Deck 12: Indirect Mechanisms of Synaptic Transmission

Question 1

When comparing direct and indirect synaptic transmission, indirect synaptic transmission

A) mediates reflex arcs in the spinal cord.
B) is mediated by ligand-gated ion channels.
C) is required for high speed, integrated motor performance.
D) is mediated by metabotropic receptors that activate intracellular second-messenger pathways.
E) mediates skeletal muscle contraction.

Answer 1

D

Question 2

When comparing ionotropic and metabotropic receptors which of the following is true?

A) Ionotropic receptors mediate their effects faster than metabotropic receptors.
B) Metabotropic receptors mediate their effects faster than ionotropic receptors.
C) A single ionotropic receptor can activate a variety of second messenger effects in the cell.
D) Metabotropic receptors can directly mediate the flux of ions across the cell membrane.
E) Metabotropic signaling within the cell is terminated when the ligand un-binds from the receptor

Answer 2

A

Question 3

How many transmembrane domains do all G protein-coupled metabotropic receptors have?

A) Each subtype of G protein-coupled metabotropic receptor has a different number of transmembrane domains.
B) All G protein-coupled metabotropic receptors has 12 transmembrane domains
C) All G protein-coupled metabotropic receptors has 7 transmembrane domains
D) All G protein-coupled metabotropic receptors has 4 transmembrane domains
E) All G protein-coupled metabotropic receptors has 5 transmembrane domains

Answer 3

C

Question 4

Each particular metabotropic receptor (e.g., a metabotropic glutamate receptor)

A) exists one-to-one with a particular G protein complex in the cell.
B) couples to only one type of second messenger signaling system in the cytoplasm.
C) can only couple to one subtype of G protein (i.e., G_i).
D) can couple to a variety of G proteins that are more plentiful than receptors.
E) competes with other metabotropic receptors for the same G protein.

Question 5

When different transmitters or hormones act through different G protein-coupled metabotropic receptors,

A) each receptor is always coupled to a different type of G protein.
B) multiple receptors can be coupled to the same type of G protein.
C) the G protein that is coupled to the receptor is determined by the transmitter or hormone that is the ligand for that receptor.
D) the second messenger cascade that is coupled to the receptor is determined by the transmitter or hormone that is the ligand for that receptor.
E) the second messenger cascade that is coupled to the receptor is always determined by the specific G protein type that is coupled to that receptor.

Question 6

The G proteins that coupled to metabotropic receptors are

A) small homomeric GTP binding proteins made up of only α-subunits.
B) heterotrimeric GTP binding proteins made up of α-, β-, and γ-subunits.
C) heterotrimeric cGMP binding proteins made up of α-, β-, and γ-subunits.
D) small homomeric GTP binding proteins made up of only β-subunits.
E) small homomeric GTP binding proteins made up of only γ-subunits.

Question 7

For G protein-coupled metabotropic receptors, GTP binds to the

A) cytoplasmic surface of the metabotropic receptor.
B) transmembrane domains of the metabotropic receptor.
C) β-subunitof the heterotrimer.
D) α-subunit of the heterotrimer.
E) the γ-subunit of the heterotrimer.

Question 8

How is G protein-mediated signaling terminated?

A) Desensitization of the G protein-coupled receptor terminates the signaling previously initiated by active G proteins.
B) Hydrolysis of GDP to GTP by the endogenous GTPase activity of the α-subunit leads to reassociation of the αβγ-complex, terminating the response.
C) Exchange of GDP for GTP by the endogenous GTPase activity of the α-subunit leads to reassociation of the αβγ-complex, terminating the response.
D) Exchange of GTP for GDP by the endogenous GTPase activity of the α-subunit leads to reassociation of the αβγ-complex, terminating the response.
E) Hydrolysis of GTP to GDP by the endogenous GTPase activity of the α-subunit leads to reassociation of the αβγ-complex, terminating the response.

Question 9

Which of the following tests would be effective at determining if a transmitter action was mediated by a G protein-coupled receptor?

