muscle physiology: cellular mechanisms of muscle contraction review of membrane permeability resting...
TRANSCRIPT
Muscle Physiology: Cellular Mechanisms of Muscle Contraction
Review of Membrane PermeabilityResting Potential of Muscle Cells
Local Membrane PotentialsAction Potentials
Neuromuscular JunctionExcitation 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
mV
-80-70
-60
0
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
mV
-80-70
-60
0
The Action Potential
If the local potential reaches a certain threshold level, it triggers an action potential
mV
-80-70
-60
0
Threshold
The Action Potential An action potential is “all-or-none” Action potentials have three phases:
- depolarization- repolarization- hyperpolarization (afterpotential)
mV
-80-70
-60
0
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 close (K+ channels stay open)
Permeability to K+ increases, K+ exits the cell, causing repolarization (inside of cell more negative)
K+ channels stay open past the resting potential (after potential)
mV
-80-70-60
0
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
presynapticterminal
motor neuron
muscle fiber
postsynaptic membrane
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
z line
actin
Sliding Filament Theory of Contraction
Resting
Contracting
Myosin heads pull on the actin filaments, bringing the Z lines together.
The I bands and H zonesshorten during contraction, but the A band stays the same size.
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 theOrgan Level