5-2 Neuromuscular Junctio
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Transcript 5-2 Neuromuscular Junctio
Neuromuscular Junction
Suzanne D'Anna
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Motor Unit
one motor neuron
all the skeletal muscles it stimulates
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Fine Muscle Control
few muscle fibers stimulated by one
motor neuron
single motor neuron may supply very
few fibers (eye)
Result:
- finer control of muscle fibers
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Coarse Muscle Control
many muscle fibers stimulated by one
motor neuron
single motor neuron may supply many
fibers (large muscle)
Result:
- less control of muscle fibers
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Neuromuscular Junction
contact or junction between motor
neuron and a skeletal muscle
- thread-like extensions of neuron
branch into many axonal terminals
- each branch forms a junction with
sarcolemma (one muscle fiber)
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Nerve Endings
individual branches of axon near
muscle fiber loose myelin sheath
divide into several bulb-shaped
structures (synaptic end bulb)
- bulbs contain neurotransmitter
acetylcholine (ACh)
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Nerve Endings
extremely close to muscle but never
touch
space is called synaptic cleft
- filled with interstitial fluid
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Motor End Plate
portion of muscle fiber membrane
adjacent to synaptic end bulb of motor
neuron
contains receptors for acetylcholine
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Polarization
muscle fiber relaxed (resting
sarcolemma)
outside sarcolemma + charge
(predominant extracellular ion is Na+)
inside sarcolemma - charge
(predominant intracellular ion is K+)
sarcolemma is relatively impermeable to
both ions
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Depolarization
(generation of the action potential)
stimulation of sarcolemma by motor nerve
patch of sarcolemma becomes permeable
to sodium ions (sodium gates open)
+ sodium ions rush into cell
inside sarcolemma + charge
outside sarcolemma - charge
this rush upsets electrical currents causing
action potential
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Propagation of the Action
Potential
+ charge inside sarcolemma changes
permeability of adjacent patches on
sarcolemma
depolarization is repeated
- therefore action potential spreads
along entire length of sarcolemma
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Repolarization
events occur in reverse
sarcolemma permeability changes
Na+ gates close
K+ gates open allowing diffusion of K+
ions out of cell
activation of sodium-potassium pump
restores ionic resting state concentrations
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Repolarization
(cont.)
occurs in same direction as
depolarization
must occur before muscle can be
stimulated again
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Sequence of Events of Muscle
Stimulation
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Muscle Stimulation
muscle fibers are stimulated by motor
neurons
impulse arrives at axon terminal of
motor neuron
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Muscle Stimulation
(cont.)
impulse depolarizes plasma membrane
opening voltage-sensitive calcium
channels (Ca+2)
calcium ions diffuse from extracellular
fluid into the axon terminal
- triggers release of acetylcholine from
synaptic end bulb
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Muscle Stimulation
ACh diffuses across synaptic cleft
ACh interacts with receptors in the motor
end plate of the muscle fiber, thus altering
its permeability to sodium ions (Na+)
sodium ions diffuse from extracelluar fluid
into muscle fiber, producing local
depolarization called end-plate potential
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Muscle Stimulation
(power stroke)
end-plate potential generates flow of
ions or current to bring adjacent
sarcolemma to threshold
current spreads in both directions
triggering action potentials
action potential initiate wave of
contraction by way of transverse tubules
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Muscle Stimulation (power stroke)
(cont.)
action potential triggers release of Ca+2
from sarcoplasmic reticulum
Ca+2 ions bind to troponin molecules on the
thin filaments
tropomyosin moves, uncovering crossbridge binding sites on actin
binding of actin and myosin causes ATP to
split releasing energy for the power stroke
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Muscle Stimulation (power stroke)
(cont.)
rotational movement of a myosin crossbridge
one power stroke of a cross-bridge
results in a small movement of the thin
filament
each cross-bridge produces many
cycles of movement during a single
twitch contraction
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Muscle Stimulation (power stroke)
(cont.)
acetylcholine is quickly decomposed by
cholinesterase
its decomposition prevents generation
of further end-plate potentials
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Sliding Filament Mechanism
during muscle contraction, neither the
thick nor the thin filaments decrease in
length
the actin (thin) filaments slide like
pistons inward among the myosin (thick)
filaments
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Sliding Filament Mechanism
(cont.)
