LS15 - Week 9 notes
LS15 - Week 9 notes Life Science 15
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This 5 page Class Notes was uploaded by AK315 on Thursday March 10, 2016. The Class Notes belongs to Life Science 15 at University of California - Los Angeles taught by Professor Phelan in Winter 2016. Since its upload, it has received 24 views. For similar materials see Life: Concepts and Issues in Biology at University of California - Los Angeles.
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Date Created: 03/10/16
Week 9 The synapse • Action Potential comes down Axon • Calcium channels open (calcium that is at higher potential outside rushes in to the lower potential area inside) • Neurotransmitter dumped in synapse • NT diﬀuses across synapse • Binds to receptors • Causing Na+ inﬂux and depolarization • At the synapse, an action potential is converted to a chemical signal releasing NT to stimulate tissue or another neuron The pleasure centers • There are pleasure centers in animal brains • In 1954, James Olds put electrodes to the mesolimbic area of bats brains and found that rats loved the sensation and would self-stimulate till the point of death from starvation (more than 700 times per hour!) • What good does it do an animal to have a set of neurons that makes them feel real good? • Which behaviors are tied to human pleasure centers? Why? ◦ Sex = pleasure. It maximizes reproductive success, although we don’t partake in sex with the expectation of maximizing reproductive success ◦ Adrenaline-ﬁlled activities; Bungee jumping etc. • What is going on in pleasure centers? ◦ Neuron is stimulated (in response to your behavior) ◦ dopamine is released into the synapse ◦ receptors on adjacent cell binds dopamine and ﬁre ◦ happiness occurs Drugs • Cocaine ◦ Cocaine binds to re-uptake receptors. Blocks them. ◦ Dopamine remains in synapse. ◦ Pleasure is intensiﬁed ◦ The message ‘something good is going on’ is not going to stop • Our brains are built with pleasure centers. Stimulating them is so pleasurable, we want to behave in ways that repeat and maximize that stimulation. • Serotonin ◦ This is another neurotransmitter ◦ It’s usually inhibitory ◦ Aﬀects appetite, sleep, anxiety and mood. ◦ Makes you content and satiated ◦ What if you block serotonin re-uptake transported protein? ▪ No more depression ▪ Prozac, Zoloft, Paxil etc. help prevent the re-uptake of serotonin and are used as anti-depressants. ▪ Wellbutrin, however, blocks the re-uptake of dopamine • How can a drug make us feel less tired and more alert? ◦ Caﬀeine ◦ Adenosine is a chemical produced as a by-product of cellular metabolism. It is like ‘cellular exhaust’. ◦ Over the course of a day, adenosine builds up n brain synapses, ◦ When adenosine receptors are ﬁlled, the ion channels open and the cell becomes less likely to ﬁre. ◦ Adenosine is like a brake to brain activity (And when you sleep, it is re- absorbed) ◦ When you sleep, adenosine gets taken away and you feel refreshed. Then throughout the day it builds up and shuts down your cells so you feel sleepy. ◦ Caﬀeine masquerades as adenosine but doesn’t make a neuron less likely to ﬁre! ◦ Additional caﬀeine eﬀects; ▪ Athletic endurance- 19.5% more endurance with caﬀeine consumption, 1 hour before bike race ▪ Learning - increased performance in maze learning by rats given caﬀeine. ◦ By interfering with normal neuron functioning, drugs can change the way we feel and function (for better or worse) ◦ There is no evidence of negative consequences of caﬀeine long term. • Why use Botox and how does it work? ◦ It gets into the terminal button at neuron/muscles synapses ◦ It degrades several proteins required for fusion of vesicles with the terminal button membrane ◦ this prevents the release of acetylcholine (neurotransmitter) ◦ And if this neurotransmitter doesn’t release, then the muscles that is meant to be contracted, does NOT contract! (it paralyzes the muscles) ◦ So basically, Botox prevents the muscle contraction ◦ LSD: Mimics serotonin ◦ Ecstasy: Increases serotonin production and blocks serotonin re-uptake ◦ Permanently damages serotonin producing cells in cerebral cortex (used in learning) and the hippocampus (used for memory) ◦ Crystal meth - stimulates dopamine and serotonin release ◦ Oxycontin - mimics an opium-like neurotransmitter in pain neurons, blocking their function. • By interfering with normal neuronal operation, drugs can alter how we look/feel/function Alcohol • Alcohol is a molecular everyman ◦ Alcohol reduces anxiety ▪ GABA is an inhibitory neurotransmitter. When GABA docks, cells won’t ﬁre. So releasing it calms you down. Alcohol mimics GABA and thus enhances its eﬃciency ◦ Alcohol produces stimulated energized feelings ▪ Alcohol increases dopamine. Dopamine makes us happy ◦ It blocks pain ▪ Alcohol stimulates endorphins release. Endorphins block pain signals ◦ It reduces depression ▪ Alcohol stimulates serotonin receptor activity. Serotonin makes us more content. ◦ Alcohol slows you down ▪ Glutamate is a NT. Alcohol blocks Glutamate receptors: slow/ slurred speech + reaction times are slowed down • Alcohol has multiple physiological eﬀects because it mimics activity at numerous diﬀerent synapses • How do our bodies process alcohol ◦ Ethanol - our body produces alcohol dehydrogenase (ACD) that binds to this, breaking ethanol down to ….. ◦ Acetaldehyde - our body produces aldehyde dehydrogenase (ALD) that binds to this, breaking acetaldehyde to ….. ◦ Acetic acid • Asians and alcohol = Asian glow (they turn red) ◦ 50% produce an inactive form of aldehyde dehydrogenase (this is coded for by our genes) ◦ Acetaldehyde levels increase (and because the aldehyde dehydrogenase isn’t working and breaking the acetaldehyde down). This build up causes consequences which are: ▪ Rapid pulse ▪ Sweating ▪ skin ﬂushing ▪ nausea ◦ 2 versions; fast ﬂushing (2 defective ALD genes) and slow ﬂushing (1 defective and 1 active ALD Gene) meaning that the slow ﬂushers can handle the drinks slowly but if they take it fast then they’re gonna have problems ◦ In fact, interestingly, it can be considered beneﬁcial that having a defective ALD Gene makes alcohol more unpleasant for you thus lowering your risk of alcoholism • Many genetic diseases - or beneﬁcial conditions - are the result of a non- functioning metabolic pathway • How might you make a drug that helps treat alcoholism? ◦ Antabuse - blocks the action of ALD. It has kind of a low success rate though because since the Antabuse pill needs to be taken everyday, alcoholics can just choose not to take the pill. ◦ Aspirin - blocks ACD which means ethanol build up occurs causing you to get drunk faster • Humans are polymorphic for the dopamine receptor gene ◦ Long version of gene - more responsive receptor ◦ Short version of gene - less responsive receptor ◦ World-wide 20% carry at least 1 copy of the long version gene ◦ They did a study of risk taking with the Dopamine receptor gene and to some extent it was found that individuals with the long gene did more risk-taking things for kicks compared to people with short gene. ◦ Basically, although there are problems with the study itself, it is quite consistent with other studies and it basically tells us how genes tend to aﬀect personality traits • Risk-taking stimulates the brains pleasure centers - some brains experience more pleasure than others • Some interesting predictors of risk-taking ◦ Spicy food preference ◦ Alcohol use/abuse ◦ Sexual novelty seeking ◦ Smoking ◦ Drug use ◦ ADHD