NROS 310 Exam 3 Study Questions || with 100% Errorless
Solutions.
Describe endocrine, paracrine, and autocrine signaling. correct answers Endocrine: An endocrine
cell releases a hormone into the blood stream to target a receptor on the target cell.
Paracrine: A signaling cell releases a local mediator to target cells (neighboring cells).
Autocrine: A cell releases a chemical signal to target itself.
How does a hormone that is released generally throughout the body end up having different
effects on (or no effects on) different cells? correct answers Hormones can have different effects
throughout the body depending on the types of GPCR pathways that are activated. Cell context
(protein and ion concentrations).
Describe what is meant by the term second messenger. For each of the following second
messengers, describe how they are generated and how they are gotten rid of: cAMP, cGMP,
Ca2+, and IP3. correct answers A second messenger is a protein who's levels increase as a
response to receptor activation, they also trigger downstream effects (cascades).
cAMP: Adenylyl cyclase is the enzyme to make cAMP. PDE breaks down cAMP. cAMP
activates PKA.
cGMP: SGC is the enzyme that makes cGMP activates PKG which phosphorylates cation
channels in rod cells and is degraded by PDE.
Ca2+: IP3 or kinases (e.g. PKA) activate Ca2+ channels. They are removed by phosphatases.
Ca2+ pump maintain homeostasis.
IP3: PLC (Pip2 to IP3 and DAG). Negative feedback step uses PPP.
Why is Ca2+ considered a second messenger but Na+ is not? correct answers Because Ca2+ is
used in the activation of pathways and other biological processes unlike Na+.
What are the main differences between ion channel coupled receptors, GPCRs, and enzyme
linked receptors? correct answers Ion channel coupled receptors: They are classical
neurotransmitter receptors where a signaling molecule binds and the channel opens.
GPCRs: Contains a seven transmembrane domain receptor for ligand binding, a heterotrimeric
subunit (alpha, beta, gamma) which is mediated by the alpha subunit binding GDP and GTP
when active separating alpha from the other two.
Enzyme linked receptors: Two halves of a molecule are separated and a ligand brings them
together which activates them through dimerization.
, What types of biological processes would be best served by a negative feedback type of
signaling? What types of biological processes would be best served by a positive feedback type
of signaling? correct answers Negative feedback best serves things that require homeostasis in
order to keep things at a set level such as heart rate or glucose level.
Positive feedback best serves thing such as childbirth (Oxytocin) and apoptosis (Programmed
cell death), for when the body needs to reach extremes.
How can a simple signaling molecule such as acetylcholine have such different effects on
different cells? correct answers Context, the receptor, and the circuitry of the brain matter
allowing for different effects from the same molecule.
GPCRs have been described as GEFs for heterotrimeric G proteins. Is this accurate? Explain
why or why not. correct answers Yes, GPCR are described as heterotrimeric because is it
contains a alpha, beta, and gamma subunit that form the G protein. This G protein will exhibit a
conformation change when a ligand binds to the GPCR causing the alpha-GDP to break off and
form alpha-GTP
Outline the signal transduction pathway by which a neuropeptide could result in both the
activation of existing ion channels and the production of additional ion channels assuming that
the effect is mediated by a GPCR coupled to adenylyl cyclase. Include the shutting off of the
system by GRKs and arrestin and include other negative feedback steps. correct answers Draw
the GPCR cAMP pathway (Lecture 21).
Where does amplification occur in the pathway you outlined for a GPCR pathway? correct
answers Amplification occurs when increased levels of cAMP activate PKA to promote
transcription factors and phosphorylation of ion channels.
What is the main effect of activating Gs on cAMP levels? What is the effect of activating Gi on
cAMP levels? How can interactions with either G protein cause an increase in cAMP? correct
answers Activation of Gs causes an increase in cAMP levels (Activates AC 1).
Activation of Gi causes a decrease in cAMP levels (Inhibits AC 1 and activates AC 2).
Activating Gs (alpha subunit activates AC 2) and alpha-GDP in the Gi (activates AC 2) resulting
in increased levels of cAMP.
What effect would the inhibition of a phosphodiesterase (PDE) have on cAMP levels? correct
answers Inhibiting PDE would cause and increase in cAMP levels.
Describe the effects of cholera toxin, pertussis toxin, GTP-gS, and GDP-bS on GPCR signaling.
correct answers Cholera toxin increases the activity of Gs leading to higher cAMP levels because
the alpha subunit is always active.
Pertussis toxin inhibits the activity of Gi leading to higher levels of cAMP levels because it
inhibits the inhibitor in AC 1.
