Week 5 Anatomy and physiology
-during contractions of a muscle, calcium ions (Ca+) binds to troponin.
This moves tropomyosin and undercover binding sites for myosin on
the actin myo lament.
-ADP and phosphate (P) are attached to myosin head from the
previous cycle of movement.
-the myosin head attaches to the exposed binding site of the actin
myo lament to form cross bridges and phosphate is released.
-energy stored in the head of the myosin myo lament is used to move
the head. This causes the actin myo lament to slide past the myosin
myo lament. The ADP is released from the myosin head as it moves.
- Bond between acting and myosin is broken when ATP molecule binds to myosin head
- ATP is broken to ADP and phosphate (energy)
- Head of myosin molecule return to upright position and is ready to bind into acting again.
- Calcium Ions present entire sequence is repeated.
-action potential introduced at the neuromuscular junction is propagated along the
sarcolemma of the skeletal muscle.
-T tubule - the action potential is propagated on T tubule membrane into the
interior of muscle so near the ends of the sarcoplasmic reticulum.
-
- The depolarisation of the T tubule membrane causes nearby voltage gated
calcium ions channels on the sarcoplasmic reticulum to open, resulting in an
increase in the permeability of the sarcoplasmic reticulum to calcium ions (Ca2+).
-(Ca+) di uses from the sarcoplasmic reticulum into sarcoplasm.
-Long lamentous tropomyosin protein lie on two sides of the actin
mo lament.
-Covering up the site where myosin can bind to the actin myo lament
-Globular troponin proteins are attached to the tropomyosin
-Tropomyosin moves, this uncovers the myosin binding sites on the
actin, myosin heads to bind and form cross bridges.
-The cross bridges play a role in the muscle contraction
NEUROMUSCULAR JUNCTIONS
- action potential arrives at the presynaptic terminal causing voltage
gated calcium ion channels to open,
- Increasing the calcium ion permeability of the presynaptic terminal cell
membrane
- Calcium ions into the presynaptic terminal and causes vesicles to
release the neurotransmitters
- (ACh) acetylcholine, from the synaptic vesicles into the presynaptic
cleft.
Di usion of acetylcholine across the synaptic cleft and
bidding of the acetylcholine to acetylcholine receptors on the postsynaptic mules
bre membrane causes an increase in the permeability of the ligand-gated
sodium ion channels.
The movement of sodium irons into the muscle
cells result in depolarisation in the postsynaptic membrane.
- what is threshold has been reached a postsynaptic take action
potential is generated and is propagated over the muscle cell
membrane
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-during contractions of a muscle, calcium ions (Ca+) binds to troponin.
This moves tropomyosin and undercover binding sites for myosin on
the actin myo lament.
-ADP and phosphate (P) are attached to myosin head from the
previous cycle of movement.
-the myosin head attaches to the exposed binding site of the actin
myo lament to form cross bridges and phosphate is released.
-energy stored in the head of the myosin myo lament is used to move
the head. This causes the actin myo lament to slide past the myosin
myo lament. The ADP is released from the myosin head as it moves.
- Bond between acting and myosin is broken when ATP molecule binds to myosin head
- ATP is broken to ADP and phosphate (energy)
- Head of myosin molecule return to upright position and is ready to bind into acting again.
- Calcium Ions present entire sequence is repeated.
-action potential introduced at the neuromuscular junction is propagated along the
sarcolemma of the skeletal muscle.
-T tubule - the action potential is propagated on T tubule membrane into the
interior of muscle so near the ends of the sarcoplasmic reticulum.
-
- The depolarisation of the T tubule membrane causes nearby voltage gated
calcium ions channels on the sarcoplasmic reticulum to open, resulting in an
increase in the permeability of the sarcoplasmic reticulum to calcium ions (Ca2+).
-(Ca+) di uses from the sarcoplasmic reticulum into sarcoplasm.
-Long lamentous tropomyosin protein lie on two sides of the actin
mo lament.
-Covering up the site where myosin can bind to the actin myo lament
-Globular troponin proteins are attached to the tropomyosin
-Tropomyosin moves, this uncovers the myosin binding sites on the
actin, myosin heads to bind and form cross bridges.
-The cross bridges play a role in the muscle contraction
NEUROMUSCULAR JUNCTIONS
- action potential arrives at the presynaptic terminal causing voltage
gated calcium ion channels to open,
- Increasing the calcium ion permeability of the presynaptic terminal cell
membrane
- Calcium ions into the presynaptic terminal and causes vesicles to
release the neurotransmitters
- (ACh) acetylcholine, from the synaptic vesicles into the presynaptic
cleft.
Di usion of acetylcholine across the synaptic cleft and
bidding of the acetylcholine to acetylcholine receptors on the postsynaptic mules
bre membrane causes an increase in the permeability of the ligand-gated
sodium ion channels.
The movement of sodium irons into the muscle
cells result in depolarisation in the postsynaptic membrane.
- what is threshold has been reached a postsynaptic take action
potential is generated and is propagated over the muscle cell
membrane
fi fffifi fi ff
fi fi fi fi