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neurotransmitter that regulates a variety of bodily processes |
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Enzyme that converts tryptophan into 5-HTP. Specific marker for 5-HT. |
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Enzyme that converts 5-HTP into 5-HT (serotonin) |
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rapidly removes serotonin from the synapse. SSRI's inhibit this process, keeping serotonin in the synapse |
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Catalyzes breakdown of serotonin to 5-HIAA. 5-HIAA levels are a measure of serotonin. Higher levels-more serotonin |
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reduce cAMP synthesis and increase opening of K+ channels-leading to hyperpolarization (decrease in firing). Influences food intake (decreases it), anxiety (reduces it), alcohol consumption (reduces it), and temperature regulation (reduces it). |
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Metabotropic receptors (& serotonin) |
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At least 15 receptors. All are metabotropic besides the 5-HT3A receptor |
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Raphe Nucleus (& serotonin) |
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Most serotogenic neurons are located in the raphe nuclei. |
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Food intake, anxiety, alcohol conusmpton, temperature regulation. -reduces all of these. May help treat schizophrenia. Also reduced serotonin during REM sleep. |
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Low levels of tryptophan INCREASED depression symptoms in women |
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neurotransmitter-exitatory; learning and memory |
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Enzyme that synthesizes glutamate. Transforms glutamine into glutamate |
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Excitatory amino acid transporter-removes glutamate from the synapse-important because too much glutamate can lead to diseases such as ALS. Also, once glutamate has been picked up, it is turned into glutamine again by glutamine synthetase, which leads it to be recycled back in the system. |
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Ionotropic receptor that leads to an influx of Na+. Leads to excitatory responses-depolarizes the cell |
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Ionotropic receptor. Glutamate and glycine bind, Mg2+ is removed, Na+ and Ca2+ enter the cell (which must be depolarized)-depolarizes the cell-excitatory responding |
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mGluR1-8. Inhibits/deactivates cAMP. Some are autoreceptors who inhibit glutamate release. |
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Hippocampus & cortex (glutamate) |
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Cerabral cortex-glutamate used throughout. Also several pathways in the hippocampus. |
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Increases the strength of synaptic conncetions, increases learning/memory, motor behavior , motor coordination. Too much causes cell death. |
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Mice that had an overexpressed NMDA receptor learned much faster than mice that did not. Demonstrates Glutamates effect on learning. |
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Inhibitory neurotransmitter |
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Enzyme that synthesizes GABA from Glutamate |
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GABA transporter-inhibition can help to treat epilepsy |
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Ionotropic receptor that lets Cl- in the cell, which hyperpolarizes the cell and causes an IPSP |
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Metabotropic receptor. Lets K+ into the cell, hyperpolarizing the cell and causing and IPSP |
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muscle relaxant, rhythmic patterns, stablizes movement, regulates memory, and regulates executive functioning |
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GABA and areas of concentration |
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cerebral cortex (regulates executive functioning), brainstem (rhythmic patterns), hippocampus (supresses memory), basal ganglia (regulates dopamergenic activity and stabalizes movement) |
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DBI may be a receptor for BDZ (binds on GABAA receptor)-when it was administered, rats reduced the amount that they drank when they were shocked because they felt the pain more. It blocked GABA from responding. |
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Projects studying drug use of 8th, 10th and 12th graders and college students to learn about patterns of use and abuse in these age groups |
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behavioral-toxicity from behavioral effects of a drug (drunk driving). acute-"short-term" "intoxication" chronic- long-term, personality changes, heart disease, lung cancer, etc. |
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1906 Pure Food and Drug Act |
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Created the FDA. Products need to be clearly labelled. |
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Regulates food, prescriptions, OTC drugs, cosmetics, medical devices, and vaccines. Does not regulate alcohol or illicit drugs. DOES regulate nicotine. Regulates new drugs, not drugs already on the market |
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Tax intended to cut down on opium and cocaine international trade. Taxed those who produce, manufacture, compound, deal in, and/or dispense opium or coca leaves, salts, derivatives, or preparations. Mostly affected physicians, dentists, vets, and retailers. |
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Drug Names (Code, Chemical, Generic, Brand) |
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Code-from pharmaceutical company Chemical- based on organic chemistry Generic- legal name Brand- based on different company names |
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5 schedules I-no medical use/high abuse potential-heroin, LSD, MDMA, THC, GHB (date-rape drug) II-high abuse potential but some medical value-opium, morphine, ritaline, amphetamines III-reduced abuse potential/medical value-barbituates, steroids IV-lower abuse potential/medical value-valium, xanax, ambien V-lowest abuse potential/medical value- low doses of codine/opium |
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Drug Enforement Agency in the Department of Justice-enforces drug laws |
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Alcohol leads to cigarettes leads to marijuana leads to cocaine leads to hard drugs. Not necessarily true. No causal relationship. |
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Craving does not depend on physiological needs. Reflected in the time/effort expended to get a drug. |
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unpleasant symptoms with cesure of drug use. |
