Download 9 Muscles and movement I:

9 Muscles and movement I:
Where hath
all my skin
gone?
MUSCLE STRUCTURE
SLIDING FILAMENT THEORY
(or, 6[ish] easy steps to contraction)
3 TESTS OF THE SLIDING FILAMENT
MODEL
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Office hours today shifted:
3:30-4:30
Practice exam soon
PK submission
Quick Quiz
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Estrogen
Estrogen promotes osteoclast death (apoptosis)
High estrogen levels at puberty are associated with epiphyseal closure
and decreased bone turnover.
Q: Why might spayed female cats have long legs?
Low estrogen levels are
associated with increased
bone turnover and decreased
bone mass.
Rate of hip fractures among
Hong Kong women between
1966 and 1995.
Q: Why might medications
that increase inorganic
composition of bone not
always be clinically
beneficial?
Q: What unusual traits were observed in the clinical case reported by Smith?
Q: Why was estrogen administered? Why was it ineffective?
Smith et al. 1994. New England Journal of Medicine 331:1056
FROM NERVE TO MUSCLE . . .
Muscle tissue represents about 40% of body weight
Q. How do motor neuron action potentials make muscles
contract?
Need to understand the
structure of muscle
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MUSCLE STRUCTURE AND
CONTRACTION
muscles
Striated
skeletal
cardiac
fibers = cells
fibrils
Smooth (unstriated)
filaments
thin filament
thick filament
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Muscle contraction is initiated at the neuromuscular junction
A single motor unit
consists of a motor
neuron and all of
the muscle fibers it
innervates.
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Striated muscle fibrils
fiber
sarcoplasmic reticulum in x-section
fibril
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Myofilament organization dictates the macroscopic appearance of muscle.
dark
=
A
ht
g
i
l
I=
sc
i
d
Z
Q: through which parts of the fiber were these sections made?
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The Sliding Filament Theory of muscle contraction
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The neuromuscular
junction is the point of
synaptic contact between
the axon terminal of a
motor neuron and the
muscle fiber it controls.
Action potentials in the
motor neuron cause
acetylcholine release
into the neuromuscular
junction.
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Q: Where in the muscle contraction cycle do ligand-gated channels
occur? Voltage-gated?
1
2
3
DHP “receptor”
senses t-tubule
voltage->ryanodine
receptor
4
ryanodine
receptor releases
Ca2+ into cytosol.
Ryanodine
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Relaxed: tropomyosin
blocks the cross-bridge
binding site on actin.
5
Ready: Ca2+ binds to
troponin:
-tropomyosin “moves”
-myosin binding
sites exposed.
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6
another 6 substeps involving ATP hydrolyzation
A-M binding, ready
6.1
ADP released,
binding site
clear
“power stroke”
powered by P
release
6.5
6.2
6.5
6.3
ATP binds to actin,
release A-M bond
ATP partially
hydrolysis
6.4
Actin head “cocked”
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THREE TESTS OF THE SLIDING FILAMENT MODEL
Q: Do sarcomeres change in length and structure when they contract? If so, which
regions contract?
at rest
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THREE TESTS OF THE SLIDING FILAMENT MODEL
Q: Do sarcomeres change in length and structure when they contract? If so, which
regions contract?
at rest
contracted
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Q: Does concentration of myoplasmic free calcium change during
contraction?
Furaptra = a fluorescent
calcium indicator
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Furaptra = a fluorescent
calcium indicator
Q: What is happening between
the time of the action potential
and the peak of myoplasmic
calcium?
Q: Why is the contractile force
generated AFTER the spike in
myoplasmic free calcium?
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Q: Does the force generated by muscles differ in muscles of different
resting length?
HINT: ARE FILAMENTS INFINITELY LONG?
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