Which of the following is true? The NMJ occurs at the synapse between the T-tubule and the SR. A skeletal muscle cell must be stimulated by a somatic motor neuron to contract. AchE breaks down ACH inside the synaptic vesicles, preventing the release of Ach. Ach must bind to AchE for contraction to occur. The action potential in the neuron at the NMJ directly stimulates the skeletal muscle fiber to generate an action potential.
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The neuromuscular junction (NMJ) is the synapse between a motor neuron and a muscle fiber. It does not occur between the T-tubule and the SR (sarcoplasmic reticulum). Step 2: Evaluate the second statement. Skeletal muscle cells require stimulation from a somatic Show more…
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At the neuromuscular junction: To terminate contraction, acetylcholine is broken down by acetylcholinesterase at the muscle cell membrane. Opening of muscarinic acetylcholine receptors increases the sodium permeability of the skeletal muscle membrane. Action potential propagation to the lower motor neuron triggers the opening of voltage gated Ca2+ channels allowing Ca2+ to flow into the cell and bind to muscle proteins triggering contraction. Action potential propagation to the lower motor neuron terminal opens voltage-gated Ca2+ channels triggering exocytosis of vesicles containing glutamate. Acetylcholine binding to acetylcholinesterase results in muscle contraction.
Adi S.
Acetylcholine binds to receptors on the motor end plate, opening sodium channels. Calcium binds to troponin, causing tropomyosin to roll away from the active sites on actin. An action potential travels down the axon of a motor neuron to the synaptic terminal. ATP binds to myosin, causing it to release actin. Sodium ions rush in, triggering an action potential that travels along the sarcolemma. Voltage-gated calcium channels open, and calcium rushes into the synaptic terminal. Myosin binds with a second actin, and the cycle repeats, resulting in muscle contraction. Vesicles containing acetylcholine fuse with the plasma membrane, releasing ACh into the synaptic cleft. The myosin head splits the ATP into ADP and phosphate, putting it back into its original position. Myosin binds with actin's active site, producing a cross-bridge. The action potential along the sarcolemma causes calcium to be released from the sarcoplasmic reticulum. The myosin head releases ADP and phosphate, causing the head to pivot towards the M line.
In a neuromuscular junction, in the presynaptic terminal, small round membranous structures are called vesicles. These vesicles contain a neurotransmitter called Acetylcholine (ACh). Ach receptors are located on the postsynaptic membrane. The gap between the pre and post is called a synapse. The following ion is necessary to rupture the vesicles: Ca2+. Binding of ACh with the receptors will open the Na+ channels on the postsynaptic membrane. Influx of sodium in the muscle fiber causes depolarization and closure of the sodium influx. Opening of the K+ ion channel will cause efflux of K+ and leads to the generation of a signal to the sarcoplasmic reticulum (SR) to release calcium into the sarcomere. Units of muscle contraction inside a myofibril are sarcomeres. They are separated by discs. Sarcomeres are present as segments within a myofibril. Influx of Ca2+ causes depolarization and efflux of K+ causes repolarization. Contractile proteins inside the sarcomere are actin and myosin; the regulatory proteins are tropomyosin and troponin. During contraction, calcium binds with the troponin-tropomyosin complex, which covers the binding sites on actin. The brain talks to the muscle at the neuromuscular junction. Rigor mortis occurs due to the stoppage of ATP production. On the myosin head, the following binding sites are present: actin and ATP. The shortening of a sarcomere is explained by the sliding filament theory. The protein spring that connects the thick filament to the Z disc is called titin. Intervertebral discs are present in the muscle tissue. Multiple nuclei are present in the muscle.
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