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Physical Dependence Model |
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Based on tolerance. Initial drug use leads to repeated drug use which leads to physical dependence which leads to attempts at abstience which leads to withdrawl which leads to relapse. Classical conditionaing also plays a part because CS's are everywhere! But it dues not account for drugs with little tolerance/withdrawl, and individual differences. |
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Positive Reinforcement Model |
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Initial use leads to positive reinforcement which leads to repeated use which leads to attempts at abstinence which leads to craving (compulsive desire) which leads to relapse (positively reinforced). It does not explain physiological behaviors, tolerance, negative consequences. It does not explain why some people do not become dependent and why craving may not occur after 1 administration. |
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When rats self administer drugs based on a progressive ratio schedule. |
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Ventral tegmental area-axons to to nucleus accumbens-rewarding pathway. Drugs hijack this pathway and reward. |
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When they no longer level press for a drug reward. High breaking point-highly rewarding substance |
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Sugars from grapes, honey, sugar cane, grains, etc. are eaten by yeast which creates ethanol and CO2. Fermentation continues until there is an alcohol concentration of 15%, when the yeast dies. |
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Alcohol is heated and the vapor is collected and cooled-then converted back into a liquid-leads to a higher concentration of alcohol. |
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Determines alcohol content. 1/2 of the percentage of alcohol. |
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Blood alcohol concentration-% of alcohol in the blood. gram/mg per 100 ml of blood. |
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.025-.05 (ED50)-measurable behavioral effects DUI-BAC > .08 DWI-BAC > .05-.07 .15-vomiting .35-unconciousness LD50-.45 |
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Unconscious, slow/irregular breathing, cold skin, death |
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Alcohol absorption & factors influencing |
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10% from stomach, 90% from small intestine. Depends on food in the stomach, and sex differences (women absorb faster-less alcohol dehydrogenase and more fat) |
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first-pass metabolism-90-95% metabolized in the liver by alcohol dehydrogenase lungs do 5% of metabolizing excreted as CO2 and water |
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metabolism at a constant rate .015% per hour |
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1st enzyme that breaks down alcohol in the stomach and liver. it breaks it into acetaldehyde |
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1st metabolite of alcohol, somewhat toxic and can lead to nausea. Breaks alcohol into ALDH |
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Acetaldehyde dehydrogenase-breaks down acetaldehyde quickly. Asians have more inactive ALDH-which leads to more acetaldehyde, which makes them feel more sick. |
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Antabuse is a drug that inhibits ALDH, and it is intended to treat alcoholism my associating drinking with negative effects (of acetaldehyde), doesn't really work |
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With chronic alcohol use, the liver spends less time releasing fats, leading it to accumulate fat. The cells then rupture and die, which is called cirrhosis. |
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agonist-enhances the effect. It is an allosteric modulator at a non-competative binding spot. GABA-A has a longer, more pronounced effect-more hyperpolarization. Chronic use leads to down regulation of GABA A or desensitization of GABA A. |
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Inhibiting an inhibitory behavior-instead of listening when the brain tells you not to do something, alcohol inhibits this response |
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antagonist-inverse agonist. Decreases the amount of glutamate being released. Chronic use-increase of glutamate receptors-up regulation |
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agonist-mimics the effect of the neurotransmitter antagonist-inhibits the effect of the neurotransmitter |
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Up regulation of glutamate and down regulation of GABA. |
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Indirect effect. Influences the mesolimbic dopamine pathway-increases firing of the VTA-inceases reward |
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Other alcohol effects (sleep, blood circulation, hormones) |
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Induces sleep, but reduces REM (critical for memory) Peripheral blood circulation increased-appear flushed but actually lose body heat. Increases corticosteroids (more violence), decreases testosterone (less sexual behavior), decreases vasopression (pee a lot- don't retain water) |
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enhance social/physical pleasure enhance sexual performance/responsiveness increase power/assertiveness reduce tension |
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40% of all traffic accidents are alcohol related. Most in 18-24 age group |
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diminished effect within 1 bout of drinking |
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increases alcohol dehydrogenase and CYP430 |
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Instrumental learning-adjust behavior-but it is task-specific. |
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tremors, intense anxiety, high BP, increased heart rate, sweating, rapid breathing, nausea, vomiting, hallucinations. Hyperexitability of the CNS |
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vitamin B1 (thiamine) deficiency-poor diet and failure to absorb nutrients. Critical for glucose metabolism. A deficiency leads to confusion, disorientation, tremors, coordination difficulties and significant memory disorder |
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leads to withdrawl symptoms and hangovers |
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a majority of individuals who commit violent offenses are under the influence of alcohol at the time of the crime. It is a correlation though. Expectations may be more important than alcohol consumption, may be cultural, and early childhood experiences may set the stage for agression |
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increase in endogenous opioid release. Leads to a decrease in endorphin release, and withdrawl leads to dysphoria |
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