Only $35.99/year

A&P 1 Lecture Exam 3 Study Guide

Terms in this set (93)

1. Release of acetylcholine.
Arrival of the nerve impulse at the synaptic end bulbs stimulates voltage‐gated channels to open. Because calcium ions are more concentrated in the extracellular fluid, Ca2+ flows inward through the open channels. The entering Ca2+ in turn stimulates the synaptic vesicles to undergo exocytosis. During exocytosis, the synaptic vesicles fuse with the motor neuron's plasma membrane, liberating ACh into the synaptic cleft. The ACh then diffuses across the synaptic cleft between the motor neuron and the motor end plate.

2. Activation of ACh receptors.
Binding of two molecules of ACh to the receptor on the motor end plate opens an ion channel in the ACh receptor. Once the channel is open, small cations, most importantly Na+, can flow across the membrane.

3. Production of muscle action potential.
The inflow of Na+ (down its electrochemical gradient) makes the inside of the muscle fiber more positively charged. This change in the membrane potential triggers a muscle action potential. Each nerve impulse normally elicits one muscle action potential. The muscle action potential then propagates along the sarcolemma into the system of T tubules. This causes the sarcoplasmic reticulum to release its stored Ca2+ into the sarcoplasm, and the muscle fiber subsequently contracts.

4. Termination of ACh activity.
The effect of ACh binding lasts only briefly because ACh is rapidly broken down by an enzyme called acetylcholinesterase (AChE). This enzyme is located on the extracellular side of the motor end plate membrane. AChE breaks down ACh into acetate and choline, products that cannot activate the ACh receptor.

Flickr Creative Commons Images

Some images used in this set are licensed under the Creative Commons through
Click to see the original works with their full license.