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(Excitation)
Each muscle cell is stimulated by a nerve impulse
_____ cell body is in CNS, but sends axons out to
muscles
____ branch so that each cell is in contact with a
neuron
Neurons, Axons
structure of the Neuromotor Junction
Neuron’s axon end
bulb filled with
vesicles of
acetylcholine (ACh)
• Synaptic cleft
• Muscle cell’s motor
end plate with
receptors for ACh
Excitation –
change in Resting
Membrane Potential
Pumps move ions across the membrane
against their concentration gradient (requires
ATP)
Na/K pump
creates and maintains a
resting membrane potential (a voltage
difference across the membrane)
Muscle cells typically have
a -90mV resting
membrane potential
Excitation steps
Nerve impulse reaches axon end bulb
↓
ACh is released into cleft
↓
ACh attaches to receptors (ligand
gated ion channels
↓
Na+ floods more quickly than K+ into the
cell and the sarcolemma
depolarizes
↓
Action Potential
Action Potential
(adjacent Na and K pumps)
1. Membrane potential (Vm )reaches threshold (-55mV)
2. Fast Na+ channels open and Na+ rushes in causing the Vm to depolarize
to +30mV.
3. The depolarization stops when the Na+ channels become inactivated.
4. Slow K+ channels have opened & K+ efflux occurs. This returns Vm
back to its resting level. This is repolarization.
Excitation – Contraction Coupling
Muscle
↓
Neighboring voltage gated Na+ channels open and
depolarization sweeps across sarcolemma and
into T-Tubules
↓
Causes Ca2+ to be released from terminal
cisternae into cytoplasm
↓
Ca2+ attaches to troponin
↓
Troponin changes shape and pulls the
tropomyosin off the myosin binding sites on
the actin
↓
Myosin heads bind to the
exposed binding sites
Muscle Contraction -
Power Stroke
When the cell is resting, Ca2+ levels in the
cell are low and myosin binding sites on
actin are physically blocked by Tropomyosin
When terminal Cisterns
releases
Ca2+ into cytoplasm
Calcium attaches to Troponin
Troponin/Tropomyosin
complex
moves which opens the Myosin
binding sites on the Actin
Power Stokes occur
. ATP hydrolysis
– The ATP binding site on myosin head contains
ATPases
• ATP ADP + P (which are attached to
myosin head)
• This energizes myosin head
. Attachment of myosin to actin to form crossbridges
– Energized myosin head attaches to myosin
binding site on actin and releases P
Power Stroke
– Spot where ADP is bound on myosin head
opens causing the head to rotate and release
ADP
– Force is generated as the head moves near
sarcomere center (actin filament slides past the
myosin filament towards M line)
Detachment of Myosin from Actin
– Myosin head stays attached to actin until ATP binds
to it at ATP binding site
– Myosin head detaches from actin
– Steps are repeated until contraction is complete
– tropomyosin blockage restored; contraction ends
For attachment of myosin to
actin –
P then ADP are
released
For release of myosin from
actin –
ATP must reattach to myosin head
Contraction is the result of
sarcomeres shortening
When relaxed the thin and thick filaments overlap
slightly
• During contraction myosin heads act as little ratchets to
pull the thin filaments to the center of the sarcomere
As a result thin and thick filaments
overlap extensively - H zone disappears
and Z lines are closer to each other
Contraction - Relaxation
Cycle repeats to shorten Sarcomeres
(muscle contracts)
Cycle is broken when calcium is
reabsorbed into Terminal Cisterns
Tropinin/Tropomyosin move back to
cover Myosin binding sites on Actin
Sarcomeres return to original length
(muscle relaxes)
Rigor Mortis
3 h after death, full rigor about 12 h. After 12 h rigor slowly
ceases, around 72 h rigor disappears
Ca 2+ leaks into cytoplasm & myosin heads
attach to actin –
rigor sets in
no more ATP and heads cant unattach
tissues decompose -
proteolytic enzymes in the lysosomes of the
muscle cells escape and begin to dissolve the myofilaments – rigor
disappears
Botulism –
blocks release of
Ach......botox