in the resting state, the ends of the actin
barely overlap the myosin
during contraction, these ends overlap
considerably while the two Z
membranes approach the ends of the
myosin filaments
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Myosin
Actin
has globular
bridges
Ca+2 ions help
cross bridges
react with actin
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ADP molecules on
surface act as sites
for linkages with
cross bridges
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Sources of Energy
phosphate system
glycogen-lactic acid system
aerobic system
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Phosphate System
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Phosphate System
ATP and creatine phosphate
together they provide energy for
muscles to contract maximally for
approximately 15 seconds
this system is used for short bursts of
energy
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Energy Source for Muscle
Contraction
immediate source is ATP (adenosine
triphosphate)
supplied by mitochondria near myofibrils
enzyme ATPase splits a phosphate group
from ATP, forming ADP (adenosine
diphosphate) and P (phosphate group)
energy released when P is split from
molecule of ATP activates myosin crossbridges
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Energy Source for Muscle
Contraction
very little ATP present in muscle fibers
if exercise is to continue for more than a
few seconds, additional ATP must be
produced
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Energy Source for Muscle
Contraction
primary energy source available to
regenerate ATP from ADP and
phosphate is creatine phosphate
contains high-energy phosphate bonds
cannot directly supply energy to a cell
3-5 times more abundant in muscle
fibers than ATP
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Creatine Phosphate
stores energy released from mitochondria
when sufficient ATP is present, creatine
phosphokinase (enzyme) promotes
synthesis of creatine phosphate
energy is stored in its phosphate bonds
when ATP is being decomposed, energy
from CP is transferred to ADP and then
quickly converted back to ATP
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Glycogen-Lactic Acid System
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Glycogen-Lactic Acid System
with continued activity, muscles require
energy after the supply of creatine
phosphate is depleted
glucose must be catabolized to
generate ATP
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Glycogen-Lactic Acid System
glucose passes into contracted muscles
via blood (facilitated diffusion)
glucose is also produced by glycolysis
(breakdown of glycogen in muscles)
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Glycolysis
series of ten reactions
splits glucose into two molecules of
pyruvic acid and two molecules of ATP
anerobic process (no oxygen)
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Glycogen-Lactic Acid System
pyruvic acid formed by glycolysis enters
mitochondria
- its oxidation produces large quantities of
ATP from ADP
some activities do not supply enough O2
to completely break down pyruvic acid
pyruvic acid is then converted to lactic
acid
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Glycogen-Lactic Acid System
(cont.)
most lactic acid diffuses from skeletal
muscles into the blood
heart muscle fibers, kidney cells and liver
cells use lactic acid to produce ATP
liver cells can convert lactic acid back to
glucose
some lactic acid is accumulated in blood
and muscles
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Glycogen-Lactic Acid System
(cont.)
can provide energy for about 30-40
seconds of maximal muscle activity,
e.g., a 50 meter swimming race
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Aerobic System
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Aerobic System
reactions that require oxygen carried by
the blood
oxygen is bonded to molecules of
hemoglobin
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Cellular Respiration
when energy is exhausted, muscles
become dependant upon cellular
respiration of glucose as a source of
energy for synthesis of ATP
muscle activity longer than 30 seconds
requires an aerobic process
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Aerobic System
conversion of pyruvic acid into CO2,
H20, and ATP
yields 36 molecules of ATP from each
glucose molecule
provides energy for muscular activity
lasting longer than 30 seconds
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Recovery Oxygen Consumption
(oxygen debt)
elevated oxygen use after exercise
above resting oxygen consumption
elevated oxygen necessary to restore
metabolic conditions to resting state
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Recovery Oxygen Consumption
converts lactic acid back into pyruvic
acid
reestablishes glycogen stores in muscle
and liver cells
resynthesizes creatine phosphate and
ATP
replaces O2 removed from myoglobin
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Recovery Oxygen Consumption
(cont.)
ATP production for metabolic reactions
(increased rate due to increased body
temperature)
ATP production for continued elevated
activity of cardiac and skeletal muscles
ATP production needed for an increased
rate of tissue repair
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Muscle Fatigue
(inability of a muscle to contract)
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Condition may result from:
- insufficient O2 delivered to muscle cells
- depletion of glycogen stored in muscle
cells
- buildup of lactic acid in body fluids
- insufficient acetylcholine
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