Movements propagated by skeletal muscle both simple and complex also require interaction with nerve. The nerves and muscle work together to help us do out conscious task with ease. The purpose of this lab is to identify how changes in such variables will affect the properties of the muscle in a human flexor digitorium superficialis (FDS) and to extrapolate the nerve changes from a sciatic nerve of a frog. Neurons are excitable cells structural features such as dendrites, cell body and axon. Excitable cells generate electrochemical impulses also known as an Action Potentials (AP), which propagate down an axon to transmit a signal to another cell. The signal may be transmitted to another neuron through a synapse of another dendrite or will form a Neuromuscular junction with a skeletal muscle cell. Skeletal muscle consists of many multinucleated muscle fibers connected to intercalation of sarcoplasmic reticulum (SR) which contains calcium ions, voltage gated (V-gated) calcium channels and transverse tubules (T-tubules), and actin fibers used for contraction. Electrochemical signals such as AP are a great way to send a signal across a cell.
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However, this requires a cell to maintain a negative electrical potential also known as the resting membrane potential (RMP). This is achieved due to the semi permeable nature of the plasma membrane and multiple V-gated ion channels that are found on it. In a nerve cell, when a dendrite receives a signal, a depolarization event occurs which causes the electrical potential to drop. If it reaches a threshold of (-55 mV) the fast V-gated Sodium channels activate at the axon hillock. This brings the membrane potential to +30 mV in a quick burst as the Na+ ions escape and the sodium channels inactivate. At this point the relatively slower V-gated K+ channels activate and the movement of K+ bring the membrane potential to -90 mV thus hyperpolarizing it. The V-gated K+ channel eventually closes and the membrane potential is brought to RMP (-70 mV) by the Cl- channels. The depolarization then travels through the nerve until it reaches another dendrite synapse or a Neuromuscular Junction (NMJ). At the NMJ, depolarization causes the V-Gated Ca2+ channels to open and in influx of Ca2+ causes the release of a neurotransmitter, acetylcholine (ACh) at the Axon terminal of a synaptic vesicles. The ACh now in synaptic trough binds to the ligand gated channels activating the influx of cations and thus creating a potential the endplates of muscle cells (EPP). This local depolarization causes the adjacent V-gated Na+, K+ channels to open thus creating an AP. ACh is broken down to avoid further stimulation of the ACh receptors. AP spreads and travels down the T-tubules and causes a conformational change in Dihydropyridine receptors (DHP) causing the Ca2+ channels found on SR to open. The influx of Ca2+ allows it to bind to troponin which causes the tropomyosin to roll of the myosin binding site on actin forming a crossbridge. Myosin heads attach to actin and in the presence of ATP and using hydrolysis undergo a power stroke pulling the Z-disks together causing the sarcomeres to shorten leading to muscle contraction. Ca2+¬¬¬ is actively pumped back into the SR by a primary (ATP) transporter. Tropomyosin covers the binding site in the presence of insufficient Ca2+ and relaxing the muscle. A motor unit consists of an Alpha motorneuron (AMn) and all the muscle fibers it innervates. One AP from an AMn will cause sufficient
However, this requires a cell to maintain a negative electrical potential also known as the resting membrane potential (RMP). This is achieved due to the semi permeable nature of the plasma membrane and multiple V-gated ion channels that are found on it. In a nerve cell, when a dendrite receives a signal, a depolarization event occurs which causes the electrical potential to drop. If it reaches a threshold of (-55 mV) the fast V-gated Sodium channels activate at the axon hillock. This brings the membrane potential to +30 mV in a quick burst as the Na+ ions escape and the sodium channels inactivate. At this point the relatively slower V-gated K+ channels activate and the movement of K+ bring the membrane potential to -90 mV thus hyperpolarizing it. The V-gated K+ channel eventually closes and the membrane potential is brought to RMP (-70 mV) by the Cl- channels. The depolarization then travels through the nerve until it reaches another dendrite synapse or a Neuromuscular Junction (NMJ). At the NMJ, depolarization causes the V-Gated Ca2+ channels to open and in influx of Ca2+ causes the release of a neurotransmitter, acetylcholine (ACh) at the Axon terminal of a synaptic vesicles. The ACh now in synaptic trough binds to the ligand gated channels activating the influx of cations and thus creating a potential the endplates of muscle cells (EPP). This local depolarization causes the adjacent V-gated Na+, K+ channels to open thus creating an AP. ACh is broken down to avoid further stimulation of the ACh receptors. AP spreads and travels down the T-tubules and causes a conformational change in Dihydropyridine receptors (DHP) causing the Ca2+ channels found on SR to open. The influx of Ca2+ allows it to bind to troponin which causes the tropomyosin to roll of the myosin binding site on actin forming a crossbridge. Myosin heads attach to actin and in the presence of ATP and using hydrolysis undergo a power stroke pulling the Z-disks together causing the sarcomeres to shorten leading to muscle contraction. Ca2+¬¬¬ is actively pumped back into the SR by a primary (ATP) transporter. Tropomyosin covers the binding site in the presence of insufficient Ca2+ and relaxing the muscle. A motor unit consists of an Alpha motorneuron (AMn) and all the muscle fibers it innervates. One AP from an AMn will cause sufficient