BSC 215 Week 8 Notes
BSC 215 Week 8 Notes BSC 215
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This 9 page Class Notes was uploaded by Jordana Baraad on Thursday October 6, 2016. The Class Notes belongs to BSC 215 at University of Alabama - Tuscaloosa taught by Dr. Jason Pienaar in Fall 2016. Since its upload, it has received 4 views. For similar materials see Human Anatomy & Physiology I in Biological Sciences at University of Alabama - Tuscaloosa.
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Date Created: 10/06/16
10/4/16 Muscles LO1: Muscle tissue Striated Skeletal (muscles that connect to bones) Cardiac (heart) Smooth (fusiform-shaped; Cells Skeletal muscle cells: long, multinucleated & connected to nerves a.k.a. “muscle fiber” or “myocite” Cardiac muscle cells: shorter,uni or binucleated, branched, involuntary connected to each other by gap junctions Smooth muscle cells: short,spindle shaped, uninucleated connected to each other by gap junctions gap junctions (cardiac and smooth) no need for innervation skeletal muscles = focus of A&P I (cardiac &smooth in A&P II) Extracellular matrix Endomysium: holds muscle cells together within muscle tissue ALL generate muscle tension LO1: Muscle cell characteristics Contractility ability of protein fibers within myocytes to draw together o NOT to shorten; fibers draw over one another (unit shortens; fibers don’t) Excitability responds to stimuli (electrical or chemical) o Electricity flowing thru nerve Acetylcholine (Ach) release electricity in muscle cells Conductivity conduct stimulus (electricity) Extensibility can be stretched up to 3x resting length o Often confused w/ elasticity—know the difference Elasticity ability to regain original state after stretching LO1: Muscle cells Smooth endoplasmic reticulum = Sarcoplasmic reticulum Extensions Store Ca ions Plasma membrane = Sarcolemma Cytoplasm = Sarcoplasm Release Ca ions into sarcoplasm musc contraction Myofibril: specialized parts of cytoskeleton Actin/ myosin –main functional units of muscle Mitochonrion make ATP; lots needed for muscle cells Nucleus: multinucleated to control long, skinny cell LO2: Skeletal muscle organization Tendon: attaches muscle to bone Bone Muscle = myofiber = muscle fiber Fascicle: groups of fibers gathered together Epimysium: Surrounds muscle & continues as tendon Perimysium: collects cells & endomysium into fasicles, continues as tendon Sarcolemma—surrounds whole thing ECM = endomecium (btwn individ muscle cells) Perimecium: dense irreg CT; surrounds fassicles Collects cells in ECM into fassicle (collection of cells) Epimecium: dense irreg CT Needs nerves and blood vessels LO3:The Skeletal muscle fiber Erythrocyte (shown for contrast) No nucleus, no striations, float around Cell size and shape: long and narrow Striations Multiple nuclei Squished up against side Skeletal myocyte LO3:The Skeletal muscle fiber Mitochondria squished in btwn Myofibril Terminal cisternae (on either side of T-tubule) Part of sarcoplasmic reticulum T-tubule Part of sarcolemma 2 main types protein: actin and myosin dark (A) bands & light (I) bands I band missing thick purple (myosin) Thick + thin = dark; thin only = light **Fav test q: what happens to A&I bands dur musc contraction LO3: Sarcoplasmic reticulum Triad Tubules of sarcolplasmic reticulum (SR) Terminal cisternae T-tubule = extension of sarcolemma—extends btwn 2 cisternae Green particles in nerve cell = Ach Neuromuscular junction causes Na channels to open Na/K pump Pumps 3 Na out; 2 K in Ca channels in term cisternae (in SR) open Stimulation of SR fr nerve signal opening Ca release T-tubule carries action potential to triad Ca interaction w/ muscle fibers contraction Riger mortis bc loss of control of Ca channels LO3: Myofibrils Filament proteins: Actin – thin filaments Myosin thick filaments Titin – elastic filaments (belongs here least) Tropomosin (long, skinny) – involved w/ Ca Troponin (short)– involved w/ Ca “drawing pins”; blocks holes flooding sarcoplasm w/ Ca troponin interaction w/ Ca tropomyosin falls off Thick: collection of myosin protiens Tail, hinge, head Hinge allows for puling on actin filaments Hole in actin filament for myosin heads to fit into Multiple myosin heads interact w/ mult actin Muscles never open (Z discs pulled apart) by self; must