PSYC*3410 Exam Info
30 multiple choice
7 short answer
Chapter 12 (Obesity and eating disorders), Chapter 13, Chapter 14, plus class
Chapter 15: Sleep Disorders
o Strong genetic influence
Nucleus Magnocellularis becomes overactive during attacks.
o Gene causing attacks is mutated orexin (hypocretin)
Those with lack of REMsleep atonia, usually have lesioned nucleus
Also spontaneous cases from birth.
Chapter 15: Drug Addictions & Rewards
The Problem (USA Stats)
60 million users of legal drugs.
5.5 million users of illegal drugs
several million users of prescription drugs
Psychoactive Drugs – drugs that influence subjective experience and behaviour by
acting on the nervous system.
Oral – most common, hardest to control (interact with stomach contents, hard to
control timing of effects and dosage between ppl)
Intragastric – infused in stomache (coma patients).
Transdermal – absorb through skin.
o Subcutaneously (SC) – under the skin
o Intramuscularly (IM) – into large muscles
o Intrathecal (usually done by doctor into spine (cerebrospinal fluid),
circulate nervous system).
o Intravenously (IV) – quickest, but dangerous.
Inhalation – lung capillaries
Mucus membranes – nose, mouth, rectum
how well a drug reaches its target depends on how well it penetrates the blood
Mechanisms of Drug Affects
Increase neurotransmitter synthesis Destroy degrading enzymes
Increase neurotransmitters released from terminal button
Drug binds to autoreceptors (block inhibitory affect on release)
Metabolism and Elimination
Liver enzymes degrade drugs – drug metabolism
Excreted in urine, sweat, feces, breath, mother’s milk
Decreased sensitivity to a drug due to exposure to it.
o Shift doseresponse curve right
Crosstolerance – exposure to one drug may lead to tolerance to similar drugs.
o Ex: alcohol and benzodiazepines
Sensitizatio – inverse tolerance
Tolerance and sensitization often develop to some effects and not others.
Various forms of tolerance:
o Metabolic tolerance
Less drug is getting to the site of action.
o Functional tolerance
Decrease responsiveness at the site of action.
• Fewer receptors
• Less responsive receptors
• Decreased efficiency of binding at receptors
Withdrawal and Dependence
Illness brought on by the elimination of a drug from the body.
Physical dependence – withdrawal experienced with cessation of drug use.
Compensatory body changes – body functions normally with drug in system.
Drug cessation – the body manifests the compensatory changes.
What is Addiction?
Continuing to use a drug despite adverse effects on social life and health.
Addiction and physical dependence can occur together or separately.
Role of Learning in Drug Use and Addiction
Contingent drug tolerance
o Ex: rats given alcohol(convulsion deterrent) before convulsion protocol
Stimuli that predict drug use become conditioned.
o Exteroceptive – environmental influences (location, friends, setting)
o Interoceptive – thoughts (associations with the drug)
Conditioned drug tolerance
Maximal tolerance effects seen in the environment in which a drug
is usually taken.
New setting can have greater effects. Compensatory changes do not happen quick enough.
Condition compensatory responses – responses opposite that of the drug.
Five Commonly Abused Drugs
Tar and 4000 other chemicals.
Nicotine the psychoactive ingredient.
o Agonist of the nicotinic acetylcholine receptor.
Buerger’s disease – ceased blood flow to extremities (very painful, amputation)
reversible if quit smoking.
First time users nausea, vomiting, sweating, couching, abdominal cramps,
dizziness, flashing and diarrhea.
Regular users: relaxed, alert, less hungry.
about 70% of experimenters become addicted.
Only 20% of attempts to quit are successful.
Twin studies: estimates 65% heritability.
Health Effects of LongTerm Smoking
Smoker’s Syndrome chest pain, labored breathing, wheezing, coughing, increased
susceptibility to respiratory infections.
Lung Disorders – pneumonia, bronchitis, emphysema, lung cancer.
Cardiovascular Disorders – high blood pressure, heart attacks, stroke, Buerger’s disease.
