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How is the strength of muscle contraction increased?

Neuron stimulation must be increased

Even though continuous depolarization and repolarization occurs in the muscle cell (i.e DHP opens and closes calcium release channels), calcium remains in the cytoplasm causing constant stimiulation and muscle contraction

Muscle contraction last longer and is stronger


Sarcoplasm reticulum

ONLY source of calcium for muscle cells


Ryanodine Receptor

Receptor on calcium release channels on sarcoplasmic reticulum

"Cork" of these channels

Stimulation from voltage-sensing dihydropyridine (DHP) receptors causes "uncorking" of the ryanodine receptor which allows for the release of calcium from the sarcoplasmic reticulum into the cytoplasm of the cell causing muscle contraction


Excitation-Contraction Coupling of muscle cells

1) Action potential from motor neuron travel to inner muscle cells along transverse T-tubules 

2) Stimulation of voltage-sensing dihydropyridine (DHP) receptors "uncorks" (Ryanodine receptorscalcium release channels on the sarcoplasmic reticulum 

3) Calcium rushes into the cytoplasm of the muscle cells

4) Calcium binds to troponin C causing an actin myosin reaction

5) Muscle contraction occurs


High concentration of calcium in the cytoplasm of the cell



Voltage-Sensing Dihydropyridine (DHP) Receptor

Receptor on cell membrane


Senses voltage (action potential) that propagates from motor neuron to T-tubules

"Uncorks"  Calcium Release Channel (through stimulation of the Ryanodine Receptor) causing release of calcium from Sarcoplasmic Reticulum to the cytoplasm of the muscle cell causing muscle contraction


What happens to Acetylcholine after it reacts with nicotinic receptors on skeletal muscle?

It gets broken down by Acetylcholinesterase (AChE) into acetyl and choline

The choline is later added to Acetyl CoA = more ACh


What happens after Acetylcholine is released from the motor neuron?

1) Acetylcholine attaches and stimulates nicotinic receptors on Ligand (chemical) Gated Channels on the cell membranes of the muscle cells

2) Opening of these ligand gated channels allow for sodium to enter the cell

3) This causes end plate potential - either goes back to resting potential or threshold is reached causing depolarization (opening of voltage-gated sodium channels) to occur in the muscle cell


Botulinum Toxin

Neurotoxin produced by Clostridium botulinum

Blocks release of ACh from nerve terminals = no fusion of ACh to nicotinic receptors = action potential not reached = paralysis


One propagation from the motor nueron produces...

...A muscle twitch


Drugs affecting skeletal muscle potential 

Curariform drugs

Botulinum toxin


Myasthenia Gavis 

A disease characterized by skeletal muscle weakness

Believed to be autoimmune disease = antibodies present that block activation of nicotinic receptor = not as many activated = action potential not reached = paralysis

One treatment = acetylcholinesterase inhibitors (neostigmine) = ACh NOT broken down = so will hopefully attach to receptors due to increased concentration


Neuromuscular Junction

Transmission of impulses from nerves to skeletal muscle fibers

Where the nerve and the muscle come together

The nerve innervates around the middle of the muscle and releases Acetylcholine to stimulate action potential and the cell membranes of muscle fibers



Acts as an antagonist blocking nicotinic receptors and causing competition for ACh (agonist)

Not enough nicotinic receptors activated = not a high enough end plate potential = threshold not reached = no action potential = paralysis

competition is dependent on concentration and afinity of curare

The respiratory muscles are affected first


Resting state of muscle cells

Resting membrane potential = -90mV


Low concentration of calcium within the cytoplasm of the cell

High concentration of calcium in the Sarcoplasmic Reticulum


Calcium release channel closed (Ryanodine Receptor not stimulated by Voltage-sensing dihydropyridine (DHP) receptors)  


How is the action potential spread to interior muscle cells?



The plasma membrane (Sarcolemma) continues into the muscle cell = T-Tubules (invaginations of the cell membrane


Action potential is spread by the way of transvers T-tubules


1) Extracellular fluid within T-tubules brings action potential to cells



How is Acetylcholine (ACh) released?

1) The action potential travels down the axon to the axon terminal of the motor neuron

2) Depolarization of the axon terminal causes Voltage-Gated Calcium Channels to open

3) Calcium rushed into the axon terminal

4) Calcium affects vesicles that contain Acteylcholine, which is then released from the axon terminal into the Synapse through exocytosis


Toxins that affect this pathway cause paralysis


What is the neurotransmitter released from motor neurons?



Relaxation of muscle cells after the excitation-contraction coupling

1) Skeletal muscle repolarizes

2) Calcium release channels are "replugged" (Ryanodine receptor) by voltage-sensing dihydropyridine receptor

3) Calcium gets pumped back in the sarcoplasmic reticulum lowering the amount of calcium in the cytoplasm of the cell (decrease of calcium in the cytoplasm of the cell causes release of calcum from troponn C)