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PSL 250 Week 6 Lectures

by: Ren K.

PSL 250 Week 6 Lectures PSL 250

Marketplace > Michigan State University > PSL 250 > PSL 250 Week 6 Lectures
Ren K.
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These are the lectures from week 6 - lectures 15 (complete vers.),16, 17, 18
PSL 250: Introductory Physiology
Class Notes
PSL, 250, Physiology, PSL250, premed, medical, Engineering, P.Dillon, Dillon, Science
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This 12 page Class Notes was uploaded by Ren K. on Saturday October 8, 2016. The Class Notes belongs to PSL 250 at Michigan State University taught by Spranger in Spring2015. Since its upload, it has received 11 views.


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Date Created: 10/08/16
PSL 250 - Lecture 15 - Hearing and Equilibrium Outer Ear ● Little amplification ● Direction detection. Tympanic membrane ● The tympanic membrane is the eardrum. ● Overlapping membranes. ● Separates outer and middle ears. ● Vibrates to external air waves. Middle Ear ● Air filled ● Amplifies sound 20x Ear Bones ● Malleus - incus - stapes ● Hammer - anvil - stirrup ○ Need to know order + english version. ● Carry waves from the tympanic membrane to the oval window. Eustachian Tube ● Drains middle ear of fluid. ○ Normally the eustachian tube is air filled - not a rigid tube. ○ Flat and flexible - collapses against itself. ○ Eustachian tubes can stick, and only if the pressure gets sufficiently high will it open up. ○ Ears pop because air forces out of eustachian tube into sinuses when you are in a plane. ○ Swelling during an infection. ● Equalizes air pressure between middle ear and sinuses. ● Normally closed - if unopenable, tubes needed in eardrum. ● When the eardrum vibrates it moves the malleus (hammer). ○ Tube can’t vibrate if there is excess fluid. ○ Eustachian tube has to pass through a hole that is within your facial bones. ○ As a result, sometimes children can’t have fluid draining out of their ears. Oval Windows ● Membrane - connects middle ear to inner ear. Inner Ear ● Fluid filled. ● Converts sound waves to electrical signals. ● Cochlea - Organ of corti. ● C: spiral shaped tube of inner ear. ● O of C: part of cochlea that transduces sound to APs. ● Waves carried to apex and back to round window. ● Round window absorbs all sound waves, no APs. ● Similar to choroid in the eye. Diagram part of lecture on inner ear ● Tectorial membrane - very stiff. ● Basilar membrane - very flexible ○ This is how we differentiate from a high pitch to a low pitch. ● Cilia on the basilar membrane - referred to as hair, embedded into tectorial membrane. ● As the soundwave pulls the cell back and forth, pulling on the hair. ● Sodium ions are able to come in and produce a potential. ● The signal is then sent out via the auditory nerve into your brain. ● Round window is virtually able to absorb all sound, preventing you from hearing a sound multiple times - no echo. ● Identical to choroid - no repetitive signal. Basilar Membrane ● Vibrates to the sound waves that come by, to the base area - its shape changes over the length. ● High frequency at the base, low frequency at the apex. ● Lowest frequency sound we can hear is 20 hz. ● If it's very loud like a power plant you can notice the sound more easily - power plant at Niagara falls. ● Highest pitch sound we can detect is 20,000 hz. ● As we age, the cochlear membrane thins meaning as we age we can detect only lower hz than 20,000 hz even if your hearing is pretty good. ● Hair cells rest on the basilar membrane. ● Hairs embedded in the tectorial membrane. Tectorial membrane ● Much stiffer than the basilar membrane, meaning that tectorial membrane experiences less movement. Frequency of sound ● Maximum range 20hz to 20,000 hz. Lose high frequency with age. ● If the frequency is reaching you at a faster rate (doppler effect) coming close - changes frequency. ● Doppler