contract opponent muscle LO4: Protein myofilament arrangement Zig-zag lines = Z-disk Sarcomere(funct unit of individ myofibril) = area btwn 2 z-disks Sarcomeres contract in muscle fiber Sacromeres & musc cells shorten; individual fibers don’t H-zone: zone of overlap M-line: central line that contraction goes toward LO4: Sliding filament mechanism of contraction Left: Light pink = I band Dark pink = H zone Both I &H get thinner H-zone defined by lack of overlap; contraction = overlap I defined by zone of non-overlap Rt: A-band unchanged in relaxation v. contraction **Why no change? Protein fibers don’t change in length Only the zones of overlap change Bc myosin pulling actin toward M-line musc contraction Sarcomere shortening; Z-discs pulled closer together Vid Ca released, binds w/ tropomyosin; myosin heads exposed on actin myofilament LO5: Membrane potential Fig: Blue = ECM; inside = sarcoplasm; separated by sarcolemma Electrochemical gradient: pos charge outside; neg charge inside Na conc higher outside • Electrical gradient: • Separation of charged particles (electrolyte pairs) across the plasma membrane (sarcolemma) • Electrical potential: • Potential energy due to barrier (sarcolemma) maintaining gradient • Voltage (V) • Difference in electrical potential between two points • E.g. 110 Volt potential difference between wall outlet & toaster. • Membrane potential • Electrical potential diff either side of the cell membrane (polarized membranes) • Resting membrane potential for myocytes = 85 mV (when ion channels closed) negative sign bc always measure outside rel to inside of cell at resting potential, ready to do work; ion flow = work being done also K leak channels in cell memb some K flows out by diffusion strong pos charge outside stops diffusion equilibrium reached due to opposing conc and electrical gradient keeps all K ions fr flowing out maintains resting potential LO5: Sodium potassium pumps help generate resting membrane potentials 2KCl > 2K+ + 2CL 3NaCl > 3Na+ + 3Cl 10/6 CQ. Which true dur musc contraction? C) H zone and I bands both narrow LO1: Action Potential x-axis: millivolts—measuring action potential when red line move, voltage/ potential changing little flat line before jump = resting potential maintained by Na/K pump also by K leak channel equilibrium state—total # cations inside/out change by creating cation (Na and K) flow never talk about anion flow steps open Na ion channels in membrane lots Na flowing into cell inside cell becomes increasingly positive (up to approx. 0 mV up to +30 mV (inside cell more pos rel to outside)) open K channels; K flows out : repolarizing left side of graph = depolarization (increasingly pos) ; rt side = repolarizing (increasingly neg) Entire graph (depolarization + repolarization ) = action potential 1. Resting phase: Gated channels are closed Na+ & K+ gradients maintained by Na+/K+ pumps & K+ leak channels 2. Depolarization phase: Na+ channels open in response to a depolarizing stimulus. Na+ enters the cell down its gradient & further depolarizes the membrane. 3. Repolarization phase Na+ channels close. K+ channels open, (can now rush out) Na can also rush out bc not facing opposition very fast reversal K+ exits the cell down its gradient & repolarizes the membrane. 4. Na+ / K+ pump restores resting potential opening/ closing at different stages; simultaneous events Na channels open depolarization; K channels open repolarization CQ2 T/F—opening of voltage gated K-chanels depolarization? F. K-chanel opening repolarization LO1 Need to bring action potential into cell so Ca can interact Green arrow = AP AP’s move by saltation fr ion channel to ion channel All muscle cells attached to nerve (motor neuron) 2 kinds channels: initial: ligand gated regenerated: voltage gated Na ion channels LO2: Neuromuscular junction Motor neurons stimulate skeletal muscle to contract • All skeletal muscle fibers are innervated / have neuron attached often, muscle cells stimulated in groups • Axon branches of motor neurons synapse with muscle fibers at neuromuscular junctions synapse = nerve + other cell (can be 2 nerve or diff type) • Synaptic vesicles at end of axons contain acetylcholine, a neurotransmitter • Acetylcholine is secreted into synaptic cleft, and interacts with acetylcholine receptors (ligand gated Na+ channels) on the motor end plate on the sarcolemma Na flows into muscle cell End plate potential generated on motor end plate Slightly diff from action potential Generated by ligandgated, not voltage gated Action potential propagated through neurilemma (voltage gated Na+ / K+ channels) Chemical signal at synapse (acetylcholine & ligand gated Na+ channels) Convert electrical chem Ach interacts Na channels opening Action potential propagated through sarcolemma (voltage gated Na+ / K+ channels) Cq3 T/F? Ach acts to open voltage gated sodium ion channels in the muscle cell membrane? F—Ach opens ligand-gated channels, not voltage-gated LO3: The big picture excitation / contraction coupling 1. Action potential from neuron results in acetylcholine secretion in synaptic cleft 2. Ligand gated Na+ channels in sarcolemma open when bound to acetylcholine 3. Generates action potential wave that travels down Ttubules of sarcolemma 4. Ttubule depolarization results in Ca2+ channels in the terminal cisternae of sarcoplasmic reticulum to open 5. Ca2+ interacts with troponin, releases tropomyosin and allows myosin heads to interact with actin, resulting in sarcomere contraction 6. Muscle relaxes when acetycholine no longer present and [Ca2+] in sarcoplasm returns to norma also must introduce Ach-degrading enzyme and contract opponent muscle LO3: Excitation phase Diff set of Ca channels responsible for exocytosis Channels Ca flow in exocytosis of Ach 1. Action potential from neuron triggers exocytosis of synaptic vesicles 2. Synaptic vesicles release acetylcholine into synaptic cleft 3. Acetylcholine binds to ligand-gated ion channels in motor end plate 4. Na+ diffuses through ion channels, depolarizing sarcolemma locally, producing an end-plate potential 5. Continuous multiple endplate potentials generate a sarcolemma action potential must generate lots end plate potentials AP bc AP is irreversible; WILL cause musc contraction LO3: Excitationcontraction coupling 1. Action potential travels down Ttubules via voltage gated Na+ channels 2. Ttubule depolarization leads to the opening of voltage gated Ca2+ channels in terminal cisternae of sarcoplasmic reticulum 2. CORRECTION mechanically-gated channels NOT voltage gated LO3: Preparation for contraction At rest, tropomyosin twists around actin, blocking its active sites Ca2+ binds to troponin, causing tropomyosin to fall off the actin, exposing the active sites CQ4 Troponin has higher affinity for Ca than it does for tropomyosin? True LO4: Contraction phase: the crossbridge cycle Where ATP introduced; also req Ca—expensive process, energywise 1. ATP hydrolysis “cocks” the myosin heads 2. Myosin heads bind to actin active sites (crossbridge) 3. Myosin releases ADP and P power stroke pulls actin towards M line 4. Binding of a new ATP “breaks” crossbridge 5. Cycle starts again CQ5 Functional unit of muscle contraction found btwn 2 Z disc is C) sarcomere Muscle relaxation 1. Acetylcholinesterase degrades acetylcholine in synaptic cleft 2. Sarcolemma returns to resting potential, and calcium channels in sarcoplasmic reticulum close 3. Calcium ion pumps return calcium to sarcoplasmic reticulum 4. Troponin and tropomyosin block active sites on actin LO5: Energy requirements • Muscle fibers require a lot of ATP adenosine of ATP also used to build DNA/ RNA red circles around highenergy phosphate anhydrous bonds only 2 of 3 bonds are highenergy ATP ADP AMP, then stop—not helpful to remove last P • Na+ / K+ pumps • The cross bridge cycle • Where do they get it from? LO5: Energy Sources 3 sources E 1. Quickest derived; quickest used up a. Source = creanine phosphate (CP) b. Directly gives phosphate to cells c. Supplements not helpful; can’t beat physio ratio i. Only so much 2. next quickest a. glycolysis works in absence of oxygen b. can’t strip electrons off pyruvate product bc no O to pass them to c. produces some ATP (2); lasts about 1 min d. lactic acid buildup—NOT cause of muscle soreness 3. takes longest; provides most a. oxygen reaches cells via hemoglobin b. myoglobin w/n cells take O to mitochondria c. mitochondria produce ATP d. When run out of glucose, switch to fatty acids e. Then, move to amino acids i. Comes from digesting muscle tissues
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