PSL300 Muscle 1 & 2 Notes PDF

PSL300 PSL300 – Muscle 1 & 2 Skeletal Muscle Smooth Muscle Cardiac Muscle Skeletal Muscle Activated by the somatic nervous system Motor neurons (motor neuron + associated muscle fibers = motor unit) Chemical signaling between motor neuron and skeletal muscle = Neuro-Muscular Ju...

PSL300 PSL300 – Muscle 1 & 2 Skeletal Muscle Smooth Muscle Cardiac Muscle Skeletal Muscle Activated by the somatic nervous system Motor neurons (motor neuron + associated muscle fibers = motor unit) Chemical signaling between motor neuron and skeletal muscle = Neuro-Muscular Junction (NMJ) NMJ= the synapse between a motor neuron and a muscle fiber (motor neuron’s axon terminal, muscle fiber) Contractile filaments in sarcomeres; striated Well developed sarcoplasmic reticulum (SR) Skeletal Muscle Muscle = group of fascicles Muscle fibers extend length of muscle from tendon to tendon Skeletal Muscle Fiber Muscle fiber made up of myofibril Sarcolemma = Plasma membrane · T-tubule system = Invaginations of sarcolemma into muscle fiber · sacroplasmic reticulum = Intracellular organelle , Catt storage - fastest contraction Motor Unit The muscle fibers of a motor unit all contract together The smoothness and precision of movement depends on the number and timing of motor units that are activated Muscle contraction begins with small motor units being activated first Muscle Fiber Types Slow-twitch oxidative fibers – Slowly contracting – Many mitochondria – Oxidative metabolism Properties of NMJ Anatomy of the neuromuscular junction – Terminal bouton = axon terminal (motor neuron) – Motor end plate = specialized muscle membrane at junction All motor neurons release acetylcholine All synapses are excitatory Communication at the NMJ 1. Action potential arrives at terminal bouton 2. Voltage-gated calcium channels open 3. Calcium enters cell triggering release of ACh 4. ACh diffuses across cleft and binds to nicotinic receptors on motor end plate Poisoning the NMJ The brain is largely protected from toxins in the blood by the ‘blood-brain barrier’. Peripheral tissues, including muscle, are exposed to circulating toxins. Toxins that block the NMJ fall into 3 types: nicotinic receptor blocker · · poison dart (Curare) Curariform · drugs · exocytosis blocker · DOtO)C · ach-esterase inhibition nerve gases · · pesticides The Mechanism of Force Generation The crossbridge cycle: how muscles generate force Skeletal Muscle Fiber Thin filament is made up of actin Thick filament is made up of myosin Structure of a Sarcomere Actin and myosin are organized in overlapping arrangement with respect to one another in units called sarcomeres · muscle contraction = Sacromere shortening instead slide another · activ and myosin do not change length , past one Thick Myofilament Thick filament is made up of myosin molecules Myosin head contains actin binding site and ATP binding site Troponin & Tropomyosin Actions No Calcium: troponin holds tropomyosin over myosin binding sites on actin – No crossbridges form between actin and myosin – Muscle relaxed Crossbridge Cycle Myosin head undergoes conformation changes swiveling back-and-forth – High-energy form High affinity for actin – Low-energy form Low affinity for actin Relies on ATP hydrolysis Crossbridge Cycle With increase in Ca++, myosin head and actin filament bind strongly Power stroke occurs, myosin head moves propelling the thin filament toward center of muscle Crossbridge Cycle Myosin releases ADP at the end of power stroke · light binding in the rigor state · ATP binds to myosin · Myosin releases actin · Myosin hydrolyzes ATP · Myosin head rotated to cooked position · Myosin binds weakly to actin Power · stroke begins when tropomyosin off moves the binding site Excitation-Contraction Coupling Sequence of events whereby an action potential in the sarcolemma causes contraction Dependent on neural input from motor neuron Requires calcium release Termination of Contraction Calcium must leave the binding sites To remove calcium from cytosol – Ca2+ ATPase in sarcoplasmic reticulum – Transports calcium from cytosol into sarcoplasmic reticulum Twitch Contraction 3 phases of muscle twitch – Latent period – Period of contraction – Period of relaxation Latent period – Excitation-contraction coupling occurring Period of contraction – Intracellular Ca++ levels are high, crossbridge cycling is occurring Period of relaxation – Intracellular Ca++ levels fall, eventually tension gradually falls to zero Summation and Tetanus In skeletal muscle, with increased AP frequency, successive twitches fuse with each other Contractile force rises Summation and Tetanus Repeated stimulation = fuse into one continuous contraction called tetanus · muscle fatigue results in rapid decrease in tension Smooth Muscle Found in internal organs, blood vessels Examples of smooth muscles: vasculature, GI tracts, urinary, reproductive, and respiratory tracts, pupil, etc… Not arranged in sarcomeres Under involuntary control by ANS Classification of Smooth Muscle By location – Vascular, gastrointestinal, urinary, respiratory, reproductive, ocular By communication with neighboring cells – Single-unit smooth muscle, or visceral smooth muscle – Multi-unit smooth muscle Single-Unit Smooth Muscle Single-unit smooth muscles – Found in the Intestinal tract and Blood vessels etc… – Exhibits spontaneous activity (but also activated by the ANS) – Able to actively exert tension in absence of external stimulation Excitation-Contraction Coupling Lacks specialized receptor regions Ca2+ is from the extracellular fluid and sarcoplasmic reticulum Ca2+ initiates a cascade ending with phophorylation of myosin light chain and activation of myosin ATPase Relaxation of Smooth Muscle Phosphatase removes phosphate from myosin Calcium removed from cytoplasm – Ca-ATPase – Ca-Na counter transport Cardiac Muscle Contractile cells and conductile cells Contractile filaments in sarcomeres; striated Intermediate development of SR Gap-junctions for synchronous beat Activity modulated by ANS (unlike skeletal muscle = somatic nervous system) Cardiac Muscle - AP AP duration 300ms in ventricles AP plateau due to slow Ca2+ channels allows time for forceful contraction from single AP Plateau allows muscle contraction to last 300ms (20-50x longer than in skeletal muscle) AP shape and duration reflects changing permeability to Na+, Ca2+ Cardiac Muscle Contraction One way to increase force of contraction: Unable to increase force of contraction by motor unit recruitment or by enhanced excitation/contraction coupling Unable to increase force of contraction by increasing stimulation frequency to tetanus Increase force of contraction by increasing muscle length (Starling law) Excitation-Contraction Coupling Significant Ca2+ source from ECF, rest from SR Contractile proteins in presence of increased cytosolic [Ca2+] power contraction (systole) Ca2+ pump in the SR removes Ca2+ from cytosol allowing for relaxation (diastole) Na+/Ca2+ membrane exchange removes Ca2+ from cytosol allowing for diastole