In a mouse mutant, all Norepinephrine (NE) synapses in the thalamus have a Protein Kinase A that cannot be activated by CAMP. Which of the following effects would occur? Check all correct answers. NE would not have target actions in thalamus Protein kinase A in the synapse could not phosphorylate its targets Adenyl Cyclase would not function CAMP could not be broken down the alpha-1 adrenergic receptor coupled pathway would still function

In a mouse mutant, all Norepinephrine (NE) synapses in the thalamus have a Protein Kinase A that cannot be activated by CAMP. Which of the following effects would occur? Check all correct answers. NE would not have target actions in thalamus Protein kinase A in the synapse could not phosphorylate its targets Adenyl Cyclase would not function CAMP could not be broken down the alpha-1 adrenergic receptor coupled pathway would still function

Human Physiology: From Cells to Systems (MindTap Course List)

9th Edition

ISBN:9781285866932

Author:Lauralee Sherwood

Publisher:Lauralee Sherwood

Chapter4: Principles Of Neural And Hormonal Communication

Section: Chapter Questions

Problem 5TAHL

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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
In a mouse mutant, all Norepinephrine (NE) synapses in the thalamus have a Protein Kinase A that cannot be activated by cAMP. Which of the following effects would occur? Check all correct answers. NE would not have target actions in thalamus Protein kinase A in the synapse could not phosphorylate its targets Adenyl Cyclase would not function CAMP could not be broken down the alpha receptor coupled pathway would still function
Changes in intracellular Ca2+ is one of the main governing factors that determines the direction of plasticity (i.e., whether a synapse potentiates or depresses). Provide a general mechanism to explain how changes in intracellular Ca2+ can result in either synaptic depression or synaptic potentiation (refer to our discussion on kinases and phosphatases).
apucreceptors ava ble at the synapse are reflected in this number. Question 2: In this chapter, we discussed a GABA-gated ion channel that is permeable to Cl. GABA also activates a G-protein-coupled receptor called the GABA receptor, which causes potassium-selective B channels to open. What effect would GABAB receptor activation have on the membrane potential? GABAB receptor activation causes potassium-selective channels to open. As a result this bringhs the
Arrange following the boxed information in sequence regarding the dissociation and reassociation of G proteins following the activation of a G protein coupled receptor. GTP-bound Ga, dissociates from B and y cuhunits Gas exchanges GTP for GDP Gas reassociates with By subunits and the rorentor reforms Binding of the ligand to a G-protein rounled recentor GTP-bound Gas binds and activates adenvlul rurlase GTP is hydrolyzed and GDP bound Gas suhunit dissoriates Conformational change Increased synthesis of CAMP from ATP
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An experimental cell line expresses K+ inward rectifier channels, Na+ leak channels, K+ channels activated by the elevated levels of cytosolic Ca2+, Cl- channels activated by PKC, aquaporins, and α-1 adrenergic receptors (GPCRs that activate Gαq/11 signalling pathway). No voltage-gated channels of any kind are present. The resting membrane potential of these cells is about –50 mV, and they are bathed in the standard extracellular solution. The intracellular concentrations of the relevant ions are as follows: K+ 130 mM, Na+ 15 mM, Cl- 30 mM, Ca2+ 10-4 mM. Q. What will happen to the cell volume if α-1 adrenergic receptor agonist is applied to the bath? Explain your answer.
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The figure below shows a signaling pathway activated by the bindiıng of adrehalMNe LU the beta-adrenergic receptor. Binding of adrenaline to the receptor causes GTP-binding and activation of G proteins. Active GTP-bound G protein activates adenylate cyclase to initiate a signaling cascade that affects cellular responses, and includes cellular changes to mediate increased heart rate and accounts for the flight-or-fight response. activated adenylate cyclase adrenaline activated B-adrenergic receptor adenylate cyclase G protein subunit 22 GTP SDP conformational ATP CAMP change in receptor heterotrimeric G protein ACAMP inactive protein kinase A active protein kinase A 4 cellular responses Consider the homozygous mutation in which a cell produces a variant of adenylate cyclase that can no longer be activated Which of the following are true in this cell? Select all that apply. Heart rate increases Protein Kinase A is not activated CAMP levels are lower than normal Heart rate decreases
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Describe the 3 main steps for activation of receptor tyrosine kinases.