A) Adding extra GTP to the cell cytoplasm to activate G protein-coupled receptors.
B) The addition of cholera toxin to inhibit G protein-coupled receptors.
C) The addition of GDP-β-s enhances and greatly prolongs agonist-induced activation of G protein-mediated responses.
D) The addition of GTP-γ-s enhances and greatly prolongs agonist-induced activation of G protein-mediated responses.
E) The addition of pertussis toxin to activate G protein-coupled receptors.

Question 10

G proteins are activated when GDP is

A) phosphorylated to GTP while bound to the α-subunit.
B) dephosphorylated to GDP while bound to the α-subunit.
C) exchanged for the GTP that is bound to the α-subunit.
D) exchanged for the GDP that is bound to the α-subunit.
E) exchanged for the GDP that is bound to the βγ-subunit.

Question 11

The particular neurotransmitter present at a synapse

A) indicates the subtype of G protein that will be coupled the receptor.
B) does not indicate the subtype of G protein or second messenger that will be coupled to the receptor.
C) indicates the second messenger that will be coupled to the receptor.
D) indicates the ion channels that will be targeted by second messengers.
E) indicates if the effect on the synapse will be excitatory or inhibitory.

Question 12

Non-hydrolysable GTP analog is an analog of GTP that

A) cannot bind to G proteins associated with metabotropic receptors.
B) is rapidly cleaved by GTPases to GDP.
C) cannot be cleaved by GTPases to GDP.
D) cannot be used in G protein-mediated signaling.
E) remains persistently bound in a heterotrimer.

Question 13

What would happen to G protein-coupled metabotropic signaling in a cell if you removed GTP from the cell cytoplasm?

A) This would enhance G protein-coupled metabotropic receptor signaling.
B) This would make G protein-coupled metabotropic receptor signaling irreversible.
C) This would not affect G protein-coupled metabotropic receptor signaling.
D) This would block G protein-coupled metabotropic receptor signaling.
E) This would cause G protein-coupled metabotropic receptors to switch to a different signaling pathway.

Question 14

What would happen to metabotropic signaling in a cell if you added cholera toxin?

A) This would irreversibly activate metabotropic signaling mediated by G_s.
B) This would irreversibly activate metabotropic signaling mediated by G_i and G_o.
C) This would irreversibly inhibit metabotropic signaling mediated by G_s.
D) This would irreversibly inhibit metabotropic signaling mediated by G_i and G_o.
E) This would have no effect on metabotropic signaling.

Question 15

What would happen to metabotropic signaling in a cell if you added GDP-β-s to the cell cytoplasm?

A) This would irreversibly activate all G protein-coupled metabotropic signaling.
B) This would irreversibly inhibit all G protein-coupled metabotropic signaling.
C) This would have no effect on G protein-coupled metabotropic signaling.
D) This would irreversibly activate G protein-coupled metabotropic signaling mediated by only G_i and G_o.
E) This would irreversibly inhibit G protein-coupled metabotropic signaling mediated by only G_i and G_o.

Question 16

What would happen to metabotropic signaling in a cell if you added GTP-γ-s to the cell cytoplasm?

A) This would irreversibly activate all G protein-coupled metabotropic signaling.
B) This would irreversibly inhibit all G protein-coupled metabotropic signaling.
C) This would have no effect on G protein-coupled metabotropic signaling.
D) This would irreversibly activate G protein-coupled metabotropic signaling mediated by only G_i and G_o.
E) This would irreversibly inhibit G protein-coupled metabotropic signaling mediated by only G_i and G_o.

Question 17

You are recording calcium channel currents using whole cell patch clamp methods from frog sympathetic ganglia neurons with GTP-γ-s included in the patch pipet. What would happen when you added norepinephrine to the solution bathing this neuron.

A) Norepinephrine would activate calcium currents for a shorter amount of time than normal.
B) Norepinephrine would switch its target and couple to potassium currents.
C) Norepinephrine would not affect calcium currents.
D) Norepinephrine would persistently activate calcium currents.
E) Norepinephrine would persistently inhibit calcium currents.

Question 18

Which of the following experiments provided experimental evidence that potassium channels in cardiac muscle cells were opened by the direct action of βγ-subunits of activated G proteins?

