Lecture 13 new (Pharmacology of Drugs and Abuse) Flashcards Preview

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Flashcards in Lecture 13 new (Pharmacology of Drugs and Abuse) Deck (63):
1

drug abuse (substance abuse)

-maladaptive pattern of use of a substance

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drug addiction (dependence)

-when an individual persists in use of alcohol or other drugs despite problems related to use of the substance
-tolerance may develop to drug
-withdrawl symptoms when use is reduced or stopped

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Percent of persons 12 years of age and over with any illicit drug use in the past month

8%

4

Percent of high school seniors that reported nonmedical use of vicodin

1 in 10

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Percent of high school seniors who have abused oxycontin in the past year

1 in 20

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percent of people aged 12 or older who reported driving under the influence of alcohol at least once in the past year

-12.4%
about 31 million people

7

positive reinforcement

-anything that increases the probability of a behavior occuring again
-food, drugs of abuse, physical violence

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reward

-positive stimuli which causes feeling of euphoria
-ex: food, drugs of abuse

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Mesolimbic dopamine system

-activated by food, water, sex, drugs of abuse
-releases dopamine in the nucleus accumbens (NAcc)

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Dopamine cell bodies

-located in ventral tegmental area (VTA)
-project to the nucleus accumbens, prefrontal cortex, and limbic areas

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How does the administration of an abused drug change the strength of excitatory synapses on DA neurons in VTA

-increases their strength

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increase in DA release at mesolimbic terminals like the NAcc (ventral striatum) results in:

-reinforcement of drug taking behavior

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negative reinforcement

-removal of an aversive stimulus that increases probability of behavior occurring again
ex: if someone has a headache they take a ibuprofen. the headache is gone so negative reinforcement has occurred

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physical dependence

-long-term use of drugs
-can produce tolerance and withdrawl

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tolerance

-decreased sensitivity to a drug following repeated use
-ex: how many drinks to behavioral intoxication?

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withdrawl

-opposite physiological effects as drug administration present during absence of use
-symptoms of withdrawal are brought to you by the body's attempts to maintain homeostasis

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heroin

-euphoria
-constipation
-relaxation
-hyperthermia

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heroin withdrawal

-dysphoria
-diarrhea
-agitation
-cold-flashes (goosebumps)

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negative reinforcement role in drug taking behavior

-removal of withdrawal symptoms reinforces drug use
-removal of unpleasant feelings not associated with the drug

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alcohol's reduction of social anxiety

-alcohol may be taken in advance when individual anticipates anxiogenic situations

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craving

-urge to self-administer the drug even after a period of abstinence

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relapse

-return to drug use after a period of drug abstinence

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feelings of getting high can become associated to....

-stimuli present at the time
-stimuli associated with drug taking thus become exciting and motivated on their own and may induce drug craving
(ex: paraphernalia, location)

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alcoholics in experiment with sight and sip of alcohol using an fMRI

-sip of alcohol AND sight of alcohol related images (cues) increased craving in alcoholics but not controls
-this also showed increase activation in mesolimbic dopamine system

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prefrontal cortex in drug addiction

-plays an important role in executive functions
-planning
-evaluation of consequences of actions
-inhibition of inappropriate action
-prefrontal lesions cause IMPULSIVITY

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Volkow (1992)

-activity of PFC of cocaine abusers during abstinence much less than normal subjects
-when performing tasks that require PFC drug addicts perform poorly compared to controls and show less PFC activation
-amount of PFC activation and weekly amound of cocaine ingestion inversely related!

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maturation of PFC

-occurs around age 20
-very few addiction cases occur after the age of 20

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Opiates

-derivative of morphine
-the active ingredient of juice from the opium poppy
-ingestion produceds analgesia, euphoria, relaxation
(ex: morphine, heroin, Vicodin, Oxycontin, Codeine)

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Egyptians use of opiates

-medicinal value
-1500 BCE

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1914 Harrison Act

-prohibited recreational use of opiates

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three major opiod receptor types

-m-opioid (MOR) receptors (analgesic and euphoric effects caused by activation)
-d opioid receptors
-k-opioid receptors

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Animals lacking MOR---> what reaction of reinforcing or analgesic effects of morphine?

INSENSITIVE

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MOR high in regions of brain that deal with...?