Shorter life span
Teratogenic Effects – abnormal fetal development, miscarriage, stillbirth, early death of
organic compound with (OH) hydroxyl functional group attached to hydrocarbon.
Obtained by fermentation of sugars.
Ethanol: the alcohol contained in beverages.
Acute Effects of Alcohol
a toxic substance
highly penetrating (lipo and hydro soluble)
a depressant at moderate to high doses.
Disinhibitor at low doses.
Acts on GABA, glutamate, and neuronal Ca2+.
Moderate doses: cognitive, perceptual, verbal and motor impairments.
Vasodilatation (skin rush), diuretic.
High dose: unconsciousness, hypothermia, respiratory depression (respiratory
block, lethal) Delayed Effects of Alcohol
Mild Withdrawal Syndrome (a few hours)
headache, vomit, nausea, tremors.
Severe Withdrawal Syndrome – in 3 phases
56 Hours Post Drinking: severe tremors, agitation, headache, nausea, vomiting,
sweating, abdominal cramps, perfuse sweating, hallucinations.
1530 Hours: convulsive activity
2448 Hours: delirium tremens (hallucinations, delusions, agitation, confusion,
hypothermia, tachycardia) – may last 34 days.
o Tolerance and physical dependence.
o Tolerance is both functional and metabolic.
Heritability of alcohol addiction estimated 55%.
Several genes identified ( e.g. alcohol dehydrogenase).
Health Effects of Chronic Alcohol Consumption
Korsakoff’s Syndrome – direct and indirect effects
o Neurotrophins, celladhesion molecules, apoptosis.
Organ inflammations and scaring:
o Liver cirrhosis, pancreatitis, gastritis.
o Increased risk of liver cancer, stomach ulcers.
Teratogen – fetal alcohol syndrome
Increased risk of breast, prostate, ovary, skin cancer.
Traffic and other accidents
Disulfiram, a potential treatment.
o Acetaldehyde intoxication
o Loss of white matter
o Reduction in number and size of neurons
o Neurotrophins, celladhesion molecules, apoptosis.
o Thiamine (Vitamin B)1 deficiency – Korsakoff’s
o Acute demyelination or necrosis of the corpus callosum.
Other demyelination syndromes
o During liver failure, possibly reversible.
Alcohol withdrawal syndrome in former abusers.
Marijuana Cannabis sativa – common hemp plant
80 other chemicals
Delta9tetrahydrocannabidiol (THC) primary psychoactive.
Two receptors: CB1, CB2 – regulate neurotransmitter release (mostly GABA) via
Endocannabinoids: anandamide, 2arachidonoylglycerol (2AG)
Acute Effects of Marijuana
Low recreational doses: very subtle: vivid sensory perception and though
High doses impair shortterm memory and interfere in tasks involving multiple
Addiction potential is low
Negative effects of longterm use are far less severe than those associated with
alcohol and tobacco.
Health Effects of Heavy Marijuana Use
respiratory problems – cough, bronchitis, asthma
ingle large doses can trigger heart attacks in susceptible individuals.
No evidence that marijuana causes permanent brain damage
Possible correlation between marijuana use and schizophrenia, but no causal link
has been shown.
Schweinsburg et al. (2010)
Adolescents (1518), 3 groups
o Recent users (within a week, abstinent 27 days)(n=13)
o Abstinent users (2760 days of abstinence) (n=13)
o Nonusers (n=18)
o Drinking and drug use, depression, anxiety, externalizing and internalizing
behavior (assessed by parents)
o Visuospatial skills, working memory, spatial working memory, IQ
Anatomical and functional Magnetic Resonance Imaging while performing the
spatial working memory tasks.
No group difference in behavioral assessments
No group differences in most neuropsychological assessments
Recent and abstinent users: small increase in vigilance (but not in memory) in the
spatial working memory task.
Recent users: greater activation of prefrontal cortex
o More effortful cognitive control?
Recent users: greater activation of insula
o Greater inhibitory effect.
Abstinent users: greater activation in right precentral gyrus.
o Linked to faster reaction time?
Meler et al. (2012), Moffit et al. (2013) Participants: 1037 people born in 1972 and 1973, enrolled as infants, longitudinal