A) Cardiac potassium channels were opened in inside-out patch clamp recordings when pure recombinant α-subunit was applied to the intracellular side of the patch.
B) Cardiac potassium channels were opened in inside-out patch clamp recordings when pure recombinant βγ-subunit was applied to the intracellular side of the patch.
C) Removal of intracellular GTP prevents the activation of cardiac muscarinic receptors from opening of potassium channels.
D) The addition of intracellular Gpp(NH)p prolongs the opening of potassium channels after activation of cardiac muscarinic receptors.
E) Muscarinic receptor-mediated activation of potassium channels is blocked by pertussis toxin.

Question 19

What would happen in muscle cells dissociated from the atrium of the heart if you added acetylcholine in the presence of an inhibitor of RGS proteins?

A) There would be a decrease in potassium channel activity.
B) There would be an increase in potassium channel activity that lasted shorter than normal.
C) There would be an increase in potassium channel activity that lasted longer than normal.
D) There would be no change in potassium channel activity.
E) There would be an increase in calcium channel activity that lasted longer than normal.

Question 20

What does it mean that inhibition of calcium channels by norepinephrine is "voltage-dependent"?

A) The inhibition of calcium channels by norepinephrine only occurs if the resting membrane potential is depolarized.
B) Norepinephrine is inhibiting a voltage-gated ion channel.
C) Norepinephrine is activating a voltage-gated ion channel.
D) The inhibition of calcium channels by norepinephrine is enhanced by depolarization.
E) The inhibition of calcium channels by norepinephrine is reduced by depolarization.

Question 21

Feedback inhibition, or auto-inhibition, is defined as

A) diffusion around sites of release to affect neighboring cells.
B) the use of a chemical signal that communicates from the presynaptic cell to the postsynaptic cell.
C) the use of a second messenger signal within the postsynaptic cell.
D) the use of a chemical signal that communicates from the postsynaptic cell to the presynaptic cell.
E) the use of a chemical signal that communicates from the presynaptic cell back onto the same presynaptic cell.

Question 22

Metabotropic receptors that couple to second messenger signaling

A) all trigger the generation of cAMP in cells.
B) can activate one of many enzymes in cells.
C) have faster action than direct metabotropic signaling.
D) all inhibit ion channels within cells.
E) all trigger the cleavage of PIP2 to generate IP3 and DAG.

Question 23

What happens when PIP2 is cleaved by phospholipase A2?

A) This cleavage generates cAMP that acts as a second messenger.
B) This cleavage generates active protein kinase A that phosphorylates proteins.
C) This cleavage generates arachidonic acid that acts as a second messenger.
D) This cleavage generates 12-HPETE that acts as a second messenger.
E) This cleavage generates inositol-1,4,5-trisphosphate (IP3) and diacylglycerol (DAG) that act as second messengers.

Question 24

In a cell with β-adrenergic receptors coupled to the cAMP second messenger system, what would happen to that signaling pathway if you blocked adenylate cyclase?

A) This would make β-adrenergic receptor activation using the cAMP pathway irreversible.
B) This would have no effects on β-adrenergic receptor signaling using the cAMP pathway.
C) This would make β-adrenergic receptor activation using the cAMP pathway last longer.
D) This would prevent β-adrenergic receptor activation from causing any effects through the cAMP pathway.
E) This would mimic the signaling pathway, causing the same effect as activation of the β-adrenergic receptor.

Question 25

In a cell with β-adrenergic receptors coupled to the cAMP second messenger system, what would happen to that signaling pathway if you blocked phosphodiesterases?

A) This would make β-adrenergic receptor activation of adenylate cylase irreversible.
B) This would make β-adrenergic receptor activation using the cAMP pathway last longer.
C) This would have no effects on β-adrenergic receptor signaling using the cAMP pathway.
D) This would prevent β-adrenergic receptor activation from causing any effects through the cAMP pathway.
E) This would mimic the signaling pathway, causing the same effect as activation of the β-adrenergic receptor.

Question 26

In a cell with β-adrenergic receptors coupled to the cAMP second messenger system, what would happen to that signaling pathway if you added forskolin?

