Anatomy & Physiology

Anatomy & Physiology Study Guide the permeability or other properties of another plasma membrane. These types of chemicals are called neurotransmitter. The permeability of the sarcolemma is altered by the release of ACh from the synaptic terminal and can trigger the contraction of the muscle fiber. The synaptic cleft separates with a space of the synaptic terminal of the neuron from the opposing sarcolemmal surface. The membrane receptors that bind ACh are located on the sarcolemmal surface, known as the motor end plate. A neuron stimulates a muscle fiber through a series of steps: • Step 1: The arrival of an electrical impulse, or action potential, at the synaptic terminal is the stimulus for acetylcholine release. An action potential is a sudden change in the transmembrane potential that travels along the length of the axon. • Step 2: When the action potential reaches the synaptic terminal, the membrane permeability changes and secretes ACh into the synaptic cleft. • Step 3: ACh molecules diffuse across the synaptic cleft and bind to ACh receptors on the surface of the sarcolemma at the motor end plate. ACh binds the receptor on the motor end plate and changes the permeability of the membrane to sodium ions. This influx continues until acetylcholinesterase (AChE) removes the ACh from the cleft. As the concentration of ACh in the cleft falls, bound ACh diffuses off the receptors and into the cleft. • Step 4: The sudden influx of sodium ions results in the generation of an action potential in the sarcolemma at the motor end plate. These electrical impulse sweeps across the entire membrane surface and travels inward along each T tubule. • Step 5: Even before the action potential has spread across the entire sarcolemma, the ACh has been broken down by AChE. Some of the breakdown products will be absorbed by the synaptic terminal and used to resynthesize ACh for subsequent release. This sequence of events can be repeated with the arrival of another action potential at the synaptic terminal. Excitation–Contraction Coupling Excitation-contraction coupling describes the generation of an action potential in the sarcolemma and the start of a muscle contraction. This coupling occurs at the triads. Once it reaches a triad, an action potential triggers the release of Ca 2+ from the sarcoplasmic reticulum. The change in the permeability of the SR to Ca 2+ is temporary, lasting only about 0.03 second. Within a millisecond, the Ca 2+ concentration in and around the sarcomere reaches 100 times resting levels. The effect of calcium release on the sarcomere is nearly instantaneous because the terminal cisternae are at the zones of overlapping thick and thin filaments. In a resting sarcomere, the tropomyosin strands cover the active sites on the thin filaments, preventing cross- bridge formation. When calcium ions enter the sarcomere, they bind to troponin, which rotates and swings the tropomyosin away from the active sites. Cross-bridge formation then occurs, and the contraction cycle begins. ATP is the energy source for muscle contraction. The ATP demands of a contracting skeletal muscle are enormous, since even small muscles have thousands of muscle fibers. In practical terms, the demand for ATP in a contracting muscle fiber is so high that it would be impossible to have all the Achieve Page 108 of 368 ©2018