Flashcards in Excitation Contraction Coupling Deck (75):
innervation of skeletal muscle
somatic motor neurons
ventral horn of spinal cord
-except cranial nerves
motor neuron and all muscle fibers it innervates
synapse vs NMJ?
-two excitable cells
-change in membrane potential both graded potentials
-synapse is junction of two neurons, NMJ is not
-one-to-one transmission at NMJ, neuron requires summation of multiple EPSPs
-NMJ always excitatory, neuron NO
-inhibition can only occur in neurons (not NMJ)
dense spot over which synaptic vesicles are clustered
-fusion of vesicles and release of ACh occurs
-oriented directly over secondary postsynaptic clefts between adjacent postjunctional folds
where there are lots of receptors
-folds increase SURFACE AREA
type of receptor in skeletal muscle?
nicotinic acetylcholine receptors
high density expression at crests of postjunctional folds
high concentration associated with synaptic basal lamina (basement membrane)
terminates synaptic transmission**
hydrolyzes acetylcholine > choline + acetate
neurotransmitter at NMJ?
vesicles produced in cell body and fast axonal transport sends them to nerve terminal
vesicles for ACh (and other non-peptides) travel down axon empty
-vesicle destined contain peptide neurotransmitters travel down axon with presynthesized peptide precursors inside
site of ACh synthesis and uptake?
synthesizes ACh from choline and acetyl CoA
allow ACh uptake by synaptic vesicle
-antiport of ACh into cell and H+ out of cell
-driven by vesicular proton electrochemical gradient
-positive voltage and low pH inside
essential for transmitter RELEASE
forms complex with SNAP-25 and syntaxin
-helps drive vesicular fusion
Calcium receptor of vesicle
-detects rises in calcium and triggers exocytosis of docked vesicles
syntaxin and snap 25
snap-25 and syntaxin on membrane coil around synaptobrevin on the vesicle to bring vesicle closer to presynaptic membrane
exocytosis of neurotransmitter?
synaptotagmin is calcium sensor
calcium triggers vesicle fusion and exocytosis
endoproteinase that digests synaptobrevin
botulinum B, D, F, G
endoproteinase that digests synaptobrevin
botulinum A, E
botulinum toxin C1
ionotropic, nicotinic AcHR channel
non-selective cation channel at muscle endplate
what happens when ACh binds receptor?
allows influx of multiple cations (non-specific)
-to raise Vm above threshold
threshold at membrane with ACh receptor?
opening of AChR channel?
Na+ and K+ become equally permeable
increase normally low permeability of sodium relative to K+
Vm shifts to value between Ek and Ena
-80 > +50
for action potential
-due to increased sodium permeability relative to potassium
type of graded potential
is an EPSP
will you run out of ACh?
no, there's a lot at the end of the neuron in vesicles
-can maintain high rate of AP transmission without significant loss of function
termination of neurotransmitter action
enzymatic destruction removes ACh from NMJ synaptic cleft
-two step reaction
contain thick and thin filaments
ordered arrangements of thick and thin filaments
z line to z line
what changes during contraction of sarcomere?
A band no change
H zone gets smaller
I band decreases in width
2 myosin heavy chain
2 alkali light chains
2 regulator light chains
rod of thick filament
heads of thick filaments
form cross-bridges binding actin on thin filament
binding sites on heavy chain?
2 important sites**
myosin ATPase site
both on heads of heavy chains
for cross-bridge formation
myosin ATPase site
for binding and hydrolyzing ATP
myosin light chain
alkali and regulatory
stabilizing and rate of ATP hydrolysis regulation
-globular actin polymerizes to alpha helix of F-actin
how many actin monomers in one turn?
regulatory proteins of thin filament
tropomyosin and troponin
blocks the myosin binding site at rest on actin
interacts with one tropomyosin molecule
interacts with 7 actin monomers
what allows regulated actin-myosin interaction?
troponin, tropomyosin, and actin interactions
structure of tropomyosin?
2 alpha helices coiled around each other
regulate binding of myosin heads to myosin binding site on actin
components of troponin
bind to single tropomyosin molecule
bind to actin and inhibit contraction
when calcium binds troponin?
tropomyosin slips away from its blocking position between actin and myosin
allows cross bridge to form and muscle contraction can occur
largest known protein
tethered from M line to Z line
appears to be involved in elastic behavior of muscle by maintaining resting length
mutation affects the length of muscle cell
action potential originating at sarcolemma propagate to the cell interior via these specialized membrane invaginations
location of T-tubules
extend into muscle fiber and surround myofibrils at junction of A and I bands
t-tubule with 2 cisternae of sarcoplasmic reticulum
L-type Ca2+ channel
responds to change in voltage
-causes conformation in ryanodine receptor
located in SR membrane
-cluster at portion of SR membrane that faces T tubules
release stored Ca2+ from SR
does not directly interact with contractile proteins
-only interacts with the binding of regulatory proteins
-troponin removes tropomyosin from myosin binding sites on actin
also need ATP hydrolysis on myosin heads (cocked)
hydrolyzes to cock the myosin
what causes power stroke?
interaction between myosin and actin uses the stored potential energy
P is released from cross bridge to trigger power stroke
-ADP is released with power stroke completion
what detaches myosin head?
binding new ATP
what is needed for contraction cycle?
ATP and calcium
cross bridge cycle
1) ATP binds myosin head - disocciation
2) ATP hydrolyzes - puts myosin in cocked state
3) cross bridge formed with actin
4) P release - myosin head changes conformation
-this is power stroke!
5) ADP released
can't unbind the myosin from actin (no ATP)
requires reuptake from sarcoplasm back into SR
what helps to remove calcium?
Na+ Ca2+ exchanger and Ca2+ pump
calcium to extracellular space
-minor mechanisms for calcium removal
-sarcoplasmic and endoplasmic reticulum Ca2+ ATPase
calcium reuptake into SR
Ca2+ binding proteins
in SR lumen can delay inhibition of Ca2+ pump activity
can increased the calcium capacity of the SR
inhibition of SERCA?
high concentrations of calcium
primary Ca2+ binding protein in skeletal muscle
-localized in SR beneath triad junction
forms complex with RyR
-facilitates muscle relaxation by buffering Ca2+
unloads its Ca2+ in vicinity of Ca2+ release channel to facilitate EC coupling
Ca2+ binding protein in smooth muscle