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PSYB65H3 (519)
Lecture

05.12.06.PSYB65.L7+L8.notes.doc

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Department
Psychology
Course
PSYB65H3
Professor
Zachariah Campbell
Semester
Fall

Description
DRUGS -most drugs work through the transmitter systems Major Classifications of Drugs: 1) Prescription drugs available in drug store with prescription  pretty much based on politics and money 2) Over-the-counter drugs available in drug store without prescription Ex. Codeine is available in Canada without a prescription, BUT in US you need a prescription. 3) Social drugs alcohol, nicotine, caffeine 4) Not produced commercially/Produced commercially but NOT for psychoactive effect marijuana, cocaine/airplane glue, etc. Tolerance -most drugs if taken repeatedly and frequently (a long time) show a DEC behavioural effect How does tolerance for drugs occur? -with repeated exposure to a drug, the brain, specifically the synapse, begins to compensate by INC/DEC the number or sensitivity of receptors (to try to bring things back to normal) stimulants with repeated exposure MORE stimulant NT’s are released so synapse gets rid of some receptors to DEC the post-synaptic response back to normal levels depressants with repeated exposure LESS stimulant NT’s are released so synapse creates more receptors to INC the post-synaptic response back to normal levels Withdrawal -when frequently and repeatedly used, drug STOPS being taken there will be a behavioural effect 2 basic responses: 1. craving for drug 2. behavioural effect OPPOSITE of effect of drug that they used to be on stimulants depressive withdrawal (draw the SIN curve) depressive withdrawal they will be tired, sleepy, lethargic, depressed, but this is not life threatening depressants over-stimulated withdrawal (draw the SIN curve reflected in the x-axis) over-stimulated withdrawal agitated, seizures, potential death -NEVER take a person off depressants (i.e. alcohol) cold turkey cuz they could die, so start the alcoholic person on another sedative/depressant like valium and then get them off the valium slowly How does withdrawal occur? -recall, after tolerance occurs for a stimulant, less receptors are at the synapse because there is excess NT’s -however, when you get off the stimulant drug cold turkey, the NT’s released quickly return to normal levels (via a DEC), BUT the receptors don’t INC quickly enough back to normal, therefore result is LOWER level of activation (the opposite effect of the drug used previously) - likewise recall, after tolerance occurs for a depressant, more receptors are at the synapse because there is less NT’s -therefore, when you get off the depressant drug cold turkey, the NT’s released quickly return to normal levels (via an INC), BUT the receptors don’t DEC quickly enough back to normal, therefore result is HIGHER level of activation (the opposite effect of the drug used previously) summary: withdrawal from stimulants very little receptors and only normal NTs therefore synapse understimulated withdrawal from depressants normal NTs with too many receptors therefore synapse overstimulated Addiction -is a behavioural term and refers to fact that a person has a craving for the drug 2 Definitions: 1) Psychological addiction  not a very useful term  behavioural dependence on drug  only means it is important to you (i.e. you can be psychologically addicted to sports) 2) Physical addiction physical withdrawal symptoms when drug taken away  can be measured with physiological measures (EEG,GSR) As a general rule: -the more rapid/powerful the effect of the drug, the more addicting the drug will be -commonly observed in drugs with multiple forms ex: cocaine (comes from Coca leaves found in Bolivia and Peru) -as leaves in tea, not addicting, mild stimulant -as white powder that is snorted it is only slightly addicting -as intravenous or crack cocaine, very powerful AND very rapid, very addicting Note: the chemical active ingredient is the SAME in all of these forms, its just the concentration/power AND the speed of ingestion that makes the difference in terms of addiction STIMULANTS -all cause cortical EEG shifts to an arousal state -all inhibit sleep -create depressive withdrawal (not life threatening) (For drugs in general: Effective Dose- dose that gives u an effect Lethal Dose- the