Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Ch.18
Drug Abuse
| Question | Answer |
|---|---|
| Operant Conditioning | Antecedent(Stimulus)-Behavior-Consequence |
| Reinforcer | strengthens a response |
| Punisher | weakens a response |
| Increase Behavior | Positive reinforcement(add something) and Negative Reinforcement(take away) |
| Decrease Behavior | Positive punishment(add something) and Negative punishment(take away) |
| Addiction from the Latin word Addicere | To Sentence/ idea is that someone is sentenced to a term of involuntary servitude of the drug |
| Symptoms of Drug Abuse Disorder | Repeated use of substance which results in tolerance of effects |
| Symptoms of Drug Abuse Disorder | Craving for the substance |
| Symptoms of Drug Abuse Disorder | Intentions to reduce use of the substance |
| Symptoms of Drug Abuse Disorder | Large amounts of time are spent seeking or using the substance, or recovering from its effects |
| Symptoms of Drug Abuse Disorder | Continued used of Substance despite significant problems in work, school, family, or social interactions related to its use |
| Symptoms of Drug Abuse Disorder | Continued use even in dangerous situations, or when substance abuse worsens physical or psychological symptoms |
| Delayed Positive Reinforcement | Prevents animal from learning to take the drug |
| nucleus accumbens | dopamine is released by addictive drugs, the release of dopamine is necessary, but not sufficient for reinforcement to take place |
| Ventral Tegmental Area (VTA) /synaptic strengthening | a single injection of a drug shows synaptic strengthening for about five days, and if the animal continues to receive cocaine for two weeks the changes persist |
| Changes to VTA | Lead to increased activation in regions that receive dopaminergic input from the VTA |
| Ventral striatum | includes nucleus accumbens and dorsal striatum |
| Synaptic changes particularly in the Dorsal Striatum | are responsible for the compulsive behaviors that occur after the continued use of an addictive drug |
| Early Reinforcing Effects | take place in the ventral striatum particularly in the NAC |
| Dorsal Striatum | Where the changes occur that make behaviors become habitual |
| Blocking Dorsal Striatum | In rats whose lever presses were reinforced by intravenous injections of cocaine, bilateral blocking of dopamine to dorsal striatum decreased lever presses |
| cocaine addicts | they show a much smaller release of dopamine in the NAC or dorsal striatum than do non-addicted people |
| addicts when showed a video of cocaine drug use | showed an increased release of dopamine in the dorsal striatum |
| addicts | response to the drug is diminished, but the response to cues associated with the drug is intensified—in the dorsal striatum. |
| risk of addiction | The likelihood of becoming addicted is a function of heredity, age, and environment |
| prefrontal cortex in adolescents | Regions of the prefrontal cortex have inhibitory connections with the striatum. The role of the PFC in judgment, risk taking, and control of inappropriate behaviors may explain why adolescents are much more vulnerable to drug addiction than are adults. |
| Adolescents & the Prefrontal Cortex | Approximately 50% of cases of addiction begin between the ages of 15 and 18 (very few begin after age 20). Early onset: more severe addiction and a greater likelihood of multiple substance abuse |
| Orexin | is synthesized in neurons in the lateral hypothalamus and released in many parts of the brain, including those that play a role in addiction, such as the ventral tegmental area, nucleus accumbens, and dorsal striatum. |
| infusion of orexin into the VTA | reinstate drug seeking that was previously extinguished. |
| MCH | melanin-concentrating hormone |
| melanin-concentrating hormone | is also synthesized in the lateral hypothalamus, and stimulates hunger and reduces metabolic rate. |
| MCH receptors | are found in the NAC on neurons that also contain dopamine receptors. |
| administering a drug that blocks MCH receptors | decreased the effectiveness of cocaine or cocaine-related cues on the animal’s behavior. Same is true with alcohol. |
| Stimulating both dopamine receptors and MCH receptors | increases firing of nucleus accumbens neurons |
| Tolerance | is the decreased sensitivity to a drug that comes from its continued use; the user must take larger and larger amounts of the drug for it to be effective. |
| Withdrawal symptoms | are the opposite of the effects of the drug itself. |
| Withdrawal | is produced when the the compensatory mechanisms are unopposed by the action of the drug (because of the absence of drug), so they are strong enough to be felt. |
