Neuromuscular Junction Lecture Notes

Introduction

• Neuromuscular Junction: Point where a motor neuron communicates with skeletal muscle to cause contraction.
• Muscle Types: There are three types: cardiac, smooth, and skeletal muscle (focus here is on skeletal).

Signal Transmission

• Neuron Signal: Electrical signal needs to be converted to a chemical signal to cross the synaptic gap.
• Action Potentials: Involves voltage-gated sodium channels opening due to charge changes.

Action Potential Process

1. Sodium Channels: Sodium enters through voltage-gated channels, making the inside positive.
2. Propagation: Domino effect with subsequent channels opening, leading to the nerve signal moving down the neuron.

Calcium's Role

• At Neuron's End: Charge change opens voltage-gated calcium channels.
• Calcium Enters: Facilitates neurotransmitter release by vesicle fusion.

Neurotransmitter Release

• Acetylcholine (ACH): Neurotransmitter released into the synapse.
• Receptors: Acetylcholine binds to specific nicotinic receptors in skeletal muscles.

Binding and Channels

• Nicotinic Receptors: Activated by acetylcholine; similar to nicotine's effect.
• Ligand-Gated Channels: Sodium enters through these channels, leading to muscle cell depolarization.

Muscle Contraction

• Depolarization: Sodium influx depolarizes muscle membrane.
• Sarcoplasmic Reticulum: Releases calcium in response to depolarization.
• Calcium's Role: Unlocks actin for myosin to bind, facilitated by ATP.

Detailed Muscle Function

• Sarcomere: Basic unit of muscle contraction with actin (thin) and myosin (thick) filaments.
• Contraction Process: Myosin pulls actin for contraction; calcium and ATP are essential.

Acetylcholine Dynamics

• Synaptic Gap: 50 nanometers wide; acetylcholine has 1 ms to bind or be degraded.
• Acetylcholine Esterase: Degrades acetylcholine, recycling it for reuse.

Muscle Relaxants

• Depolarizing Relaxants (e.g., Succinylcholine):

  • Mimics acetylcholine, binding longer and maintaining depolarization.
  • Leads to initial contraction (fasciculations) followed by paralysis.

• Non-depolarizing Relaxants:

  • Inhibit acetylcholine binding, preventing depolarization and contraction.
  • Can be reversed by drugs inhibiting acetylcholine esterase.

Conclusion

• Quick overview of the neuromuscular junction and related pharmacology.