Control of Muscle

Question 1

Recall the basic layout of the nervous system.

Answer 1

Layout of the nervous system:
Central (CNS)-
- brain & spinal cord
Peripheral (PNS)-
- efferent (motor)
– somatic (skeletal muscle)
– autonomic (cardiac/smooth muscle)
- afferent (sensory)-
– somatic
– visceral

Cell body - resides within the CNS containing dendrites and nucleus in the cell body
Along the length of the axon is myelin that allows quick and efficient nervous impulses
Synapse located at the end of the neuron

Question 2

Describe the structure of a neuromuscular junction.

Answer 2

Specialised features-
- synaptic vesicles containing a neurotransmitter (ACh)
- junctional folds (folded sarcolemma) - increases surface area of NMJ for more efficient communication
- receptors at ‘mouth’ of folds
- acetylcholinesterases
- specialised synapse for one way communication

Neurotoxins:
Toxins and medications can affect the functioning of the NMJ

Classes of neurotoxin:
- Presynaptic/transmitter release inhibitor - inhibiting the NMJ at the presynaptic level (start of the synapse)
- Receptor inhibitor - receptors on postsynaptic, attach where ACh would bind to cause a muscular effect - neurotoxin inhibits/binds/destroys receptors to inhibit the effect
- Acetylcholinesterase inhibitor - prevents ACh being broken down in they synapse resulting in prolonged muscle contractions

Question 3

Discuss the basic mechanism of synaptic communication and the events at a NMJ that lead to an action potential in a skeletal muscle fibre.

Answer 3

1. Action potential propagates down axon
2. Depolarised presynaptic membrane causes opening of voltage-gated Ca2+ channels → Ca2+ ions diffuse into presynaptic nerve cytoplasm
3. Presence of Ca2+ ions causes synaptic vesicles to move and fuse to presynaptic membrane
4. Acetylcholine diffuses across cleft and binds with receptors on postsynaptic membrane
5. Binding of Acetylcholine causes ligand-gated ion channels to open - Na+ ions move into the muscle cell causing depolarisation of the motor end plate (end plate potential)
6. End plate potential causes opening of further voltage-gated ion channels along the muscle fibres - an action potential is propagated
7. Acetylcholinesterase breaks down Acetylcholines to acetyl and choline molecules

Question 4

Explain the mechanism of excitation-contraction coupling.

Answer 4

Depolarisation of the postsynaptic membrane causing contraction:
- Sarcoplasmic reticulum wrapped around the individual muscle fibres
- T-tubules - tubes that run form the muscle membrane deep into the muscle tissue (closely related to SR)

1. Muscle action potential propagated
2. Depolarisation of T-tubule causes opening of Ca2+ channel between myoplasm and S.R.
3. Calcium released from sarcoplasmic reticulum - ‘calcium transient’
4. Calcium binds to Troponin C - a protein involved in muscle contraction - to initiation the cross-bridge cycling process

Muscle contraction will not occur without the presence of Calcium ions

After contraction:
Ca2+ ions in myoplasm are pumped back into the sarcoplasmic reticulum
Pump = Ca2+ ATPase → this pump requires energy (ATP)
Absence of Ca2+ ions in the sarcoplasm means the muscle no longer contracts

Question 5

Appreciate the concept of a skeletal muscle motor unit.

Answer 5

Muscle innervation:
Each skeletal muscle is innervated by a motor neuron
Each neuron can innervate a few or many fibres
Motor neurons are excitatory only - only bring about positive responses
Skeletal muscle does not contract with innervation from motor neurons
The pattern of muscle contraction - strength, duration & speed

Motor unit:
One motor neuron and all the muscle fibres that it innervates
Ratio of nerve:muscle fibres varies depending on the function of the muscle
Strength (eg: limb) - many fibres controlled by one nerve
Control (eg: eye) - few fibres controlled by one nerve
Can control muscle force by recruiting more/fewer motor units or by controlled force within a motor unit