Transcript Document 7870168

Nerve Stimulus Excites the Muscle Cell
• A muscle cell must receive a stimulus to begin the
excitation-contraction coupling
– Series of events linking electrical signal to muscle contraction
– Muscle cells can be stimulated by ACh
• ACh- Acetylcholine- neurotransmitter
1. Nerve impulse reaches axon terminal
• Axon- long extension of nerve cell, relays stimulus
• Neuromuscular Junction- axon branches as it enters muscle,
each branch goes to 1 muscle fiber
• Synaptic cleft- small space between axon terminal & muscle
fiber
2. Voltage-gated Ca2+ channels on axon terminal open Ca2+ goes
in synaptic vesicles fuse with membrane
• Synaptic vesicles- sacs filled with neurotransmitter
3. Exocytosis of ACh
• Motor end plate- folded part of sacrolemma with millions of ACh
receptors
Animated Neurotransmission
Resting Potential- Polarized
• Partial negative charge inside a neuron or
muscle cell at rest
– More K+ inside, more Na+ outside
– Both K+ & Na+ diffuse through cell membrane, K+
can get out easier than Na+ can get in
– Polarized- difference in charge inside & outside
the cell
Resting membrane potential
K+
-
K+
-
K+
Na+
-
Na+
Na+
K+
+
Na+ K
K+
K+
-
++
Na
K
- Outside the cell Membrane
Na+ Na
K+ +
Cytoplasm
K+
Na+
K+
-
Na+
Na+
K+ +
K
K+
K+
-
Action Potential (AP)- Depolarized
• When muscle cell is stimulated by ACh, chemically
gated ion (Na+ & K+) channels open
• Na+ flows in faster than K+ flows out
Depolarization- change of charge (action potential)
– Causes a ripple effect along sarcolemma, voltage gated
Na+ gates open
– Also causes slower K+ gate to open, K+ rushes out
Repolarization- return to resting charge
• Active transport is used to move Na+ back outside
& K+ back inside
– Refactory period- cell cannot be stimulated again until
repolarization & active transport of ions is
complete
Animated Neurotransmission
K+
-
K+
-
K+
Na+
Na+
Na+
- +
Na
K+
Na+
K+
++
Na
K
- Outside the cell - Na+ Na+
+
Na+ K
Membrane
K+
Na+ - + Cytoplasm
+
K
Na
Na+
Na
K+ +
K+
Na+
Na+
Na+
K+ +
K
K+
K+
-
Action
Potential
Excitation-Contraction Coupling
•
AP ends before signs of contraction are
obvious
1. AP goes along sacrolemma & down T tubules
•
AP in T tubules causes release of Ca2+ from
adjacent terminal cisternae
2. Ca2+ binds to troponin, causing it to move
myotroponin away for actin active site
3. Mysosin heads form cross bridges with
active sites on actin & pull thin filaments
toward center of sacromere (power stroke)
Excitation-Contraction Coupling
Excitation-Contraction Coupling 2
Actin Myosin Bridge
ATP and the Power Stroke
• Myosin heads have ATP attached to them,
used for E to “cock” heads back
– Release ADP & P
• Myosin attaches to active sites to form
“cross-bridges”
• Myosin head returns to its lower E position
once cross bridge is formed, moving the thin
filament (power stroke)
• ATP binds to myosin head, actin filament is
released
Actin Myosin Bridge
Contraction
• Full contraction of the muscle cell requires
30+ repeats of power stroke action
– Process repeats until Ca2+ is no longer available
• Acetylcholinesterase
– enzyme that digests acetylcholine to ensure
contraction does not persist without nervous
stimulation
• No more acetylcholine Ca2+ is reabsorbed
by SR by active transport (uses more ATP)
Actin Myosin Bridge
Rigor Mortis
• When breathing stops, no more O2 can’t
make ATP
• Dying cells cannot keep extracellular Ca2+ out
– Ca2+ goes into muscle cells and promotes myosinactin cross-bridges
– ATP is still being consumed at the cross bridge,
when it runs out, detachment becomes
impossible stiffness
• Usually starts to set in 3-4hrs postmortem,
peaks about 12 hrs postmortem
– As muscle protein begin to break down, rigor
mortis gradually goes away