Which of the following is true of ACh (acetylcholine)? O It cannot be degraded within the synaptic cleft to which it was released; it must be internalized and degraded by the cell that receives it O It is always excitatory because it causes the entrance of Na+ into a cell which leads to an increase in intracellular mV O It is released via exocytosis from the axon terminal of a somatic motor neuron O It is released via exocytosis from all pre-ganglionic motor neurons of the ANS

Which of the following is true of ACh (acetylcholine)? O It cannot be degraded within the synaptic cleft to which it was released; it must be internalized and degraded by the cell that receives it O It is always excitatory because it causes the entrance of Na+ into a cell which leads to an increase in intracellular mV O It is released via exocytosis from the axon terminal of a somatic motor neuron O It is released via exocytosis from all pre-ganglionic motor neurons of the ANS

Human Anatomy & Physiology (11th Edition)

11th Edition

ISBN:9780134580999

Author:Elaine N. Marieb, Katja N. Hoehn

Publisher:Elaine N. Marieb, Katja N. Hoehn

Chapter1: The Human Body: An Orientation

Section: Chapter Questions

Problem 1RQ: The correct sequence of levels forming the structural hierarchy is A. (a) organ, organ system,...

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Aerobic, or low-intensity, muscle training eventually results in A more muscle fibers more capillaries C more glycogen D more myoglobin E B and D are correct B
Anatomically, the motor endplate potential is characterized by synaptic boutons active zones junctional folds Ach receptor-channels all the above
Once an action potential reaches a neurotransmitter release site, the release of the neurotransmitter is triggered by: The influx of Na* through voltage-gated channels. O The efflux of Na* through voltage-gated channels. The influx of K* through voltage-gated channels. The efflux of K+ through voltage-gated channels. The influx of Ca²+ through voltage-gated channels. O The efflux of Ca2+ through voltage-gated channels.
What would happen if we reduced the quantity of acetylcholinesterase in the synaptic cleft, after ACh is released from the pre-synaptic terminal? Can pick more than one We would increase the amount of choline and acetyl CoA produced in the cleft. We would have more ACh left in the cleft than if we had a 'normal' quantity of acetylcholinesterase. The ACh in the cleft would remain in the cleft for a longer period of time. We would have greater postsynaptic potentials generated.
are these True or False? Receptors on the post-synaptic cell membrane that bind the acetylcholine are voltage-gated channels (channels that open in response to a change in the electrical charge of the membrane). When a muscle cell is not contracting its cell membrane is negative on the inner surface. The effect of a neurotransmitter on the muscle cell membrane is to modify its ion permeability properties temporarily.
What does the binding of ACh to nicotinic receptors of skeletal muscle cells directly cause? Closing of calcium channels Cross-bridge cycling O Hydrolysis of ATP O Inhibition of acetylcholinesterase O Skeletal muscle depolarization
What drives K+ ions through voltage gated channels while funny channels are also open? O pifference in K+ concentration across the PM O pressure potential O Both difference in K+ concentration across the PM and Membrane potential (difference in charge across the membrane) O Osmotic potential O Membrane potential (difference in charge across the membrane)
hen an action potential arrives at the nerve terminal of a neuromuscular junction, which of the following statements best describes the events that occur? Depolarisation of the nerve terminal causes the release of ACh which activates nicotinic receptors on the skeletal muscle membrane to cause Ca2+ entry and muscle contraction. Depolarisation of the nerve terminal opens voltage-gated Ca2+ channels, Ca2+ entry brings vesicles containing ACh to the membrane which form fusion pores causing the release of ACh which activates voltage-gated Na+ channels at the end-plate. Depolarisation of the nerve terminal opens voltage-gated Ca2+ channels, Ca2+ entry brings vesicles containing ACh to the membrane which form fusion pores causing the release of ACh which binds to muscarinic receptors at the end plate. Depolarisation of the nerve terminal opens voltage-gated Ca2+ channels, Ca2+ entry brings vesicles containing ACh to the membrane which form fusion pores…
Matching (may not use all choices; may use some choices more than once) 45. Sección Release of inhibitory neurotransmitter 46. Decreased concentration of leaky sodium channels in the membrane Arsenic poisoning prevents mitochondria from making ATP 47. 48. Extreme sodium deficiency 49. Acetylcholinesterase concentration is decreased 50. Overdose of Potassium Chloride 51. Increased concentration of leaky potassium channels in the membrane Salto de columna A. Makes RMP more negative B. Makes RMP less negative
In muscles, acetylcholine is released by the _________________________and opens specific channels that allow the ion ______ to depolarize the membrane. motor neuron, sodium motor neuron, potassium muscle fibril, sodium muscle fibril, potassium
The patient's muscle weakness, dizziness, and nausea are all due to hypokalemia. How does hypokalemia lead to muscle weakness? O hypokalemia leads to hypopolarization which results in fewer action potentials arriving at skeletal muscles O hypokalemia leads to hyperpolarization which results in fewer action potentials arriving at skeletal muscles O hypokalemia leads to hypopolarization which leads to too many action potentials arriving at skeletal muscles O hypokalemia leads to hyperpolarization which results in too many action potentials arriving at skeletal muscles
Acetylcholine is an excitatory neurotransmitter that is responsible for initiating muscle movement. Consider the scenario where a mouse was bitten by a snake that injected venom into their circulatory system. The venom has an inhibitory effect on the reuptake of acetylcholine from the synaptic cleft. Explain how the mouse’s body would respond to the venom as well as the venoms effect at the cellular level.