NMJ, sliding filament theory, and Sarcomeres

the Neuromuscular junction

where a nerve and muscle fiber join

motor end plate

specialized part of the sarcolemma located at the neuromuscular junction

• has many folds

synaptic vesicles

where neurotransmitters are stored before being released into the synaptic cleft

synapse- synaptic cleft

a gap between the motor neuron endings and the motor end plate

acetylcholine

neurotransmitter that crosses synaptic cleft

cholinesterase

an enzyme that breaks down acetylcholine

sarcolemma

specialized cell membrane that surrounds a skeletal muscle fiber or cardiomyocyte

the steps of sliding filament theory

1. myosin head bonds with ATP

2. and hydrolyzes it to make ADP and P

3. myosin head binds to actin- cross bridge

4. phosphate is released

5. power stroke pulls actin

6. ADP is released

7. new ATP binds to myosin head so it can detach from actin

tropomyosin

actin’s regulatory protein that blocks myosin heads from bonding

troponin

more protein that blocks myosin building cites

role of calcium ions

are released when neuron stimulates muscle, bind to troponin and lets tropomyosin move so myosin heads can bind

sarcomere

the smallest functional and contractile unit of striated muscle tissue, between z bands

black diagonals = z bands

blue = actin

red = myosin

I band = lighter, only actin

A band = darker, myosin filaments

H zone = only myosin, lighter

myofilaments

actin and myosin

sarcomela

membrane of the muscle fiber

sarcoplasmic reticulum

parallel network of tubes used for transport

sarcoplasm

the specialized cytoplasm of a muscle cell

Duchenne Muscular Dystrophy

a mutation in the gene that codes for dystrophin (supports signaling, absorbs contraction stress, and conects cell framework)

• the body cant repair muscle tears and cell death fast enough

• muscle tissue is replaced with fat and scar tissue

  • leads to muscle weekness

motor unit

group of muscle fibers controlled by one motor nueron

action potential

triggers skeletal muscle contraction through a process called excitation-contraction coupling, converting an electrical signal from a motor neuron into a physical movement of the muscle

nicotinic receptors

ligand-gated ion channels on the end plate that acetylcholine binds to

• when open allow sodium to enter, depolarizing the membrane, producing end-plate potential

process of neuromuscular junction

1. acetylcholine binds to nicotinic receptors on end plate

2. nicotinic receptors open to allow sodium to enter cell

3. sodium depolarizes the membrane → producing end-plate potential

4. when end-plate potential is high enough, voltage-gated sodium channels outside end plate activate

5. outside channels allow even more sodium in, fully reversing polarity of cell membrane

6. voltage gated potassium channels open so potassium can move out of cell → returning memrane voltage to original value

7. that generates action potential, which spreads through muscle via other channels and t tubules to reach sarcoplasmic reticulum

8. activates calcium channels to release calcium into cytosol of muscle cells

9. calcium sets off sliding filament theory

acetylcholinesterase

enzyme that removes all extra acetylcholine molecules that don’t bind with receptor or are done activating a receptor

• terminates synaptic activation → gives muscle relaxation

SYNAPTIC VESICLES

where neurotransmitters are stored

*these are released into the cleft  and tell the muscle to contract

Oxygen Debt

not have enough oxygen  causes lactic acid to accumulate in the muscles → Soreness

Hypertrophy

muscles enlarge 

Atrophy

muscles become small and weak due to disuse

Myasthenia Gravis

• Means "grave muscular weakness." 

• Autoimmune disease

• Acetylcholine receptors are damaged

ALS, or amyotrophic lateral sclerosis

a progressive neurodegenerative disease.   

The motor nerves degenerate and stop sending messages to the muscles, causing atrophy.

Symptoms get worse over time

rigor mortis

adenosine triphosphate (ATP)—the energy molecule required for muscle fibers to relax—after breathing and blood circulation stop

• muscles remain contracted after death

Tetanus

causes cholinesterase to not break down the acetylcholine in the synapse.  This results in a person's muscles contracting and not relaxing.

Botulism

 Prevents the release of acetylcholine at the neuromuscular junction, causing flaccid paralysis (paralization)

Strychnine

Lowers the threshold level for an action potential, making it more likely the muscles will contract

• Blocks glycine receptors, preventing inhibition of motor neurons and causing severe muscle spasms

Curare

Blocks acetylcholine receptors on muscle cells, preventing stimulation of muscle contraction and causing flaccid paralysis