shift - tell if the sound is moving towards you (13,000 hz like fire truck coming close) or moving away (11,000 hz if a fire truck is coming away) Timbre ● Overtones allow source distinction. ● Types of musical instrument or individual voice. ● Total signal = fundamental frequency + overtone(s). ● Voice monitor - timbre for frequency of the voice. ○ Can identify individual perfectly because each person has a unique set of vocal chords even if they’re doing a vocal impersonation i.e. doing a pretend impression of Johnny Cash. ● Good singers have smooth fundamentals - pure notes. In an image, it looks less jagged. ● A pure note - reach a particular frequency to make the note sound better. Amplitude of Sound ● Amplitude of sound. ● Height of sound wave - higher wave = more hair cell movement and more APs to brain. Deafness ● Loss of hearing Conductive Deafness ● More common than nerve deafness. ● Soundwave is blocked from accessing hair cells. ● Wax, ear drum damage, middle ear bone damage. ● Hearing aid can help with conductive deafness; by amplifying sound to vibrate oval window directly. Nerve Deafness ● Damage to hair cells or auditory nerve. ● Need cochlear implants to treat. ● Frequency deafness: loud repetitive sounds at one frequency pull out hair cells in one place. ● Dual wave processor for cochlear implants to hear variable frequencies - before you could only hear a monotone frequency. ● For children who have this - inherited deafness and can be treated by cochlear implants. ● 97% people choose to have cochlear implant, vs 3% cochlear implant denied. Equilibrium ● Vestibular apparatus - detect changes in motion. ● Acceleration. Rotational Acceleration ● 3 semicircular canals detect changes in rotational motion. ● All are oriented in a mutually perpendicular manner. ● Fluid filled as fluid lags motion, fluid pulls on hair cells. Semicircular Canals ● Hair cells embedded in the cupula - inertia. ● Generates GP that lead to AP ● When hard rotation stops 25- 30 seconds to equilibrate. Linear acceleration ● Hair cells embedded in gel with otoliths ● Acceleration pulls on hair cells ● Gravity constant causes tonic signal know the position of the head Utricle Saccule ● Detect linear acceleration ○ U: horizontal motion ○ S: vertical motion ● Mismatch of these signals lead to motion sickness excess - rides or loss (space flight) or poorly designed video games. PSL 250 - Lecture 16 - Efferent Nervous system Sympathetic Structure ● The sympathetic structure is part of the autonomic nervous system. ● Sympathetic chain ganglia is parallel to the spinal cord. ● Input from the cord, medulla, hypothalamus. ● No direct cortical control. ● When people are under a lot of stress it activates the sympathetic nervous system. Postganglionic Neurons ● Short neurons ● Use acetylcholine (Ach) as NT to post ganglionic neurons in the ganglia. Preganglionic Neurons ● Long neurons ● Activated by preganglionic neurons ● User norepinephrine (NE) as neurotransmitter. ○ Epinephrine = Adrenaline ○ NE = Noradrenaline ● Adrenal medulla behaves like Post-G neuron. Parasympathetic Responses ● Decrease the heart rate ● Increase GI contraction and secretions ● Increase pancreatic secretions ● Contracts urinary bladder ● Relaxes internal anal and urinary sphincters. Agonists and Antagonists ● Pharmaceuticals can mimic or antagonize autonomic NS ● Para: mimic increase or antagonize decrease digestive activity etc. ● Sym: increase BP in shock, decrease BP in hypertension. Sympathetic Responses ● Respond to emergencies. Fight or Flight response ● Designed to remove danger. ● Increases the blood flow to skeletal muscles and the heart. ● Concurrent activation of motor units. ● Decreased activity of digestive and related functions. ● Relaxation of digestive system causes the stomach pain associated with unpleasant situations. Receptor Types - Adrenergic Receptors ● All bind NE from postganglionic neurons Alpha adrenergic receptors ● Cause