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Psych 204
| Question | Answer |
|---|---|
| What are the side effects of alcohol? | -Euphoria -Anxiolytic -stimulant at low doses -Sedative at high doses -Disinhibition -Reduction in motor coordination |
| How is the metabolism of alcohol different from other drugs? | The rate of oxidation is constant over time and does not occur more quickly with a higher blood concentration, unlike other drugs. |
| Describe the enzymatic breakdown of alcohol. | alcohol > +alcohol dehydrogenase > acetaldehyde> +acetaldehyde dehydrogenase > acetic acid |
| What happens when the two acetaldehyde dehydrogenase genes are homozygous for inactive form? | Sever flushing occurs (severe reaction) because acetaldehyde levels remain high. |
| What are Cyp450 enzymes? | They are enzymes that metabolize alcohol and other drugs. Regular alcohol consumption leads to an increase in the number of Cyp450 enzymes. |
| What are the long term effects of alcohol on tolerance? | (Chronic/long-term use) drug disposition tolerance occurs- changes metabolism. Behavior tolerance also occurs |
| What is the cause of a "hangover"? | Residual acetaldehyde in the body Alcohol-induced gastric irritation Rebound drop in blood sugar Excess fluid loss the previous night Toxic effects from congeners |
| What are delirium tremens? | A rebound phenomenon representing a hyper-excitable state of the CNS following the prolonged depressant effects of alcohol. |
| What are the areas other than the CNS that alcohol effects? | The cardiovascular system The renal-urinary system The reproductive system The gastrointestinal system The liver |
| What is the outcome of alcohol being such a simple molecule? | It readily crosses cell membranes , including the blood-brain barrier. |
| What neurotransmitter(s) does alcohol act on? | Glutamate GABA Dopamine The opioid system |
| What are alcohols effects on Glutamate? | Reduces effectiveness at the NMDA receptor Reduces release in the hippocampus In withdraw, release returns to normal but acts on up-regulated NMDA receptors (increased quantity) |
| What are the effects of alcohol on the GABAergic system? | (Acute) Enhances effects at the GABAa receptor allowing Cl- conductance (Chronic) repeated exposure reduces GABAa mediated chloride influx Makes animals more sensitive to the GABA antagonist-due to down regulation Cross tolerance occurs with sedative |
| What are the effects of alcohol on dopamine? | Increased DA in the Mesolimbic pathway |
| What are alcohols effects on the opioid system? | Modulates pain, mood, feeding, reinforcement, response to stress Enhances endogenous opioid activity |
| What are the effects of the alcohol dependence treating drug Disulfram/Anabuse? | The drug inhibits acetaldehyde dehydrogenase thereby increasing the availability of acetaldehyde which leads to negative effects. |
| What is the effect of nicotine on dopamine? | Directly stimulates the flow of DA in the NAc Stimulates release of glutamate which triggers additional release of DA Within a few minutes GABA is inhibited which results in even high levels of DA in the NAc Also blocks MAO |
| What is the most effective treatment for nicotine dependence? | Varenicline(Chantix) which is a nAChR agonist on the alpha 4 and beta 2 receptors It is a full agonist at alpha7 beta3 and beta4 |
| Which receptors does nicotine specifically target? | The alpha4 and beta2 binding site on nAChR receptors because they are of high affinity |
| Why does nicotine (an agonist) cause up-regulation of receptors? | As continuous binding occurs, de-sensitization and internalization of receptors occur and in response nicotine up-regulates receptors. |
| At what age range is the highest rate of cocaine use? | 18-25 |
| What are the highest producing countries of the coca plant? | Colombia Peru Bolivia |
| When and by whom was cocaine isolated and purified? | In 1860 by Albert Neiman |
| Describe the manufacture process in making cocaine. | Leaves from the coca plant > coca paste (80% cocaine) > converted to hydrochloride and crystallized. |
| Why can't cocaine be smoked in powder form? | Because it breaks down in heat. |
| Why is cocaine able to pass through the blood-brain barrier? | Because it is lipophic |
| How long is the high and half life of cocaine? | High- 30 minutes or less Half life- 30-90 minutes |
| What happens when cocaine is mixed with alcohol? | Cocaethylene is produced, which has a similar biological activity as cocaine but a longer half life leading to increased toxicity. |
| Why is crack "more" addictive than powder cocaine? | Because smoking it effects the brain much faster than powder cocaine or IV use. |
| Where does cocaine act in the brain? | It binds to monoamine transporters and blocks the reuptake of seratonin(5-HT), dopamine (DA), and norepinephrine (NE). |
| For which transporter does cocaine have the highest affinity (most strongly bind to)? | 5-HT fiollowed by DA and then NE. |
| What cause cocaine to act as a local anesthetic? | The drug blocks the v-gated Na channels thus blocking nerve conduction. |
| What is the difference between cocaine and amphetamines in reference to the level of DA in the mesolimbic pathway? | The intensity and high of cocaine is dependent upon baseline levels of DA activity in the pathway and this is not the case with amphetamines. |
| Why is the D3 receptor inportant to the use of cocaine? | Because a D3 receptor antagonist, such as SB-277011-A blocks the enhanced brain reward produced by cocaine use. |
| If cocaine has such a small amount of withdrawal symptoms, then why is it so hard to stop? | Immediate after effects cause DA levels to descend to below normal levels leading to craving and dysphoria. Also tolerance and sensitization play a role. |