| Positive reinforcement | provokes drug taking in the first place, reduction of withdrawal effects could play a role in maintaining drug addiction. |
| negative reinforcement | The withdrawal effects are unpleasant, but as soon as the person takes some of the drug, these effects go away |
| Classical conditioning | stimuli that have been associated with drugs in the past can elicit craving. |
| Anti-addiction posters | Their effect on people who were trying to break a drug habit: an urge to take the drug again |
| Reinstatement Model | mice were given saline to extinguish behavior and once the lever press produced the drug, the behavior was reinstated |
| Extinction | a form of learning, not forgetting |
| vmPFC | ventromedial prefrontal cortex |
| ventromedial prefrontal cortex | plays a critical role in extinction |
| Lesions of the ventromedial prefrontal cortex | impair the extinction of a conditioned emotional response |
| Stimulation of the vmPFC | inhibits conditioned emotional responses |
| Extinction training | activates neurons located in the vmPFC. |
| Stimulation of the ventromedial prefrontal cortex | blocked the reinstatement of responding that is normally produced by a free shot of cocaine (or the presentation of a stimulus associated with cocaine reinforcement). |
| Dorsal Anterior Cingulate Cortex | Reinstatement of lever pressing for infusions of cocaine was abolished by stimulating the (dACC), a region of the dorsal PFC that has excitatory connections with the NAC. |
| ventromedial prefrontal cortex | plays a role in craving suppression |
| dorsal anterior cingulate cortex | plays a role in craving activation |
| Medial Prefrontal Cortex | Activity in the MPC of cocaine abusers (in abstinence) is lower than that of healthy controls |
| When addicts are performing tasks that normally activate the prefrontal cortex | their medial prefrontal cortex is less activated than that of healthy controls |
| Medial Prefrontal Cortex | The amount of activation of the medial prefrontal cortex is negatively correlated with the amount of cocaine that cocaine abusers normally take each week. |
| People with long history of drug abuse | the same deficits on tasks that involve the prefrontal cortex as people with lesions of this region and show structural abnormalities of the prefrontal cortex |
| cocaine and tobacco abusers | an average decrease of 5–11% in the gray matter of various regions of the prefrontal cortex |
| cocaine and methamphetamine abusers | decreases in the gray matter volume of the cingulate cortex and limbic cortex |
| gambling and tobacco abusers | evidence of loss of behavioral control caused by decreased activation of the dorsomedial PFC |
| alcoholic patients | Prefrontal gray matter volumes were 10.1% lower |
| schizophrenic patients | Prefrontal gray matter volumes were 9.0% lower |
| alcoholic and schizophrenic patients-comorbidity | Prefrontal gray matter volumes were 15.6% lower |
| Stressful situations | can cause former drug addicts to relapse. |
| Corticotropin Releasing Hormone | plays a role in development of adverse effects on health produced by stress and on the development of anxiety disorders |
| Corticotropin releasing hormone (CRH) | link between stressful experiences and drug craving |
| Administration of CRH | can reinstate drug taking behavior |
| Administration of a drug that blocks CRH receptors | can reduce the likelihood of relapse from drugs or drug cues. |
| Infusion of a CRH receptor antagonist | prevents reinstatement of drug-taking by a stressful stimulus |
| Infusion of CRH into the VTA | causes relapse |
| cocaine-dependent women | subjective level of stress induced craving - positive correlation with stress cue condition-related corticostriatal-limbic activation |
| cocaine-dependent men | subjective level of drug-induced craving - positive correlation with drug cue condition-related corticostriatal-limbic activation |
| In cocaine-dependent women | correlations between drug-cue related craving and activation: observed (in the hippocampus, insula, orbitofrontal cortex, putamen, and midbrain) |
| In cocaine-dependent men | correlations between drug-cue related craving and activation: observed (in the hippocampus, insula, and anterior and posterior cingulate) |
| Opiates | Significant tolerance, Exposure to unsanitary instruments, Crosses placenta, Toxicity of diluting substances and uncertain strength of batch |
| Neural Basis of Reinforcing Effects of Opiates | pain tolerance, hypothermia, sedation, Increases dopamine production in the NAC by 150-300% |
Created by:
Dalea
Popular Neuroscience sets