increase in tissue activity. ● Alpha 1 leads to increase of IP3 leads to an increase of Ca++ release from SR. ● Alpha 2 leads to a decrease of cAMP causing a decrease in Ca++ pump leading to a net increase in Ca++. ○ Calcium pumps pump calcium out of your system. Beta 1 Adrenergic receptors ● Increase Ca++ in the heart - open Ca++ channels ● Increase heart activity Beta 2 Adrenergic receptors ● Increase in cAMP leads to an increase of Ca++ pump and a decrease of the Ca++ ● Blood vessel dilation and lung. ● Bronchodilation = more blood, more air. Parasympathetic Structure - Part of autonomic nervous system. ● Two neuron series - ​all neurons use Ach as NT ● Cholinergic activation controls day-to-day homeostatic maintenance. Preganglionic Neurons ● Long neurons - spinal cord to organ. ● Synapse at ganglia on organs with postganglionic neurons. Postganglionic Neurons ● Short neurons - travel from ganglia to cells Parasympathetic Responses ● Decrease the heart rate ● Increase GI contractions and secretions. ● Increase pancreatic secretions. ● Contracts urinary bladder. ● Relaxes internal anal and urinary sphincters Motor Neurons ● Alpha motor neurons gets multiple inputs - up to 10,000 ● Motor neurons get input from stretch receptors, withdrawal reflexes, cerebellum (learned activities) , cortex (conscious control) ● Both constantly receive IPSPs and EPSPs to alpha motor neurons. ● Asking - are we there yet, have we reached the required threshold. ● They become myelinated. ● Lack axon terminals - have one axon terminal known as the Neuromuscular junction. Neuromuscular junction ● Motor neuron synapse with skeletal muscle fiber (cell) ● Abbreviated as NMJ ● Motor end plate ( very large synapse ) ● Single AP in neuromuscular junction = always produce reaction. ● Muscles are controlled by neuromuscular junction AP - 1 muscular contraction for 1 AP. ● 1:1 Ratio for APs and contractions. Acetylcholine Release ● Presynaptic AP leads to the entry of Ca++ entry leads to Ach release. ● Ach binds to the receptors on the muscle membrane. Endplate Potential ● Endplate potential or EPP is much larger than the EPSP. ● Ach binds to the receptor leading to an increase of Na+ entry rate causing them to reach threshold. ● One motor neuron AP leads to one muscle AP ● Control of motor neuron APs controls muscle cell activation. Acetylcholinerase - AchE ● AchE degrades Ach to choline and acetic acid. ● Reuptake of choline, diffusion away of acetic acid. NMJ poisons YASSS ● Inhibit the diaphragm - makes you not able to breathe. ● Black widow spider venom: Releases all Ach ● Botulinum toxin: blocks Ach release ● Curare: block Ach receptors PSL 250 - Lecture 18 - Motor Units Motor Unit ● Motor neuron and muscle fibers it innervates. ● Motor neuron AP activates all the fibers in a motor unit Recruitment ● Small MUs first, then the larger motor units. ● Allows gradation of force. ● Maximum force requires all MUs active simultaneously Asynchronous Recruitment ● For submaximal forces - rotate activation of MUs. ● Maintain force - cannot simultaneously optimize force and continuous activity. Twitch ● Single AP = single muscle activation ● 1 neural AP leads to one muscle AP leads to one twitch. ● Sub-maximal force - not enough Ca++ reaches all troponin for full activation Tetanus ● Summation of twitches - many APs ● Enough Ca++ so that all myosin heads reach actin. ● Unrelated with the bacterial infection Tetanus. Length- Tension Relation ● Lo - Muscle length at which maximum force occurs ● Resting skeletal muscle length is near Lo ● Not force ™ - Lo is a length. ○ Thats is a test question ™ . Falloff at Long lengths ● Reduced overlap of thick and thin filaments. Falloff at Short Lengths ● Thick filaments compression against the z line. ● Thin filaments overlap and interfere with each other. ● Reduced Ca++ release Force-Velocity Relation ● Heavy loads can only be moved slowly. ● Light loads can be moved quickly. Inverse Relations ● High