Solutions.
Describe endocrine, paracrine, and autocrine signaling. correct answers Endocrine: An endocrine
cell releases a hormone into the blood stream to target a receptor on the target cell.
Paracrine: A signaling cell releases a local mediator to target cells (neighboring cells).
Autocrine: A cell releases a chemical signal to target itself.
How does a hormone that is released generally throughout the body end up having different
effects on (or no effects on) different cells? correct answers Hormones can have different effects
throughout the body depending on the types of GPCR pathways that are activated. Cell context
(protein and ion concentrations).
Describe what is meant by the term second messenger. For each of the following second
messengers, describe how they are generated and how they are gotten rid of: cAMP, cGMP,
Ca2+, and IP3. correct answers A second messenger is a protein who's levels increase as a
response to receptor activation, they also trigger downstream effects (cascades).
cAMP: Adenylyl cyclase is the enzyme to make cAMP. PDE breaks down cAMP. cAMP
activates PKA.
cGMP: SGC is the enzyme that makes cGMP activates PKG which phosphorylates cation
channels in rod cells and is degraded by PDE.
Ca2+: IP3 or kinases (e.g. PKA) activate Ca2+ channels. They are removed by phosphatases.
Ca2+ pump maintain homeostasis.
IP3: PLC (Pip2 to IP3 and DAG). Negative feedback step uses PPP.
Why is Ca2+ considered a second messenger but Na+ is not? correct answers Because Ca2+ is
used in the activation of pathways and other biological processes unlike Na+.
What are the main differences between ion channel coupled receptors, GPCRs, and enzyme
linked receptors? correct answers Ion channel coupled receptors: They are classical
neurotransmitter receptors where a signaling molecule binds and the channel opens.
GPCRs: Contains a seven transmembrane domain receptor for ligand binding, a heterotrimeric
subunit (alpha, beta, gamma) which is mediated by the alpha subunit binding GDP and GTP
when active separating alpha from the other two.
Enzyme linked receptors: Two halves of a molecule are separated and a ligand brings them
together which activates them through dimerization.
, What types of biological processes would be best served by a negative feedback type of
signaling? What types of biological processes would be best served by a positive feedback type
of signaling? correct answers Negative feedback best serves things that require homeostasis in
order to keep things at a set level such as heart rate or glucose level.
Positive feedback best serves thing such as childbirth (Oxytocin) and apoptosis (Programmed
cell death), for when the body needs to reach extremes.
How can a simple signaling molecule such as acetylcholine have such different effects on
different cells? correct answers Context, the receptor, and the circuitry of the brain matter
allowing for different effects from the same molecule.
GPCRs have been described as GEFs for heterotrimeric G proteins. Is this accurate? Explain
why or why not. correct answers Yes, GPCR are described as heterotrimeric because is it
contains a alpha, beta, and gamma subunit that form the G protein. This G protein will exhibit a
conformation change when a ligand binds to the GPCR causing the alpha-GDP to break off and
form alpha-GTP
Outline the signal transduction pathway by which a neuropeptide could result in both the
activation of existing ion channels and the production of additional ion channels assuming that
the effect is mediated by a GPCR coupled to adenylyl cyclase. Include the shutting off of the
system by GRKs and arrestin and include other negative feedback steps. correct answers Draw
the GPCR cAMP pathway (Lecture 21).
Where does amplification occur in the pathway you outlined for a GPCR pathway? correct
answers Amplification occurs when increased levels of cAMP activate PKA to promote
transcription factors and phosphorylation of ion channels.
What is the main effect of activating Gs on cAMP levels? What is the effect of activating Gi on
cAMP levels? How can interactions with either G protein cause an increase in cAMP? correct
answers Activation of Gs causes an increase in cAMP levels (Activates AC 1).
Activation of Gi causes a decrease in cAMP levels (Inhibits AC 1 and activates AC 2).
Activating Gs (alpha subunit activates AC 2) and alpha-GDP in the Gi (activates AC 2) resulting
in increased levels of cAMP.
What effect would the inhibition of a phosphodiesterase (PDE) have on cAMP levels? correct
answers Inhibiting PDE would cause and increase in cAMP levels.
Describe the effects of cholera toxin, pertussis toxin, GTP-gS, and GDP-bS on GPCR signaling.
correct answers Cholera toxin increases the activity of Gs leading to higher cAMP levels because
the alpha subunit is always active.
Pertussis toxin inhibits the activity of Gi leading to higher levels of cAMP levels because it
inhibits the inhibitor in AC 1.
