lecture 5&6

• Neuromuscular Junction is the site where motor neurons and skeletal muscle fibers are chemically linked.
• Calcium entry from the ECF induces a much larger Ca2+ release from the sarcoplasmic reticulum.
• Acetylcholine is the neuromuscular junction neurotransmitter.
• The smallest functional unit of skeletal muscle is the sarcomere, composed of various microfilaments and supporting structures.
• Myosin forms the thick filaments in the sarcomere.
• Actin is the main structural component of the thin filaments in the sarcomere.
• Sarcomeres shorten during contraction, with the thin filaments sliding over the thick filament, requiring ATP energy and resulting in an all-or-none response.
• The shortening of the sarcomere occurs along the entire length of the muscle fiber, with the strength of a muscle contraction depending on how often the individual muscle fibers are stimulated to contract and how many muscle fibers contract within a given muscle.
• The mechanisms of contraction involve the cross-bridge cycle, where myosin cross bridges extend out from the thick filaments to the thin filaments, with the cross-bridge heads functioning as ATPase enzymes.
• During contraction, cycles of cross-bridge binding and bending pull the thin filaments inward, with the concentration of Ca2+ in the sarcoplasm rising when the muscle cell is stimulated to contract.
• The attachment of Ca2+ to troponin causes movement of the troponin-tropomyosin complex, exposing binding sites on the actin, allowing the myosin cross bridges to attach and undergo a power stroke.
• Contraction refers to the activation of myosin’s cross bridges (force-generating sites), with shortening occurring when the tension generated by the cross bridge exceeds forces opposing shortening and contraction ending when cross bridges become inactive, the tension generated declines, and relaxation is induced.
• When action potentials cease, the Ca2+ release channels in the sarcoplasmic reticulum close, allowing the active transport Ca2+ ATPase pumps in the sarcoplasmic reticulum to accumulate Ca, removing it from the sarcoplasm and sarcomeres.
• Cardiac muscle is striated and contains sarcomeres, with each myocardial cell tubular in structure and joined to adjacent myocardial cells by electrical synapses, or gap junctions.
• The myosin proteins are stacked perpendicular to the long axis of the thick filaments, allowing them to bind to actin all along the length of the thick filament.
• Action potentials can cross from one myocardial cell to another.
• Multiunit smooth muscle requires nerve stimulation by the ANS, with neurotransmitter (NT) released along a series of synapses called varicosities.
• Excitation-contraction coupling in cardiac muscle involves depolarization of the plasma membrane during action potentials, when voltage-gated Na+ channels are opened, causing voltage-gated Ca2+ channels to open in the transverse tubules.
• The Ca2+ released from the sarcoplasmic reticulum binds to troponin and stimulates contraction.
• A Ca2+ (ATPase) pump actively transports Ca2+ into the cisternae of the sarcoplasmic reticulum, allowing relaxation of the myocardium and producing a concentration gradient favoring the outward diffusion of Ca2+ for the next contraction.
• Single unit (Unitary) smooth muscle is spontaneously active (myogenic), with some cells acting as pacemakers, and has gap junctions to spread electrical activity.
• This allows some Ca2+ to diffuse from the extracellular fluid into the cytoplasm, stimulating the opening of Ca2+ release channels in the sarcoplasmic reticulum.
• In contrast to skeletal muscles, which require neural stimulation to contract, action potentials in the heart originate in myocardial cells; stimulation by neurons is not required.