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Lecture 5A - Barbiturates.docx

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Carleton University
PSYC 3403
Tarry Ahuja

Lecture 5A– Barbiturates Chapter 7 Lecture 5A – February 5, 2014 More Depressants: Barbiturates & Antiepileptic Drugs Midterm exam: Feb 26 th T and F, MC, Short answer, diagram. 30% of grade Chapters 1,2,3,7,12,13 Q&A session witth – 2-3 th 1-2 Thurs (feb 13 , Feb 25 ) Paper: What are you talking about? Kills x people. Active components. Who it affects, how it works. Use three research papers talking about your topic (All following the same view). It doesn’t have to refer to treatment options, it could be about population type, method of administration ect. Pick something that is prevalent, why does it affect the body and brain? At the end of the doc, take home message – what is most important about it (ie. Research from these papers have shown that we need to reevaluate our treatment options) Alcohol: is considered a depressant because of how it affects your brain chemistry, not based on how you feel. Overview • barbiturates – specific depressants • nonbarbiturate sedative-hypnotics • GHB - general anesthetics • antiepileptic drugs Barbiturates • phenobarbital was introduced as a sedative in 1912 • originally mechanism of action was unknown • classified by chemical structure Barbiturates (structure) Lecture 5A– Barbiturates Phenobarbital Barbiturate Nucleus Barbiturates (mechanism) • nonselective neuronal depression - Knows that barbiturates cause depression (nonselective because we don’t know why) • depress polysynaptic diffuse (one cell talking to another cell and that to another – it slows the communication between the cells) brain-stem neuronal pathways in: • the brainstem • cerebral cortex • depression was dosage-dependent Lecture 5A– Barbiturates - Dosage-dependent is important because it lets us know how it affects a system. 1mg will have a different response than 3 mg. (ie. Alcohol is dose- dependent, because you have a different response based on 1 drink or 8 drink) Barbiturates (mechanism) • reduce electrical and metabolic activity - Affects ability to do activity • decreases in whole-brain glucose metabolism - Refers to a technique that was groundbreaking 20-30 years ago. Someone performs a task once they are administered a glucose shot that is radioactively marked. Perform a task while having a brain scan. Brain needs to use glucose to perform a task/is energy. - Glucose metabolism is a direct measure of brain activity • reduction of excitatory activity or increased inhibitory activity Barbiturates (glutamate)(type of receptor) • research has shown: • barbiturates act as NMDAR antagonists - Blocks the receptor from receiving glutamate • amnestic properties due to changes in glutamatergic transmission - Linked to us decreasing/modulating that glutamate transmition (blocking the transmittion of glutamate) • lower blood flow to brains areas associated with memory - Hypocampus ect. - Memory problems during drug use and after regarding what happened because you can’t remember something later if you can’t remember anything when it happened. Barbiturates (GABA ) A • current research shows the involvement of GABA receptorA • enhancement of GABA transmission - GABA is an inhibitory transmitor. Barbiturates increase GABA causing depression • increased Cl- influx accounts for: (Cl- = chloride) • sedative-hypnotic actions • anesthetic properties - Sedative-hypnotic = sleepy/knocks you out Lecture 5A– Barbiturates Barbiturates (GABAA) • can open Cl- channel in the absence of GABA • increased toxicity of barbiturates • high doses can produce amnesia and a state of dementia - When you take a barbiturates, it floats around and opens a GABA channel and allows chloride through. It increases the level of inhibition and leads to toxicity. - Amnesia and dementia was originally one of the main uses. Dementia (table 7.1)(pg. 241) • in demented state 5 of 12 components are altered: • sensorium (disorientation to time & place) • affect (expressi
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