Synaptic Transmission at the Neuromuscular Junction
1. An Action Potential (AP) is conducted down the somatic motorneuron down to the synaptic knob.
2. The reversal in electrical polarity at the synaptic knob causes an opening of “voltage-gated” Ca+2 channels (Voltage gated calcium ion channels open and allow calcium ions to flow inside due to the voltage change). Calcium ions are very important for the release of neurotransmitters and secretion of hormones by endocrine cells.
3. Calcium flows into the synaptic knob and it’s this influx that causes these vesicles to form and release/secrete neurotransmitters. In other words, the entry of Ca+ into the synaptic knob causes the exocytosis (secretion) of the nerotransmitter Acetylcholine (ACh).
4. The ACh diffuses across the synaptic cleft and binds to “nicotinic” ACh Receptor Site Proteins on the membrane of the Skeletal Muscle Cell (Fiber). The first chemical they discovered that affects this receptor site, happened to be nicotine so that’s why it got the name, nicotinic cholinergic receptor.
5. Activation of the ACh Receptor Sites causes an opening of “ligand-gated” Sodium Ion Channels.
6. As sodium ions flow into the Skeletal Muscle Cell, it depolarizes to the threshold potential, triggering an Action Potential.
7. As the action potential spreads along the cell, it causes the muscle cell to contract.
8. The ACh which is attached to the receptor site, is split into acetate and choline by acetylcholinesterase (ACHase), an enzyme of the skeletal muscle cell membrane.
9. The “ligand-gated” sodium ion channels close, permitting the skeletal muscle cell to relax.
10. The acetate & choline are actively transported back-up into the synaptic knob (“Active Reuptake”) to be re-synthesized.
Eventually, we’re going to talk about a neurotransmitter in our brain called Serotonin. There’s a class of medicines called Selective Serotonin Reuptake Inhibitors (SSRI). This concept of reuptake will appear when we investigate how these drugs works.
» Ach attaches to an ACh receptor site -> Increased permeability to sodium, meaning the ligand-gated sodium ion channels open -> Sodium rushes into muscle fiber -> Depolarization (less negative) -> Action Potential -> Muscle Contraction. Textbooks call this depolarization an End Plate Potential (EPP).