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Lecture 8

Lecture 8 PSYb65.docx

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John Campbell

Lecture 8 PSYb65 Depressants – categorized into barbiturates, non-barbiturates, alcohol o Barbiturates  helps people sleep/relax but doesn’t allow for REM sleep  work through Gava(primary inhibitory amino acid neurotransmitter in brain), increase of gava=slow things down, barbiturates bind to Gava receptors  decreases activity in the brain  also synergistic with other sedatives (additive if you put them together, not independent)  biggest group they’re used for are elderly  withdrawal: potential for seizures depending on how much you’ve taken them, can administer other depressants in place to reduce withdrawal (alcohol) o Alcohol  CNS depressant, produced by yeast digesting sugar and excreting alcohol  most damaging to society – largest admissions to mental hospitals (40%), 55% of all arrests, 50- 75% yo all homicides, 50% of death by car accidents, 20% suicides  US prohibited sale of alcohol from 1920-30, drop in all these problems, by 1930 all those numbers were back up in addition to more problems , people making methyl alcohol  leads to blindness/death…repealed the law…lesson: if people really want a drug in a free society, they’ll find a way to do it  Instead of trying to take it away, educate people about it  Physiology – absorbed directly through stomach wall, very high source of energy, 200 cals per ounce, fastest source of energy because it goes straight into blood stream, cannot enter any metabolic pathway that can turn it into fat, causes brain to decrease ADH production (causes to excrete more fluids)  leads to dehydration  Effects Gava receptor or slowing metabolic activity/altering membrane excitability, don’t know for sure how it works  Behavioural effects: depends on dose level, low: dis-inhibition of cortex (arousal state), high: direct inhibitory effect on brain (slurry words)  CNS depressed, can kill you in large doses  Long term alcohol consumption  atrophy in brain (dendrites in cortex and cereb
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