A) This would make β-adrenergic receptor activation using the cAMP pathway irreversible.
B) This would make β-adrenergic receptor activation of adenylate cylase last longer.
C) This would have no effects on β-adrenergic receptor signaling using the cAMP pathway.
D) This would mimic that activation of the PIP2 pathway.
E) This would mimic the signaling pathway, causing the same effect as activation of the β-adrenergic receptor.

Question 27

Which experimental approach could provide evidence that norepinephrine uses the cAMP second messenger system to modulate calcium channels?

A) Apply a blocker of adenylate cylclase to determine if the modulation of calcium channels is also blocked.
B) Apply a blocker of phospholipase C to determine if the modulation of calcium channels is also blocked.
C) Apply a blocker of phospholipase A2 to determine if the modulation of calcium channels is also blocked.
D) Apply a blocker of protein kinase C to determine if the modulation of calcium channels is also blocked.
E) Apply a blocker of phosphatidylinositol 3-kinase to determine if the modulation of calcium channels is also blocked.

Question 28

An example of convergent signaling mediated by indirectly coupled receptors is…

A) Phospholipase C cleaving PIP₂ to generate both DAG and IP₃.
B) GABA and Norepinephrine receptors both using G proteins to mediate signaling.
C) Muscarinic receptors in guinea pig sympathetic neurons that can affect five different potassium currents.
D) GABA receptor activation of both G_i and G_o proteins that leads to the opening of potassium channels and the closing of calcium channels.
E) A rat superior cervical sympathetic neuron modulated by multiple transmitters acting through many different G protein-coupled pathways that influence several types of ion channels.

Question 29

Endocannabinoids are formed by

A) adenylate cyclase cleavage of membrane phospholipids.
B) phospholipase A2 cleavage of cAMP.
C) phospholipase C or D cleavage of cAMP.
D) adenylate cyclase cleavage of cAMP.
E) phospholipase C or D cleavage of membrane phospholipids.

Question 30

Which of the following neurotransmitters is not stored in synaptic vesicles?

A) Glutamate
B) Acetylcholine
C) Endocannabinoids
D) Norepinephrine
E) Dopamine

Question 31

Anterograde signaling is defined as

A) diffusion around sites of release to affect neighboring cells.
B) the use of a chemical signal that communicates from the presynaptic cell to the postsynaptic cell.
C) the use of a second messenger signal within the postsynaptic cell.
D) the use of a chemical signal that communicates from the postsynaptic cell to the presynaptic cell.
E) the use of a chemical signal that communicates from the presynaptic cell back onto the same presynaptic cell.

Question 32

Nitric oxide

A) is packaged into synaptic vesicles for release.
B) is moved across cell membranes by a transporter that uses ATP as the energy for transport.
C) is moved across cell membranes by a transporter that exchanges sodium ions for nitric oxide.
D) is moved across cell membranes by facilitated diffusion.
E) diffuses directly across cell membranes.

Question 33

Nitric oxide is a(n)

A) peptide transmitter.
B) amino acid transmitter.
C) gas transmitter.
D) small molecule transmitter.
E) enzyme.

Question 34

How is nitric oxide synthesized?

A) Nitric oxide is synthesized from heme oxygenase (HO) after activation by the calcium-calmodulin complex.
B) Nitric oxide is synthesized from heme oxygenase (HO) after activation by guanylate cyclase.
C) Nitric oxide is synthesized from guanylate cyclase after activation by the calcium-calmodulin complex.
D) Nitric oxide is synthesized from nitric oxide synthase (NOS) after activation by the calcium-calmodulin complex.
E) Nitric oxide is synthesized from nitric oxide synthase (NOS) after activation by guanylate cyclase.

Question 35

How does the transmitter nitric oxide mediate its actions in cells?

A) Nitric oxide diffuses across cell membranes and binds to an ionotropic receptor.
B) Nitric oxide diffuses across cell membranes and only stimulates guanylate cyclase to synthesize cGMP.
C) Nitric oxide diffuses across cell membranes and stimulates guanylate cyclase to synthesize cGMP or can s-nitrosylate proteins.
D) Nitric oxide diffuses across cell membranes and only s-nitrosylates proteins.
E) Nitric oxide diffuses across cell membranes and binds to a metabotropic receptor.

