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Psychology (7,782)
PSYB65H3 (519)
Ted Petit (310)
Lecture 8

Lecture 8

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Department
Psychology
Course
PSYB65H3
Professor
Ted Petit
Semester
Winter

Description
Lecture 8 Main Teaching Points Depressants --  CNS Depressants  Sometimes known as sedative hypnotics  Anything that causes the CEREBRAL CORTEX to go into a more relaxed state ( the EEG shifts to a more relaxed/drowsy state)  Major categories: 1) Barbiturates 2) Alcohol 3) Non-barbiturates BARBITURATES – POWERFUL DEPRESSANTS!  GENERALLY: Lowers brain excitability  MECHANISM OF ACTION: Primary method of influence: GABA - Primary inhibitory neurotransmitter in the CNS. - Barbiturates bind to GABA receptors and activate them! - By activating these receptors; it SLOWS DOWN the activity in the brain (turning ON the INHIBITORY centre)  Almost all are synergistic – for drugs to be synergistic, they have to work using very similar mechanisms - and that they can add to each other (multiply each other’s effects) or cancel each other out (they cancel the withdrawal effects of each other) - Most will prevent the withdrawal effects of the other e.g. barbiturates + alcohol = synergistic but DEADLY.  Barbiturates are prescribed normally for: - sleep induction as a sedative. Induces people to go to sleep. Most commonly used in elderly individuals (sleep-wake cycles become erratic as we grow OLD) Although induces sleep, reduces REM sleep - used to treat epilepsy! (e.g. valium derivative) - Acts as an anti-anxiety drug. (calms you down)  WITHDRAWAL: - When person comes off of it: brain becomes hyper-excitable! - This may result in seizures and death – depends on how much and how long LIFE THREATNING! (NEVER TAKE OFF OF DEPRESSANTS DIRECTLY!) - Alcohol will stop the withdrawal symptoms from barbiturates (B/C ALCOHOL IS SYNERGISTIC WITH BARBITURATES) ALCOHOL: VERY POWERFUL INFLUNCE ON OUR SOCIETY  CNS depressant  Made by yeast - yeast digests sugar and secretes alcohol  Causes more problems than any other drug in society - Very negative effect on society as a whole!  Things it does: - Accounts for the largest number of admittance to mental hospitals / psychiatric wards (20-40%) - Accounts for 55% of all arrests - Accounts for 50-75% of all homicides - Accounts for 50% of all driver deaths - Accounts for 20-30% of all suicides  Experiment: United States passed a law (called PROHIBITION) in which people could not manufacture or sell alcohol (1920-1933) - Percentages decreased for a little but didn’t last long - By 1930, all of the numbers (statistics) had gone right back up to where they were before prohibition – people started drinking again! - Lesson learnt: If anyone wants anything, they can get it - The numbers were back up and there were additional problems: o Prohibition of alcohol resulted in manufacturing of alcohol that is not pure – methyl alcohol aka METHANOL causes blindness (we drink ethyl alcohol aka ETHANOL)  MECHANISM OF ACTION: - Alcohol directly absorbed through the stomach wall  One of the fastest source of energy that is available to humans  doesn’t require breaking down - extremely CALORIC:  Contains a tremendous amount of energy – 200 calories / ounce of alcohol  Just second to pure FAT. - Its metabolic pathway is such that it cannot be stored as fat (so you don’t become FAT b/c of alcohol itself)  PROBLEM: One can still get fat because the body starts using alcohol as its energy source and stores everything else as fat - Causes the brain to decrease production of anti-diuretic hormone (ADH)  Causes more excretion of fluids  Excreting more fluids then taking in! Leads to DEHYDRATION!  CNS Effects – [disinhibit = lack of restraint; free of restraint/inhibition] - In part, alcohol has an effect on GABA-ergic system (which are inhibitory) - Primarily has an effect on cell metabolism by depressing it, and membrane excitability/actions – might be combination of all three - Exact result of cortical result depends on the dose level:  At low levels (1-2 drinks at the most), causes (disinhibition) excitation in cortical EEG – at low amounts it inhibits / depresses inhibitory centers, therefore the rest of the brain is allowed to become more active [AROUSAL STATE – DISINHIBITS THE CORTEX] At low levels of alcohol, people are actually able to function better at tests – reflexes are faster than those whom are completely sober – inhibition of inhibitory centers allow faster reaction in a given amount of time  At high levels, it depresses the cortex DIRECTLY. Continual drinking will depress activity in medulla which depresses respiration (may result in death) (We do have a reflex though which detects high levels of alcohol in blood and causes us to throw up)  Long Term Effects – long term at very high levels - Atrophy of the brain – especially in dendrites – dendrites look like shrivelled up (happens in cortex and cerebellum) o Severe enough to be seen on CAT scan – reduction in size  Withdrawal Effects – depends on severity; is as severe and as likely to cause death as someone who has come off of narcotics (heroine / morphine) - Hallucinations - Tremors - Convulsions / Seizures - Possibly death IT CAN KILL THOUGH! TAKES HIGHER LEVELS OF ANY DRUG TO GET WITHDRAWAL SYMPTOMS!  Tolerance – some tolerance does develop - Appears that primary mechanism is the change in the level of liver enzymes  Fetal Alcohol Syndrome (FAS) - Caused by the female drinking du
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