pages 187-191. stimulus generated capabilities: ◦ irritability (also called...

Pages 187-191

Stimulus generated capabilities:◦ Irritability (also called responsiveness)—ability

to receive and respond to a stimulus◦Contractility—ability to shorten when an

adequate stimulus is received

Movement capabilities:◦Extensibility—ability of muscle cells to be

stretched◦Elasticity—ability to recoil and resume resting

length after stretching

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Skeletal muscles must be stimulated by a motor neuron (nerve cell) to contract

Motor unit: consists of one motor neuron and all the skeletal muscle cells stimulated by that neuron◦ (page 232 provides more elaboration about the

neurological make up of the motor unit)

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Figure 6.4a Motor units.

Spinal cord

Motor neuroncell bodies

Muscle Musclefibers

(a)

Axon terminals atneuromuscular junctions

Motorunit

1

Motorunit

2

Nerve

Axon ofmotor

neuron

Figure 6.4b Motor units.

Branchingaxon tomotor unit (b)

Axon terminals atneuromuscular junctions

Musclefibers

Neuromuscular junction◦ Where the axon terminal (end) of the motor

neuron “meets up with” the sarcolemma (plasma membrane) of a muscle These two components NEVER touch

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Synaptic cleft ◦ Gap/space between axon terminal and muscle◦ This gap is filled with interstitial (tissue) fluid

Neurotransmitter ◦ A chemical messenger released by the nerve

when the nerve impulse reaches the end of the axon terminal

◦ Acetylcholine (ACh) is the neurotransmitter that stimulates skeletal muscle

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Action potential reaches axon terminal of motor neuron.1

Slide 2

Nerve impulse

Nucleus

Myelinated axon of motor neuron

Axon terminal ofneuromuscularjunction

Sarcolemma ofthe muscle fiber

Synaptic vesicle containing AChAxon terminal of motor neuronMitochondrion

SarcolemmaFusing synapticvesicleSarcoplasmof muscle fiber

Folds ofsarcolemma

AChreceptor

Ca2+Ca2+

Synapticcleft

ACh

1. Calcium channels open◦ calcium ions enter the axon terminal

2. The presence of Calcium causes the release of acetylcholine (ACh) by way of vesicles

◦ ACh diffuses across the synaptic cleft (the gap) and attaches to receptors on the sarcolemma (membrane) of the muscle cell

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Slide 3

Action potential reaches axon terminal of motor neuron.

2 Calcium (Ca2+) channels open, andCa2+ enters the axon terminal.

1

Synaptic vesicle containing AChAxon terminal of motor neuronMitochondrion

SarcolemmaFusing synapticvesicleSarcoplasmof muscle fiber

Folds ofsarcolemma

AChreceptor

Ca2+Ca2+

Synapticcleft

ACh

Slide 4

Action potential reaches axon terminal of motor neuron.

2 Calcium (Ca2+) channels open, andCa2+ enters the axon terminal.

3 Ca2+ entry causes some synapticvesicles to release their contents(acetylcholine, a neurotransmitter)by exocytosis.

1

Synaptic vesicle containing AChAxon terminal of motor neuronMitochondrion

SarcolemmaFusing synapticvesicleSarcoplasmof muscle fiber

Folds ofsarcolemma

AChreceptor

Ca2+Ca2+

Synapticcleft

ACh

4. If enough ACh is released, the sarcolemma becomes temporarily more permeable to sodium (Na) and potassium (K ) ions

◦ Sodium rushes into the cell◦ Potassium leaves the cell ◦ This causes an imbalance of charge: the

sarcolemma becomes depolarized

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Slide 5

Action potential reaches axon terminal of motor neuron.

2 Calcium (Ca2+) channels open, andCa2+ enters the axon terminal.

4

3 Ca2+ entry causes some synapticvesicles to release their contents(acetylcholine, a neurotransmitter)by exocytosis.

Acetylcholine diffuses across thesynaptic cleft and binds toreceptors in the sarcolemma.

1

Synaptic vesicle containing AChAxon terminal of motor neuronMitochondrion

SarcolemmaFusing synapticvesicleSarcoplasmof muscle fiber

Folds ofsarcolemma

AChreceptor

Ca2+Ca2+

Synapticcleft

ACh

Slide 6

Ion channel insarcolemma opens;ions pass.

Na+ K+

5 ACh binds and channels open thatallow simultaneous passage of Na+ intothe muscle fiber and K+ out of themuscle fiber. More Na+ ions enter thanK+ ions leave, producing a local changein the electrical conditions of themembrane (depolarization). Thiseventually leads to an action potential.

5. Depolarization opens more sodium channels that allow sodium ions to enter the cell Once started, the action potential cannot be stopped The action potential travels throughout the surface

of the sarcolemma via t-tubules of the sarcolemma, causing the muscle to contract

6. The enzyme Acetylcholinesterase (AChE) breaks down acetylcholine into acetic acid and choline to end muscle contraction

Slide 7

Ion channel closed;ions cannot pass.

Degraded ACh

K+

Na+ACh

Acetylcholine-sterase

The enzyme acetylcholinesterasebreaks down ACh in the synaptic cleft,ending the process.

6

Cell returns to its resting state when:1. Potassium ions diffuse back out of the cell

Sodium-potassium pump moves sodium and potassium ions back to their original positions

The muscle is ready to receive another stimulus

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Calcium binds to regulatory proteins called troponin and tropomyosin◦ troponin stimulates tropomyosin to uncover

the actin binding sites ◦ This exposes myosin-binding sites◦ myosin heads on the thick filaments attach

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The attached heads pivot, sliding the thin filaments toward the center of the sarcomere, and contraction occurs (muscle shortens)

ATP provides the energy ◦ This continues as long as ionic calcium is present

Figure 6.7 Diagrammatic views of a sarcomere.

Myosin Actin

Z

I

Z

I

H

A

(a) Relaxed sarcomere

A

Z

I

Z

I

(b) Fully contracted sarcomere

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