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19 Cards in this Set
- Front
- Back
acute effects of cocaine |
euphoria, increased energy, mental alertness; decreased appetite; increased HR; increased BP; vasoconstriction; hyperthermia; mydriasis |
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chronic effects of cocaine |
addiction; irritability; mood disturbances; restlessness; paranoia; auditory hallucinations |
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acute effects of heroin |
rush (45sec-mins), on the nod aka sedation/tranquility (about 1 hr), depressed resp, clouded mental functioning, nausea and vomiting, analgesia, constipation, pin point pupils
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chronic effects of heroin |
addition, collapsed veins, abscesses and bac infections, infection of heart lining and valves, rheumatologic problems, adrenal/gonadal homeostasis, mood swings, malnutrition and chronic constipation |
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what is drug reinforcement |
a form of behavioral plasticity in which behavioral changes occur in response to acute exposure to a reinforcing drug; drugs are classified as REINFORCERS if the probability of drug seeking behavior is increased in response to drug exposure |
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what causes this rapid and powerful association |
hypothesis= the result of drug's ability to directly influence PRE EXISTING BRAIN SYSTEMS; these systems normally mediate the reinforcement produced by NATURAL REINFORCERS such as food, sex, social interaction, or even compulsive internet use |
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what is drug addiction |
a complex phenomenon that involves a biological process= the effects of repeated exposure to a biological agent (drug) on a biological substate (brain) over time; the long term alteration of neuronal circuits leads to the complex behaviors of craving, dependence, tolerance, etc |
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TOLERANCE= |
MORE DRUG REQUIRED; THIS IS ON THE TEST |
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SENSITIZATION= |
LESS DRUG REQUIRED; THIS IS ON THE TEST |
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what brain system is involved? |
mesencephalic DA systems= mesolimbic tract (arousal, memory, behavior), nigrostriatal tract (modulation of EPS), mesocortical tract (cognition, socialization), tuberoinfundibular tract (inhibition of prolactin release) |
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the mesolimbic DA system |
mesolimbic dopamine system as a major neural substrate for the reinforcement produced by opiates, psychostimulants, ethanol, nicotine, and cannabinoids |
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self administration in rats |
animals will self administer amphetamine and dopamine into the NAc; lesions of the mesolimbic DA neurons attenuate the reinforcing effects of iv cocaine; other drugs (ethanol and cannabinoids) cause increased DA release in the NAc |
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what does cocaine do |
blocks the reuptake of dopamine into the presynaptic neuron |
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summary: |
with chronic drug abuse the brain depends on the drug to maintain rewarding feelings (activate pathway); NATURAL REINFORCERS ARE NO LONGER EFFECTIVE |
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acute drug state aka the first time you take cocaine |
increased mesolimbic DA and decreased cAMP; DECREASED CAMP IN THE NAC OPPOSES REINFORCEMENT; acute inhibition of this system may also contribute to drug craving and relapse in addicted subjects |
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chronic drug exposure |
produces an up regulation of the cAMP pathway in the NAc which could underlie tolerance to reinforcement |
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look at slide 56 on drug dependence and reinforcement lecture |
do it |
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short term abstinence |
withdrawal; increased glu, NE and decreased DA and 5-HT |
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LONGER LASTING MOLECULAR AND CELLULAR ADAPTATIONS TO NAC |
THIS IS ON THE EXAM; TRANSCRIPTION FACTORS= gradual accumulation of proteins such as deltaFosB during chronic tratment with many classes of addictive drugs; deltaFosB is very stable, after its slow ACCUMULATION in NAc may represent a molecular switch that gradually converts acute responses into relatively stable adaptations that underlie long term responses such as craving (once it's flipped on, it stays on) |