-positive reinforcement (nucleus accumbens)-analgesia (PAG, spinal cord)

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Opioid Receptors

-G protein coupled
-activation leads to neuronal inhibition

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cause of disinhibition by use of opiates

-inhibition of inhibitory (GABA) neurons
-this increases DA release in mesolimbic targets (gx: Nacc)

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Lesion of mesolimbic dopamine system

-only decrease (not completely blocked) opiate reinforcement
-there may be other reinforcing mechanisms at work

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treatment for opiate use

-methadone maintenance

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methadone

-potent opiate administered orally
-low steady long lasting levels of MOR agonism in brain
-does not produce addictive high like heroin because oral administration = slow absorption
-already agonist at MOR, heroin injection is of little euphoric consequence
-most likely a life-long maintenance solution

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cocain

-alkaloid dound in the leaves of the coca plant native to South America
-from 1850-1880 cocaine was a popular cure-all
-regulated by harrison narcotic act of 1914
-begining in 1970s wave of increasing cocaine use in US (IV, snorting, crack)
-15% users----> addicts

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Freud believed which drug to treat alcoholism, depression, morphine addiction, digestive disorders, pain

COCAINE

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Cocaine effects

-blocks monoamine transporters
----> blocks the reuptake of dopamine, norepinephrine, serotonin
-it increases DA concentration in NAcc

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Cocaine treatment

-no treatment to antagonize DA (dysphoria/ataxia)
-no FDA approved medications for cocaine addiction

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cocaine treatment

-cocaine vaccine contains antibodies that bind to cocaine molesules and inhibit drug from crossing BB barrier
-does not stop craving
-some addicts will risk an OD by trying to take more cocaine until vaccine is saturated
-at this point the addict will die from the other effects of the drug (taking too much)

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Nicotine

-active ingredient in cigarettes/chewing tabacco
-alkaloid found in the leaves of the tobacco plant native to South America
-1500 popular in durope in pipes, cigars, chew
-mid-1800s new advances in curing tobacco leaves/ cigarette machine popularized smoking

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Leading cause of preventable death in developed countries

-tobacco use

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Nicotine effects

-binds to nicotinic ACh receptors (activates them_
-DA projection neurons excited/DA release increased in NAcc
-ion channels open allowing Ca++ influx

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6-OHDA lesions of dopaminergic pthway from VTA to NAcc

-significantly attenuate nicotine self administration
CLARIFY!!!!

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Nicotine treatment

-replacement therapy with gum or transdermal patch is more effective than placebo (most successful with counseling program)
-once smoking subsided, nicotine dose can be gradually decreased

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Non-nicotine component of smoking also addictive

-smokers rate the euphoria or regular or non-nicotine cigarettes in 7 seconds (less time than it takes nicotine to get to the brain)
-there may be rewarding component transferred to act of smoking after continued use

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Ethanol

-most commonly used psychoactive drug in the US/most drug abused (after caffeine)

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who/when was the first beer brewed?

-by the Egyptians in 3700 BCE
-8000 BCE mead was brewed from fermented honey

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American tavern

-focal point in each town for conducting business, local politics, and mail delivery

53

18th ammendment

-1920
-amendment probhibiting sale, manufacture, importation, and transport of liquior

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appeal of the 18th ammendment

-1933
-repealed by congress under FDR

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Regulation of alcohol today

-regulated by age, circumstance (operating a vehicle), and taxation

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Effects of Ethanol

-agonist at GABAa receptors
-low doses----> euphoria (anxiolytic
-high does---> loss of coordination, sedation

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GABA agonism

-how ethanol produces sedation
-GABA A antagonists block ethanol binding site on GABA receptor preventing GABA induced sedation

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Ethanol is an antagonist at....

-NMDA glutamate receptors
-non-copetitive channel blacker of the NMDA receptor (reduced Ca++ and NA+ influx)

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Reduced glutamate in hippocampus leads to...

-reduced LTP and decrease declarative memory formation

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NMDA receptor acitvation does what to DA neurons in VTA?

-inhibits DA neurons
-alcohol disinhibits VTA DA neurons
-leads to an overall increased DA in NAcc

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ethanol treatment

-opiate antagonists reduce the rienforcing value of alcohol

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naltrexone

-opiate receptor antagonist used to treat alcoholics

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naltrexone symptoms in alcohol users

-increased latency to first sip
-reduced rewarding value of drinks
-reduced amount consumed
therapy---> higher success