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FRCA Muscles (Cardiac (Excitation-Contraction coupling (Termination …

- - - - Phase 0 (rapid depolarisation): threshold potential -65mV. Rapid depolarisation to 20mV. Opening fast voltage-gated Na channels
        Phase 1 (early rapid depolarisation): Na channels close, fast K channels open towards plateau.
        Phase 2 (plateau): L-type Ca channels slowly open, Ca influx. K slow delayed rectifier channels open to let K out.
        Phase 3 (repolarisation): gradual inactivation of Ca channels. K channels remain open to allow outflux
        Phase 4 (electrical diastole): RMP is maintained due to K efflux through K inward rectifier channels
      - Absolute refractory period (200ms)
        Relative refractory period after that
  - - - Plasma membrane Ca-ATPase pump (PMCA): uses ATP to actively remove Ca2+
      - Na/Ca exchanger (NCX): removes 1 Ca for influx of 3 Na. Driven by low intracellular Ca concentration (maintained by Na/K ATPase pump)
      - SR/ER Ca-ATPase pump (SERCA): Uses ATP to sequester Ca into SR
  - - - Middle (Wenckebach pathway)
      - Posterior (Thorel pathway)
      - Anterior (Bachmann): also relays to LA via Bachmann bundle
    - - Right
      - Left anterior
      - Left posterior
- - - - ANS: Single-unit SM is usually innervated by sympathetic AND parasympathetic neurons
      - Hormones and circulating molecules: e.g. O2, CO2, NO, adrenaline, NorAd, histamine, PG, 5HT
      - Stretch: Stretch of SM sheet triggers contraction. In arteries this is called myogenic response. In GI tract peristalsis is triggered with stretch
      - Pacemaker activity: Heart (SA node) and GI tract (interstitial cells of Cajal) have spontaneously depolarising membranes. This occurs 12/min in duodenum, 3/min in colon etc.
    - - Lack of T-tubules: action potentials propagated rapidly through gap junctions. Caveolae increase surface area and facilitated Ca2+ entry
      - Ca2+: lack T-tubules and poorly developed SR mean SM uses other methods to increase Ca2+ influx:
        
        Voltage-gated Ca2+ channels
        
        Ligand-gated Ca2+ channels
        
        Stretch-responsive Ca2+ channels
      - Calmodulin: Ca2+ binds to calmodulin. This complex then activates SM contraction through:
        
        Myosin light-chain kinase (MLCK): sarcoplasmic enzyme MLCK is activated, phosphorylates myosin light-chains and allows it to form cross-bridges with actin filaments
        
        Caldesmon: Troponin is absent in SM, but replaced by Caldesmon. Ca2+/Calmodulin complex binds to caldesmon to cause conformational change, unblocking myosin binding site and permitting actin-myosin crossbridge cycling
        
        Calponin: this protein inhibits the ATPase activity of myosin head (activated by Ca2+ alone or Ca2+/Calmodulin complex
- - - - Myocytes: surrounded individually by endomysium
        
        Sarcoplasmic reticulum: modified ER acting as Ca2+ store
        
        T-tubule: invaginations of muscle surface membrane (sarcolemma) to relay action potentials deep into myocyte interior
        
        Glycogen stores
        
        many Myofibrils: contractile apparatus arranged in parallel spanning entire length of myocyte, anchored to sarcolemma at either end (to contract and shorten)
        
        long Myofilaments consisting of sarcomere continuous end to end
        
        Sarcomeres: functional unit of skeletal muscle between 2 Z lines
        
        Thin filament (actin)
        
        Double helical strand of Fibrous (F) actin consisting of strings of Globular (G) actin subunits. (300-400 actin molecules)
        About 7nm diameter
        Each G actin can bind to myosin head
        Each thin filament has a tropomyosin strand running along groove which blocks active sites of thin filament when muscle is relaxed.
        Each tropomyosin has troponin complex bound to it (T, I, C). T binds tropomyosin, I is an intermediate link, C allows Ca2+ to bind and uncover myosin binding site
        
        Thick filament (myosin)
        
        Titin core to anchor to Z lines.
        Myosin (golf-club shaped): tail of 2 intertwined chains and double globular head.
        About 15nm diameter
        
        Sarcolemma (cell membrane)
        Resting membrane potential -90mV
        Synaptic activity at motor end plate causes depolarisation of sarcolemma, triggering action potential along myocyte surface membrane (Endomysium)
      - Epimysium covers whole muscle
      - Perimysium covers around 100 myocytes
      - Special features:
        
        Muscle fibre may span entire length of muscle, diameter 50micrometer
        
        Myocytes are multinucleate
        
        Striated (cardiac and skeletal) due to regular sarcomeres
  - - - Myosin heads bind ATP (hydrolysed to ADP and Pi). Energised myosin heads able to bind actin molecules and form cross bridges.
        Energised myosin head flexes on its actin binding site to provide power stroke to move actin closer to centre of sarcomere (ADP and Pi dissociate from head)
        Fresh ATP binds to myosin head, causing dissociation from actin filament.
        Z lines move closer together, width of I band decreases. No change to A band (thick filaments do not shorten)
- - - - Afferent:
        
        Type 1α afferent neurons: receive input from both nuclear bag and nuclear chain. Receive information about static intrafusal length and rate of change
        
        Type 2 afferent neurons: receive input from nuclear chain fibres only (only relay information about static length)
      - Efferent:
        ɣ motor neurons innervate contractile outer portions of intrafusal fibres. Each ɣ motor neuron innervates a few muscle spindles
      - Voluntary contractions involve α-motor and ɣ-motor neuron. Outer part of intrafusal fibre contracts to prevent slackening of spindle despite shortening of extrafusal fibres. Therefore sensitivity of muscle spindles is maintained.
- - - - Striking patellar tendon causes contraction of quadriceps leading to extension of knee.
        Sensory: muscle spindles of quadriceps sense stretch
        Afferent: type 1a afferent neuron to dorsal root then to ventral horn of spinal cord
        Synapse: in ventral horn, the afferent neuron synapses directly with α-motor neuron using glutamate
        Efferent: α-motor neuron travels to quadriceps where it innervates several muscle fibres
        Effector organ: quadriceps contracts in response to α-motor neuron activity
        
        Some type 1a afferent neurons branch in spinal cord through interneurons to neurons of antagonistic muscles to relax them (hamstrings) using glycine are neurotransmitter
        
        Descending inputs from brain may modulate intensity of reflexes:
        Knee-jerk is lost following repeated rapid patellar strikes.
        Jendrassik manoeuvre results in increased ɣ-motor neuron firing, increasing background stretch in spindle