force (load) = low velocity ● Low force (load) = high velocity ● Hard to throw a 100 kg stone fast vs 1 kg stone Stretched muscles ● Stretching before activation (windup) uses top of L-T curve. ● Better force maintenance. ● Also, activating stretch reflexes. - reflex contraction of stretched muscles. Power curve ● From FV curve. PSL 250 - Lecture 17 - Muscle Structure and E-C coupling Striated Muscle Structure ● Skeletal - connects to 2 tendons - tendons attach to bone. ● Cardiac - smaller cells - attached end to end. ● Smooth muscle - 10 microns wide ● Cardiac muscle - 30 microns wide ○ Linked together like stacked soup cans. ○ It is a flat area loaded with gap junctions ○ Activation passes from one cell to another because of these gap junctions, giving a nice uniform heartbeat. Muscle Fibers ● Muscle cells = muscle fibers. ● Runs length of muscle in skeletal muscle ● Changes size (thickness) but no mitosis. ● Have the same muscle cells today that you were born with. ● Are not static in any term - can hypertrophy. ● If you lift heavy weights - raise muscle mass. ○ Also dependent on testosterone. Endocrinologic difference. Striations - Stripe pattern. ● Lines in skeletal and cardiac muscle ● Two bands light and dark, occur because of filaments lined up in the muscle in register. ○ In register - lined up together + start and stop at the same point. ● Filaments overlap - overlap increases during muscle contraction. ● Any place with myosin - appears dark vs no myosin - appears light Dark and light bands ● Dark bands contain thick filaments may also have some thin filaments ● Light bands have no thick filaments, only thin. Sarcomere ● Unit of contraction, z line to z line. ● Thin filaments are anchored to the z lines. ● Thick filaments are connected to thin filaments during contraction. ● What one sarcomere does, all do in a fully active fiber. Thin filaments ● Actin polymer backbone - double stranded helix. ● On 5 separate chromosomes, so no one ever has an actin mutation. ● Tropomyosin - long thin protein polymer runs along actin. ● Troponin - binds to tropomyosin. Thick filaments ● Myosin polymer of filamentous proteins ● Extension of myosin is cross bridge ● Crossbridge head can bind to actin and generate force. T-Tubules sarcoplasmic reticulum ● Tt are invaginations of muscle membranes carry APS into muscle fiber interior ● SR develops from ER stores Ca++ ● Connected to TT by voltage sensitive protein ● AP down tt open ca++ channels in SR Excitation contraction coupling ● Electrical events leading up to muscle contraction Skeletal Action potential ● Starts at NMJ synapse ● NT Ach binds to receptor opens Na+ channels and starts AP spread in both directions. Release of calcium ● At t-tubule, AP travels inward - altering the protein within the t-tubule, leading to the opening of Ca++ channels in SR near the T-tubules, causing Ca++ to be released. ● Ca++ pumps at the middle of SR resequesters Ca++ and causes relaxation. Troponin calcium binding ● Ca++ binds to troponin on the thin filament. ● Causes tropomyosin to shift. Tropomyosin shift ● Ca++ bound troponin causes tropomyosin to shift into actin groove, exposing A-M binding site. Actin-Myosin Binding ● A and M connect ● Myosin already has ATP bound and converted to ADP*Pi with ADP*Pi still bound. Force Generation ● ADP*Pi is released causing the change in myosin shape, and the myosin head twists leading to force development. ● No filament sliding, no change in overlap. ● Pi release is key to force development. Filament sliding ● Filaments slide to decrease force on crossbridge head - more overlap. ● Goes to the lowest energy state force = 0 ● New ATP binds to Myosin, actin is released, and process repeats as long as Ca++ is elevated. Relaxation ● Cessation of APs stops Ca++ release from the SR ● Calcium pumps return released Ca++ to SR ● Tropomyosin reblocks AM binding site. ● Muscle relaxes


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