Question 36

How is nitric oxide (NO) terminated after release?

A) NO is taken back up into cells by a transporter.
B) NO is degraded by a specific enzyme in the synaptic cleft.
C) NO is a reactive gas that is inactivated when it reacts with proteins or superoxides.
D) NO remains active until it diffuses away from the synapse.
E) NO action is not terminated.

Question 37

Why are the physiological effects of Nitric oxide (NO) affected by phosphodiesterase inhibitors?

A) Phosphodiesterase inhibitors prevent re-uptake of NO into cells.
B) Phosphodiesterase inhibitors prolong the lifetime of cGMP.
C) Phosphodiesterase inhibitors prolong the lifetime of cAMP.
D) Phosphodiesterase inhibitors prevent the enzymatic breakdown if NO.
E) Phosphodiesterase inhibitors block the reaction of NO with proteins.

Question 38

What is the concentration of calcium in cell cytoplasm?

A) 100 nM
B) 100 µM
C) 1 µM
D) 100 mM
E) 1 mM

Question 39

What is a "calcium microdomain"?

A) The calcium within the synaptic cleft after nerve terminal activity
B) The elevation of cytoplasmic calcium within the entire neuron after activity
C) A small localized volume of the cytoplasm within which calcium is elevated after entry across the plasma membrane or release from intracellular stores
D) The total amount of calcium within a cell at rest
E) The total amount of calcium outside of a cell at rest

Question 40

Ionotropic nicotinic acetylcholine receptors are known to excite cells based on the flux of sodium ions into the cell cytoplasm when these channels are activated near resting membrane potential. However, how can the calcium flux through these receptors lead to an inhibitory influence?

A) Calcium flux through nicotinic receptors can act back on the nicotinic receptor to inhibit it.
B) Calcium flux through nicotinic receptors directly depolarizes the cell.
C) Calcium flux through nicotinic receptors directly hyperpolarizes the cell.
D) Calcium flux through nicotinic receptors can activate a calcium-activated potassium channel whose potassium flux hyperpolarizes the cell.
E) Calcium flux through nicotinic receptors can activate a calcium-activated potassium channel whose potassium flux depolarizes the cell.

Question 41

Which protein is most commonly used by cells to bind cytoplasmic calcium and trigger biochemical events within the cell?

A) Aequorin
B) Fura-2
C) Calmodulin
D) BAPTA
E) Nicotinic acetylcholine receptors

Question 42

When we are excited or frightened, our heart rate increases. Explain how nervous system uses either direct or indirect transmission to mediate this type of response?

Question 43

How many different types of G protein-coupled metabotropic receptors are present in the nervous system? Include five different examples of G protein-couple metabotropic receptors and how each can maintain transmitter specificity, but all be coupled to G proteins.

Question 44

Explain how G protein-coupled receptors become activated after binding neurotransmitter ligand?

Question 45

How is the lifetime of activated G proteins controlled?

Question 46

What is the difference between direct and indirect actions of receptor activated G proteins on ion channels?

Question 47

By what G protein-coupled signaling mechanism does stimulation of the vagus nerve slow the heartbeat?

Question 48

When using the cell-attached patch clamp recording technique to record single potassium channel currents from cardiac muscle cells, explain why muscarinic receptor agonists applied to the bath outside of the patch are unable to activate these potassium channels?

Question 49

How is cAMP used as a second messenger in indirect actions of metabotropic receptors?

Question 50

Explain how norepinephrine causes an increase in the rate and force of contraction of the heart.

Question 51

Compare and contrast convergence vs. divergence of signals generated by indirectly coupled receptors?

Question 52

List four factors that determine how a cell responds to transmitters.

Question 53

How are endocannabinoids synthesized, released, and used to modulate synapses?

Question 54

How is Nitric oxide generated as a result of acetylcholine acting on vascular smooth muscle cells?

Question 55

Describe 4 mechanisms that cells use to regulating the cytoplasmic calcium concentration.

Question 56

Explain why synaptic interactions mediated by indirect mechanisms typically develop more slowly and last much longer than those mediated by direct mechanisms