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Ch.18
Drug Abuse
Term | Functions |
---|---|
Environmental Risk Index /Swedish study | (adoptive parental history of Divorce, Death, Criminal Activity, and Alcohol Problems, adoptive sibling history of Drug Abuse and Psychiatric or Alcohol Problems) strongly predicted the risk for Drug Abuse |
Risk for Drug Abuse was Significantly Higher for /Swedish study | Genetic Risk Index (biological parental or biological sibling history of Drug Abuse, Criminal Activity, and Psychiatric or Alcohol Problems) |
Risk for Drug Abuse was Significantly Higher for /Swedish study | Adopted Offspring of Biological Parents with Drug Abuse Biological Full and Half siblings of Adopted Children with Drug Abuse, Adoptive Siblings of Adopted Children with Drug Abuse |
cocaine | genes that produce sirtuins modify responsiveness to the addictive potential |
nicotine addiction | Variations in the gene for the α5 acetylcholine |
alcoholism | genes for alcohol dehydrogenase, play a role in susceptibility |
Specific factors | likelihood of taking and becoming addicted to a particular drug |
General factors | likelihood of taking and becoming addicted to any of a number of drugs |
Cannabis/hippocampus | contains a large concentration of THC receptors, resulting in memory problems when used Effects similar to those produced by hippocampal lesions |
Cannabis/Two primary chemicals | THC - produces anxiety, psychotic behavior (in large doses) Provides the “high” feeling Partial agonist of cannabinoid receptors CBD - antianxiety and antipsychotic effects NOT reinforcing Antagonist of cannabinoid receptors |
Cannabis/Reinforcements | THC acts directly on dopaminergic terminal buttons, increasing the release of dopamine |
Cannabis/Marijuana | has stimulating effects on dopaminergic neurons |
Alcohol/Reinforcements | is also attributed to the release of endogenous opioids |
Alcohol/Effects | Low doses: mild euphoria and anxiolytic effects High doses: incoordination and sedation Destabilization of cell membrane |
Alcohol/Two primary sites of action: | Indirect agonist of GABAA Indirect antagonist of NMDA |
Though a few weeks with abstaining bring nicotinic receptors to pre-exposure levels, cravings still remain | Decreased gray matter of frontal cortex Increased size of insula |
Nicotine/Neural Effects of ACh: activation and desensitization | Nicotine, unlike ACh, is not destroyed by AChE Nicotine activates receptors Low, stable levels of nicotine convert many receptors to a desensitized state In response desensitization, nicotinic receptors increase |
Nicotine/Neural Basis of reinforcement | Stimulation of acetylcholine receptors Stimulation of dopaminergic neurons of the mesolimbic system Stimulation of endogenous cannabinoids Suppression of MCH |
Nicotine/Prevalence of nicotine addiction | Approximately ⅓ of the world’s adult population smokes nicotine 25% of pregnant women in the US expose their fetuses to nicotine |
Stimulants/Long-term exposure: | Decrease in number of dopamine transports (even after 3 years of discontinued use) Increased risk of Parkinson’s Damage serotonin terminals and trigger apoptosis |
Stimulants/Effects | IV administration increase concentration of dopamine in the NAC, psychotic behavior (e.g., hallucinations, delusions of persecution, mood disturbances, repetitive behaviors), Result of over-activity of dopaminergic synapses, Mimics schizophrenia |
Stimulants/Effects | feelings of euphoria, alertness, energy, stereotyped movements (e.g., head bobbing, persistent locomotion, Lab animals known to inject to overdose |
Stimulants/Neural Basis of Reinforcement: | Potent dopamine agonists Cocaine binds with and deactivates transporter proteins, blocking the reuptake of dopamine directly stimulates the release of dopamine The level and rate these changes happen makes these the most reinforcing of all drugs |