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Muscle Physiology: Cellular Mechanisms of Muscle Contraction Review of Membrane Permeability Resting Potential of Muscle Cells Local Membrane Potentials Action Potentials Neuromuscular Junction Excitation Contraction Coupling Membrane Permeability Recall that the plasma membrane is selectively permeable Carrier proteins help transport in selective manner Some forms of carrier-mediated transport require ATP In active transport, movement is unidirectional, and cells can concentrate things within (or move them out) Some substances are polar, carry charge The Resting Potential The resting potential is the difference in charge between the inside and outside of the cell The cell produces proteins with negative charge (inside cell) The concentration of Na+ is higher outside the cell than inside - low membrane permeability (Na+ channels closed) - Na+/K+ pump moves 3 Na+ out, brings in 2 K+ The Resting Potential (cont) + The concentration of K+ is higher inside the cell than outside - Na+/K+ pump brings in K+ - some K+ channels open, K+ trickles in + The Ca++ concentration higher outside the cell than inside As a result, there is a net difference in the charge across the plasma membrane (about -70 mV), with the inside of the cell more negative than the outside of the cell. Depolarization and Repolarization The cell’s resting potential is -70 mV (negative inside) Making the inside of the cell more positive (-60 mV) is depolarization Returning the cell from -60 mV to -70 mV is repolarization Making the inside of the cell more negative (-80 mV) is hyperpolarization 0 mV -60 -70 -80 Changes in Resting Potential: K+ Small changes in resting potential reflect changes in K+ concentration across the membranes K+ has a tendency to leave cells due to concentration gradient, enter cells due to charge Changing [K+] outside the cell will change how much K+ exits, and thus change the resting potential Changing the cell’s permeability to K+ will change the resting potential as well Ion Channels for Na+ and K+ The permeability of cells to Na+ and K+ can be regulated by opening and closing their ion channels Na+ channels are voltage sensitive: open in response to depolarization Na+ channels are ligand-gated: open in response to substances like calcium, acetylcholine K+ channels are also voltage-sensitive, but open more slowly than Na+ channels The Na+/K+ Pump Carrier protein which brings into the cell 3 Na+ for each 2 K+ it puts out of the cell This accounts for about 15% of the negative membrane potential Requires ATP Activity increases if intracellular Na+ goes up Local Potential A stimulus applied to the cell membrane results in a local depolarization of the cell Reflects opening of Na+ channels (increased permeability to Na+) Local potentials are graded: the larger the stimulus, the larger the response (depolarization) Local potentials do not spread (propogate) very far across the plasma membrane 0 mV -60 -70 -80 The Action Potential If the local potential reaches a certain threshold level, it triggers an action potential 0 mV -60 -70 -80 Threshold The Action Potential An action potential is “all-or-none” Action potentials have three phases: - depolarization - repolarization - hyperpolarization (afterpotential) 0 mV -60 -70 -80 Threshold Changes in ion permeability during Action Potentials When threshold is reached, Na+ and K+ channels open (more slowly) When membrane potential becomes positive (+20 mV), Na+ channels 0 close (K+ channels stay open) mV Permeability to K+ increases, K+ exits the cell, causing repolarization -60 -70 (inside of cell more negative) -80 K+ channels stay open past the resting potential (after potential) Refractory Period after an Action Potential There are periods after an action potential during which it is more difficult or impossible to have another action potential Absolute Refractory Period: For some short period after an action potential, it is impossible to have another action potential Relative Refractory Period: For some longer period after an action potential, having another action potential requires a stronger stimulus (higher threshold) Propagation of Action Potentials Action potentials begin locally, but spread throughout the entire cell membrane Action potentials to NOT spread from cell to cell in skeletal muscle, but are initiated by neuronal stimulation Neuromuscular Junction Action potentials are caused by stimulation from motor neurons, at the neuromuscular junction (NMJ) A motor unit = a neuron and all the muscle fibers it innervates motor neurons contact muscle fibers at synapses presynaptic terminal: vesicles of acetylcholine postsynaptic membrane: receptors for acetylcholine synaptic cleft: space between the two, contains acetylcholinesterase presynaptic terminal motor neuron postsynaptic membrane muscle fiber Initiation of Action Potentials by the NMJ The motor neuron has an action potential, resulting in increased Ca++ in the presynaptic terminal This results in release of vesicles containing acetylcholine into synaptic cleft Acetylcholine binds to postsynaptic membrane, causing opening of Na+ channels and entry of Na+ into cells (depolarization) If depolarization reaches the threshold level, an action potential in the muscle fiber occurs Excitation Contraction Coupling How does an action potential (induced by motor neuron) result in contraction of muscle cells? - the action potential is propagated through the membranes of the t-tubule system to the sarcoplasmic reticulum - depolarization of the sarcoplasmic reticulum results in the release of stored Ca++ - increased cytoplasmic Ca++ binds to troponin in the sarcomere - troponin moves off of the active site on actin, exposing it to myosin Excitation Contraction Coupling (cont) - myosin heads bind to actin, forming cross bridges - the myosin heads pull on the actin filaments (using energy) - ATP binds to myosin, allowing the release of the myosin head from the actin - the free myosin head now binds to the next actin, and pulls it - at the fiber level, contraction is all or none actin z line Sliding Filament Theory of Contraction Myosin heads pull on the actin filaments, bringing the Z lines together. The I bands and H zones shorten during contraction, but the A band stays the same size. Resting Contracting Relaxation Phase Eventually, the depolarization signal from the neuron stops, leading to decreased acetylcholine in the synaptic cleft, and cessation of action potentials Ca++ is taken back up into the sarcoplasmic reticulum troponin covers up the binding site on actin, so myosin can’t bind the muscle fiber returns to original size due to force of gravity, antagonist muscles, elasticity Relaxation Takes Energy! Energy (ATP) is required for the following events to occur, allowing muscle to relax: - ATP must bind to myosin to allow release from actin head - ATP is required for the sarcoplasmic reticulum to take up Ca++ , decreasing cytoplasmic Ca++ levels - ATP is required to maintain the Na+/K+ pump - energy is required to produce acetylcholinesterase Next Lecture..... Muscle Physiology at the Organ Level