The Neuromuscular Junction and Cross Bridge Cycling Flashcards
muscle fiber contraction
- decision to move is activated by the brain - a signal is transmitted down the spinal cord to motor neurons
- motor neurons activate muscle fibers
- neurons and muscle cells are excitable cells - capable of action potentials - capable of changing their resting membrane potentials
resting membrane potential
voltage across the plasma membrane
action potential
type of electrical signal - a large change in resting membrane potential
- action potentials are converted to chemical signals to cross the synaptic cleft (small gap between cells)
- action potential crosses from a neuron to a muscle cell via a neurotransmitter - acetylcholine (Ach)
Ion channels
rapidly changing the membrane potential in neurons and muscle cells requires the opening/closing of channels
- allow some ions to pass and not others
- movements of ions through channels changes membrane voltage
- two classes of ion channels: chemically and voltage gated
chemically gated ion channel
opened by chemical messengers such as neurotransmitters
voltage-gated ion channels
open/close in response to voltage changes - underlie all action potentials
small depolarizations
in skeletal muscle fibers, chemically gated ion channels cause small depolarizations. small depolarizations trigger voltage gated ion channels to create action potentials
anatomy of a motor neuron
- skeletal muscles are stimulated by somatic motor neurons
- axons: long, threadlike extensions of motor neurons; travel from central nervous system to skeletal muscle
- each axon divides into many branches as it enters a muscle
- each axon branch terminates in an axon terminal
- axon terminals form neuromuscular junctions (motor end plates) w muscle fibers
- each muscle fiber has only one neuromuscular junction
anatomy of a neuromuscular junction
axon terminal and muscle fiber are separated by a gel-filled space; synaptic cleft
- synaptic vessels: membrane-bound sacs stored within the axon terminal; contain Ach
- on muscular fiber side, infoldings of sarcolemma called junctional folds contain millions of ACh receptors
- neuromuscular junction = axon terminal + synaptic cleft + junctional folds
four steps that allow skeletal muscle contraction
- events at the neuromuscular junction
- muscle fiber excitation
- excitation-contraction coupling
- cross bridge cycling
first 3 steps of events at the neuromuscular junction
- action potential arrives at the axon terminal
- voltage-gated ca2+ channels open; ca2+ ions enter the motor neuron
- entry of ca2+ ions causes the release of ACh neurotransmitter into the synaptic cleft via exocytosis
steps 4 and 5 of events at the neuromuscular junction
- ACh diffuses across the synaptic cleft to ACh receptors in the junctional folds
- ACh binding opens chemically gated ion channels
steps 6/7 of the events at the neuromuscular junction
- na+ ions enter the muscle fiber and k+ ions exit the muscle fiber. net movement of na+ creates local change in membrane potential/end plate potential
- once the membrane potential hits a threshold value (abt -55mv) an unstoppable action potential propagates along the sarcolemma
- Ach is degraded by acetylcholinesterase and diffuses away from the junction. this stops neural transmission to the muscle fiber
myasthenia gravis
autoimmune disease in which the immune system destroys ach receptors
- symptoms caused by shortage of ach receptors:
- dropping eyelids
- difficulty swallowing
- difficulty talking
- generalized muscle weakness
aesthetic botox
botulinum toxin
- reduces the amount of ach released from the motor neuron - decreases muscle contraction (reducing wrinkles)
muscle fiber excitation
- resting sarcolemma is polarized - a voltage exists across the membrane, cell’s interior is negative compared to the outside
- action potentials result from predictable sequences of electrical changes
occurs in 3 steps - generation of end plate potential (epp)
- depolarization
- repolarization
muscle fiber excitation: depolarization
generating and propagating an AP
- if epp causes enough of a change in membrane voltage to reach a critical level called threshold, voltage-gated na+ channels in the membrane will open
- large influx of na+ triggers an AP
- AP is unstoppable - leads to muscle fiber contraction
- AP spreads across sarcolemma from one voltage-gated na+ channel to the next causing additional depolarizations
muscle fiber excitation: repolarization
restoration of normal electrical resting conditions
- na+ voltage-gated channels close; k+ voltage-gated channels open
- k+ effluxes out of the cell; restores initial resting membrane potential
refractory period
muscle fiber cannot be stiumlated for a specific amount of time - until repolarization is complete
- ionic resting state is restored by na+-k+ pumps
- na+ is pumped back out, k+ is pumped back in
excitation contraction coupling
events that transmit an ap along the sarcolemma (muscle fiber excitation) are couples to the sliding of myofilaments (contraction)
- aps are brief and end before any contraction is seen
- an ap doesn’t act directly on the myofilaments - it triggers a rise in intracellular ca2+
- an ap is propagated along sarcolemma and down into t tubules
- voltage sensitive proteins in t tubules stimulate the release of ca2+ from SR
- release of ca2+ leads to muscle fiber contraction
cross bridge cycling relaxed
- at low intracellular ca2+ concentration
- tropomyosin blocks the active sites on actin
- myosin heads cannot attach to actin
- muscle fiber remains relaxed
- in response to ap, voltage sensitive proteins in t tubules change shape and cause SR to release ca2+
cross bridge cycling contracting
- at higher intracellular ca2+ concentration
- ca2+ binds to troponin
- troponin changes shape and moves to tropomyosin away from myosin-binding sites
- myosin heads bind to actin and form cross bridges
- cycling is initiated leading to sarcomere shortening and muscle fiber contraction
- when nervous system stimulation ceases, ca2+ is pumped back into the SR and contraction ends
4 steps of cross bridge cycle
- cross bridge formation
- working (power) stroke
- cross bridge detachment
- cocking of myosin head
* cross bridge cycles will repeat as long as actin’s binding sites are uncovered. cycles will cease when ca2+ moves back into SR, troponin changes shape, and tropomyosin covers actin’s binding sites
cross bridge formation
high energy myosin head attaches to the thin filament’s active site
working ( power ) stroke
myosin head pivots and pulls the thin filament towards the m line
cross bridge detachment
atp attaches to myosin head, cross bridge detaches
cocking of myosin head
energy from hydrolysis of atp cocks myosin head back into high energy state
rigor mortis
- 3-4 hours after death, skeletal muscles begin to stiffen (peak @ 12hrs)
- atp isn’t being synthesized so intracellular ca2+ levels increase - ca2+ can no longer be pumped back into SR
- higher levels of ca2+ promotes cross bridge formation
- without atp myosin heads stay bound to actin site, constant state of contraction
- muscles will stay contracted until muscle proteins break down and myosin is released