toxic dose that kills you) Caffeine -more in coffee than tea -makes you urinate -is a stomach irritant -can create some tolerance but not very significant/great -withdrawal (physical) only occurs if you are drinking 6-8 cups of coffee a day -gives u headaches on withdrawal (b/c using it treats headaches) -constipation on withdrawal (b/c it stimulates bowel movement) -very non-toxic (must drink to 70-100 cups to die) How it works? -inhibits the breakdown of cyclic-AMP increased amounts of cyclic-AMP  increased glucose production and heightened rates of cellular/metabolic activity Nicotine -found in tobacco leaves -is highly addicting -some tolerance does develop but not extreme -withdrawal is a depression How it works? -mimics acetylcholine at the receptor site stimulating the post-synaptic cell -causes release of adrenalin which increases heart rate and blood pressure Cocaine -found in leaf of Coca plant -leaf contains about 2% cocaine -is a mild stimulant -increases heart rate and respiration - if injected intravenously in high doses it can be toxic, stops the heart by acting on heart muscle -some tolerance occurs -depressed withdrawal, physical and emotional but not life threatening -the faster-acting and stronger form of drug, the more addicting - Coca leaf in tea cocaine intravenous and crack How it works? -prevents reuptake of norepinephrine  increasing activity of noradrenergic neurons Amphetamine -medical use was discovered in 1932 (fairly new) -reduction in fatigue -causes reduction in fatigue-associated decrement in performance -similar to cocaine (in mechanism of action) but more prowerful (see next point) -causes INC activity in a fibre pathway: Medial Forebrain Bundle (part of the hypothalamus) a.k.a. reward system therefore makes you feel good (sex and food) 2 primary medical uses for amphetamines: 1. Hyperactivity in children/ADD: -they use amphetamine derivatives “Ritilin” -in about 50-75% of ADD kids show improvement in behaviour -helps the kids focus and there is no tolerance to the focusing effects 2. Weight/appetite control: -causes reduction in appetite, banned in 1973 for weight control -was banned because ppl develop tolerance to the appetite suppressant effects within 2-4 weeks and then begin to eat a lot again! 3 types of amphetamines: D, L, and methamphetamine Amphetimines work in 4 ways: 1. causes norepinephrine to leak from presynaptic terminal w/o AP 2. increases norepineph. released with AP 3. blocks reuptake of norepin. 4. directly mimics effect of norepin at receptor site THEREFORE VERY POWERFUL stimulant Note: also works on dopamine system Tolerance: -usually no tolerance to focus effects in ADD, can stay on same dose for yrs -become tolerant to appetite suppressant effects in 2-4 weeks (rapid) -takes much longer to develop tolerance to mood elevating effects Withdrawal (remember, opposite of drugs effect): -depressive withdrawal, tiredness, INC in appetite -these effects last for less than a week -not life threatening High levels of use (of cocaine or amph) over a long time associated with social and behavioural problems: 1) Compulsive behaviour (arranging pencils) 2) “cocaine bugs” - feeling that there are bugs under their skin, sometimes use knife to try to scratch out the bugs creating soars 3) suspicious and hostile, can lead to extreme violence 4) paranoid psychosis think ppl are out to get them  both auditory and visual hallucinations of a paranoid nature in a setting of clear consciousness (everything seems perfectly normal not like LSD’s effect which is wacky) indistinguishable from schizophrenia typically leads to violence this caused by effect on dopamine DEPRESSANTS/SEDATIVES/HYPNOTICS 3 categories: barbiturates, non-barbiturates, alcohol -creeate overstimulation withdrawal symptoms (could cause death) Non-barbiturates -ex. Benzodiazepines such as Valium Barbiturates -broad spectrum grp of drugs that depress the brain How it Works? -bind to GABA receptors therefore directly stimulate GABA receptors -GABA is the primary inhibitory amino acid NT in the brain -thereby these drugs inhibit brain function -lower brain excitability -lower EEG activity -barbiturates are synergistic with other depressants -they work through a similar mechanism they work together, add/multiply to each other, compound the ef
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