Transcript Muscle Physiology - Cal State LA

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
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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
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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
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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+
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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+
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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
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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
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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
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If the local potential reaches a certain threshold level,
it triggers an action potential
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mV
-60
-70
-80
Threshold
The Action Potential
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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
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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
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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
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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
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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
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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
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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