| How does cocaine effect neuronal growth? | Abnormal growth in the dendrites may occur causing them to weave around each other (especially relevant to the anterior cingulated cortex ACC, which involved in learning and attention. |
| Why do amphetamines have such a potent effect on the DA system? | Because their chemical structure is closely related. |
| What are the differences in symptoms of ampethamine use compared to cocaine? | They are more energizing and produce less paranoia Have a higher likelihood of psychotic reactions |
| Describe the neurotransmitter processing involved with using meth. | Rapid release of dopamine Blocks reuptake of dopamine Also releases NE and possibly seratonin Euphoria lasts for 8-24 hours |
| What is possibly the most serious health problem from chronic meth abuse? | Damage to the neurons of several parts of the brain including the frontal cortex, hippocampus and the striatum. Meth actually destroys neurons through apoptosis. |
| What is the irony of long term use of stimulants in treating ADHD? | They increase concentration in the short-term but when given over long periods of time they neither improve school achievement nor reduce behavior problems. |
| What are the neurotoxic effects of MDMA? | Neurons damage is exacerbated by high ambient temp. The rapid release and over-stimulation of serotonin may cause irreversible damage to nerve endings. |
| Which prescription drugs affect MDMA effects the most? | Ritonavir(Norvir)-inhibits multiple CYP450 enzymes MAOI's have been reported to cause death or toxicity in combination. SSRI's nearly fully abolish MDMA effects |
| What is the function of the Mu opioid receptor (MOR)? | Morphine-induced analgesia Positive reinforcement Cardiovascular and respiratory depression, cough control, nausea and vomiting Sensorimotor integration |
| What is the function of the delta opioid receptor(DOR)? | Similar to that of the MOR, more restricted Modulating olfaction, motor integration, reinforcement, cognitive function, spinal and supraspinal analgesia |
| What are the function of the kappa opioid receptor (KOR)? | Very distinct distribution compared to that of MOR and DOR Pain perception, gut motility, dysphoria, water balance, feeding, temp. Control, neuroendocrin function |
| What are the three families of opioid peptides produced endogenously in the body? | Enkephalins Endorphins Dynorphins |
| What are the three ways endogenous opioids inhibit nerve activity? | Postsynaptic inhibition-open K+ channels Axoaxonic inhibition- Close Ca+ channels Presynaptic autoreceptors- reduce transmitter release |
| Why is co-localization important to opioids? | Opioids are neuromodulators of other neurotransmitter systems Their effects would be highly dependent on baseline activation |
| What are opiates function in the spinal cord? | Direct inhibition through release by inhibitory interneurons to block pain signaling in the dorsal horn |
| What are opiates functions in the midbrain? | The the midbrain is electrically stimulated, a profound reduction of pain perception with chronic pain occurs (Disinhibits through blockage of presynaptic GABA release) |
| What are opiates functions in the cortex? | They effect pain perception directly in the cortex Responsible for the emotional component of pain |
| How does he body react to emotional pain? | The body reacts to emotional and physical pain in the same way and release opioids to alter the perception of pain |
| Do opiates show complete tolerance? | Yes, with enough exposure to the same dose it will elicit no subjective high except the removal of withdrawal pain. |
| Is methadone an agonist, partial agonist, or agonist-antagonist? | It is a partial agonist. |
| What are the two main theories of opiate addiction? | The physical addiction-withdrawal is bad enough to guarantee continued use The psychological addiction- "a coping problem" |
| What is the active ingredient in marijuana? | D9-tetrahydrocannabinol (THC) |
| Why does marijuana increase appetite? | It interacts with peripheral signals, like leptin, insulin, ghrelin, and satiety hormones affecting energy balance and adiposty. |
| Does the tar from cigarettes or marijuana contain a higher concentration of carcinogens? | Marijuana- increasing the risk of bronchitis, chronic cough, and phlegm production. Although cigarettes smokers tend to smoke MORE than marijuana users so overall there is more tar build up |
| Marijuana receptor (CB1) | CB1- metabotropic, it is a G-protein couples receptor, INHIBITORY,, (inhibits cAMP and voltage sensitive Ca++ channels, activates K+ channel) it is located on axon terminal rather than cell body. |
| Marijuana receptor (CB2) | CB2- responds to THC, active mostly in the immune system. |
| What are the three important cannabinoid drug? | Dronabinol- synthetic THC (CB1 agonist). Nailone- THC analog (CB1 agonist). Rimonabant- SR141716 (CB1 antagonist). |
| What is the body's naturally endogous cannabinoids? | Archidonoyl ethanolamide or anandamide. 2-arachidonoilgylcerol (2-AG). They are only produced when needed and not stored, as when there is a rise in Ca+ |
| How does the cannabinoid system interact with the opioid system? | Mu opioid antagonists block THC effects on reinforcement by reducing GABA release from interneurons. |
| Negative side effects of marijuana. | THC can suppress LH THC can acutely reduce sperm counts THC can suppress immune function |
| Where is the CB1 receptor located? | On the axon terminal, unlike most other receptors. |
Created by:
Justin Gibson
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