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Lecture 8

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Department
Psychology
Course
PSYB65H3
Professor
Forget
Semester
Fall

Description
Lecture 8 Depressants - also known as sedative hypnotics - causes cortex to go into a relaxed state - 3 types: 1. Barbiturates 2. Non-barbiturates 3. Alcohol Barbiturates: Mechanism: work through GABA => primary inhibitory amino acid transmitter => bind to GABA receptors and lowers brain excitability - most depressants are synergistic w each other – work w similar mechanisms and enhance each other or cancel each other’s withdrawal’s effect - eg barbiturates w alcohol - prescribed for sleep induction, most commonly in elderly due to disturbance of circadian rhythms and inability to sleep in elderly Withdrawal: brain becomes hyper-excitable after coming off depressants; if person has been taking barbiturates for a long time there is a chance of seizures/convulsions => alcohol will stop the withdrawal symptoms Alcohol: - made by yeast digesting sugar and excreting alcohol - accounts for largest number of admissions to mental hospitals => 20-40% of all admissions - 55% of all arrests => one of the parties was drinking - 50-75% of all homicides => a person was drinking - 50% of driver deaths => one of the parties was drinking - 20-30% of all suicides => the person had been drinking - experiment of prohibition in the US => Jan 1920 - Dec 1933, until law was re-appealed making alcohol legal again => all the statistics dropped for alcohol problems, but didn’t last long - by 1930 (10 years in) all the statistics had moved up back to where they were before prohibition => ppl were drinking illegally, finding ways around the law - illegal products result in impurities and no inspection => drinking alcohol is ethyl alcohol; if accidentally ingest methyl alcohol it causes blindness - better to educate ppl rather then completely banning alcohol Chemistry and metabolism of alcohol: - absorbed directly through the stomach wall without breaking down => one of the fastest sources of energy available - contains a lot of energy => 200 calories/ounce, but cannot be stored as fat => body uses the energy from the alcohol preferentially, but everything else consumed gets stored as fat - causes a decrease in ADH, resulting in higher excretion of fluids => excrete more than intake, resulting in dehydration Central nervous system effects of alcohol: - in part works on the GABAergic system, may affect metabolism, alter membrane excitability => not clear what is responsible for CNS depressant effects – may be combination - low levels of alcohol cause a disinhibition/excitation in cortical EEG => inhibits inhibitory centres, depressing centres => the rest of the brain allowed to become active - as person consumes more and more alcohol, the whole brain becomes inhibited => ppl slow down, become unstable - at low levels of alcohol ppl are able to function better – reflexes faster 1 => due to inhibition of inhibitory centres - at high levels depresses the cortex, and eventually depress activity in medulla, thereby depressing respiration – can result in death => body reacts at a certain threshold and person throws up, if drinking quickly the threshold is reached, but if drinking very slowly can move past the threshold without reflexive vomiting Long-term effects: atrophy of the brain, especially in dendrites (shrivel up), occurring in both cortex and cerebellum => severe enough to see on a CAT scan Withdrawal: hallucinations and tremors, convulsions/seizures and possibility of death => as severe and as likely to cause death as in a person withdrawing from narcotics Tolerance: some tolerance; change in liver enzymes as opposed to alterations in synapse plasticity - lethal dose (LD) is 10 times the effective
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