Acetylcholine is a neurotransmitter that, when bound to its receptor, causes the receptor to open achannel that allows the flow of Na+ ions into neurons.When the Na+ ions begin to flow into the neuron, this change in the net charge across the neuronalcell membrane often triggers Ca2+ ion channels to open.In this scenario, the acetylcholine receptor would be acting as achannel, and the Ca2+ channels would be classified asvoltage-gated; leakyligand gated; voltage-gatedsymporter; antiporterNone of the above.ion Which of the following specifically explains why glucose uptake into intestinal cells happens in onlyone direction.O The Na+/Glucose transporter has a binding affinity for both Na+ and Glucose.The Na+/Glucose transporter will only undergo a conformational change when both Na+ and glucose arebound.O Na+ ions are always present at higher concentrations OUTSIDE of the intestinal cells.Na+ ions are always present at higher concentrations INSIDE of the intestinal cells.

Introduction:- Neurotransmitters are the chemical signalling molecules which helps in the…

Acetylcholine is a neurotransmitter that, when bound to its receptor, causes the receptor to open a channel that allows the flow of Na+ ions into neurons. When the Na+ ions begin to flow into the neuron, this change in the net charge across the neuronal cell membrane often triggers Ca2+ ion channels to open. In this scenario, the acetylcholine receptor would be acting as a channel, and the Ca2+ channels would be classified as voltage-gated: leaky O ligand gated; voltage-gated symporter; antiporter None of the above. ion

Acetylcholine is a neurotransmitter that, when bound to its receptor, causes the receptor to open a channel that allows the flow of Na+ ions into neurons. When the Na+ ions begin to flow into the neuron, this change in the net charge across the neuronal cell membrane often triggers Ca2+ ion channels to open. In this scenario, the acetylcholine receptor would be acting as a channel, and the Ca2+ channels would be classified as voltage-gated: leaky O ligand gated; voltage-gated symporter; antiporter None of the above. ion

Biology: The Dynamic Science (MindTap Course List)

4th Edition

ISBN:9781305389892

Author:Peter J. Russell, Paul E. Hertz, Beverly McMillan

Publisher:Peter J. Russell, Paul E. Hertz, Beverly McMillan

Chapter39: Information Flow And The Neuron

Section: Chapter Questions

Problem 1TYK

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Assume presynaptic excitatory neuron A terminates on a postsynaptic cell near the axon hillock and presynaptic excitatory neuron B terminates on the same postsynaptic cell on a dendrite located on the side of the cell body opposite the axon hillock. Explain why rapid firing of presynaptic neuron A could bring the postsynaptic neuron to threshold through temporal summation, thus initiating an action potential, whereas firing of presynaptic neuron B at the same frequency and the same magnitude of EPSPs may not bring the postsynaptic neuron to threshold.
Conformational changes in channel proteins brought about by voltage changes are responsible for opening and closing Na+ and K+ gates during the generation of an action potential. (True or false?)
When action potentials arrive at a synapse between a neuron and another cell, they stimulate the release of molecules of a ________ that diffuse over to that cell.
You learned in this chapter that Na+/K+ active transport pumps in the plasma membrane of the axons are responsible for creating the imbalance between Na+ and K+ inside and outside of the neuron that produces the resting membrane potential. In early research studying the role of ions and the involvement of active transport of ions in neural signaling, investigators used the giant axon of a squid as a model. The diameter of a giant axon is far greater than that of a mammalian axon, which enabled researchers to isolate it easily and use it in in vitro experiments. In one early experiment, researchers investigated the active transport of Na+ out of the axon in response to the presence of cyanide. Experimentally they hooked up a section of axon to a syringe, immersed the axon in artificial seawater, introduced radioactive 22Na (as 22NaCl) into the axon, and then quantified the transport of 22Na out through the axons plasma membrane. The rate of 22Na transport out of the axon was determined by measuring the radioactivity released into the fluid sur- rounding the axon over a period of time. The Figure shows the results of the experiment. What is the effect of cyanide on Na1 transport out of the squid axon? How do the data show the effect? Source: P. C. Caldwell et al. 1960. The effects of injecting energy-rich phosphate compounds on the active transport of ions in the giant axons of Loligo. The Journal of Physiology 152:561590. Cengage Learning 2017
Acetylcholine is a neurotransmitter that, when bound to its receptor, causes the receptor to open a channel that allows the flow of Na+ ions into neurons. When the Na+ ions begin to flow into the neuron, this change in the net charge across the neuronal cell membrane often triggers Ca2+ ion channels to open. In this scenario, the acetylcholine receptor would be acting as a channel, and the Ca2+ channels would be classified as voltage-gated; leaky ligand gated; voltage-gated symporter; antiporter None of the above. ion
In an experiment, the extracellular [Na+] surrounding a nerve cell was reduced from 145 to 45 mM. Which of the following is the most likely effect of this on action potentials? No action potentials would occur because the concentration of extracellular Na+ is too low. The membrane potential would become more negative so the threshold for action potential generation could not be reached. The nerve cell would still produce an action potential but its amplitude would be reduced and the depolarisation phase would be slower. The nerve cell would still produce an action potential but its amplitude would be reduced and the depolarization phase would be more rapid.
In the figure to the left, name the 4 phases of the action potential (Note: you have to write in where phase 4 occurs). Describe what happens in each phase with a focus on Na+ and K+ flow through channels and the membrane potential. Discuss the importance of threshold. How does this relate to the concept of APs being all or none?
Assume the membrane is only permeable to Na+ and K+, the electrical model of axon membrane is the following: Outside A INa gna ENa Ex D Inside The membrane potential at rest and at peak is -70mV and 45mV respectively; the potential of Sodium ion is 60mV and the potential of Potassium ion is -80mV. Find the ratio 9Na at rest and at peak. gK
After discussing his case with his physician, he learned that he had probably been the victim of pufferfish poisoning. The active toxin in the tissues of this fish is a chemical called tetrodotoxin (TTX). Tetrodotoxin is in a class of chemicals known as neurotoxins because it exerts its effects on neurons. The specific action of tetrodotoxin is that it blocks voltage-gated sodium ion channels. Define the following phrases and terms associated with the signs and symptoms of Dr. Westwood’s TTX poisoning: diaphoresis motor dysfunction paresthesias cyanotic hypoventilating bradycardia gastric lavage oxygen saturation As mentioned in the case description, tetrodotoxin is a molecule that blocks voltage-gated sodium ion channels. What is a voltage-gated sodium ion channel and what is its function? When nerve cells are at rest, there is an unequal amount of positive and negative charges on either side of a nerve cell membrane. This charge difference creates an electrical potential.…
Dendrotoxins, produced by the mamba snakes (Dendroaspis), are inhibitors of the voltage-gated K+ channels. What phase of the action potential would this toxin affect? How would it affect ion permeability during this phase? How would ion movement be affected?
The venom of many cobras contains a potent neurotoxin that binds to ligand-gated Na+ channels,causing them to open. Unlike ACh, which binds to and then rapidly unbinds from ligand-gated Na+ channels, the neurotoxin tends to remain bound to ligand-gated Na+ channels. How does this neurotoxin affect the nervous system’s ability to stimulate skeletal muscle contraction? How does it affect the ability of skeletal muscle fibers to respond to stimulation?
A drug that blocks Na+ channels in neurons does so not only in the axon but also in the dendrites and cell body. What overall effect would this have on action potential generation?