreased digestion • reduced body weight • peripheral side effects • increased Heart Rate • increased Blood Pressure 6 Tuesday, October 4, 2016 • increased Respiration Rate • dilation of Airways dilation of Pupils • • inhibited Digestion • decreased Salivation • urinary Retention • increased Cellular Metabolism • increased Body Temperature toxic effects: • • headache • dizziness • confusion • agitation • fatigue insomnia • • nasal Bleeding • seizures • cardiac Arrest • stimulant Psychosis • effects on cardiovascular system increases demand (increases heart rate and blood pressure) • • reduces heart function • constricts coronary artery, reducing oxygen reaching heart • exerts direct toxic action on heart • potential consequences: • cardiac arrhythmia • heart stoppage or cerebral stroke • sympathetic control of cardiac muscle • a2 autoreceptor • B1 receptor • over activation of B1 receptors by NE contributes to cardiac arrhythmia • increase force of myocardial contraction • increase rate of contraction • excess stimulation leads to arrhythmias • stimulant psychosis • paranoia • delusions • hallucinations • stereotypes • therapeutic uses • local anesthetic • middle ear, pharynx, larynx, muscosae of the nose, cornea, iris, urinary tract, rectum • reduces blood flow to site • substitutes include procaine and lidocaine • “Uber Coca” • Freud used himself to record cocaine’s psychological effects • didn’t pay enough attention to its anesthetic uses • better than ether and chloroform because they cause vomiting • Koller: dropped cocaine in eye of a dog - felt nothing when needle later poked it 7 Tuesday, October 4, 2016 • likely that Freud neglected this because the other effects are so strong 8


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