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Ch.18

Drug Abuse

TermFunctions
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
Created by: Dalea
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