Deck 9: Ion Transport Across Cell Membranes

Question 1

Unlike secondary active transport, primary active transport

A) relies on the movement of sodium down its electrochemical gradient.
B) is exemplified by sodium-calcium exchange.
C) is reversible.
D) depends on sodium-potassium ATPase.
E) uses energy provided by hydrolysis of ATP.

Answer 1

E

Question 2

In the absence of transport mechanisms, ions would only move across the membrane along their electrochemical gradient. What consequences would this have?

A) The concentration gradients and the potential across the cell membrane would disappear.
B) The concentration gradients across the membrane would be recovered through passive mechanisms relying on Donnan equilibrium.
C) The resting membrane potential of the cells would become more hyperpolarized.
D) Neurons would continuously fire action potentials.
E) Astrocytes, not neurons, would rest at 0 mV.

Answer 2

A

Question 3

What drives primary active transport?

A) Ion exchange
B) Sodium
C) Potassium
D) Water
E) The hydrolysis of ATP

Answer 3

E

Question 4

What drives secondary active transport?

A) Metabolic energy
B) ATP
C) Ion flux down their electrochemical gradient
D) Osmotic pressure
E) Diffusion

Question 5

Why is the sodium-potassium exchange pump said to be electrogenic?

A) Because it transports the same number of positively charged ions in and out of the cell membrane
B) Because it transports unequal numbers of sodium and potassium ions across the membrane
C) Because ion binding requires a change in membrane potential
D) Because ion transport can only be triggered by electrical stimuli
E) Because it has an electroneutral stoichiometry

Question 6

What is the first event for ion transport through the sodium-potassium exchange pump?

A) Sodium binding to the inward-facing sites of the pump
B) Potassium binding to the inward-facing sites of the pump
C) Potassium binding to the outward-facing sites of the pump
D) ATP hydrolysis
E) ATP phosphorylation

Question 7

How does the sequence of events underlying ion transport through the sodium-potassium exchange pump end?

A) Dephosphorylation of the pump
B) Binding of sodium ions
C) Intracellular binding of potassium ions
D) Release of potassium ions into the cytoplasm
E) Opening of an aqueous pore in the protein

Question 8

How does rise in intracellular sodium concentration affect the resting membrane potential through the activity of the sodium-potassium exchange pump?

A) It would trigger membrane depolarization.
B) It would not lead to significant changes in the resting membrane potential.
C) It would trigger membrane hyperpolarization.
D) It would change the stoichiometry of the transport process.
E) It would promote phosphorylation and desphosphorylation of the pump, which would make the cell membrane leakier.

Question 9

What is one of the main functional consequences of increasing cytoplasmic levels of calcium in muscle fibers?

A) Trigger muscle relaxation
B) Prevent acetylcholine receptor activation
C) Inhibit action potential propagation
D) Speed up action potential propagation
E) Initiate muscle contraction

Question 10

What is one of the main functional consequences of increasing cytoplasmic levels of calcium in neurons?

A) Promote neurotransmitter release
B) Hyperpolarize the resting membrane potential
C) Change the membrane capacitance
D) Depolarize the threshold for action potential initiation
E) Change the driving force for sodium ions

Question 11

Which intracellular organelles contribute to return the intracellular calcium concentration to its resting levels?

A) Golgi apparatus and cell nucleus
B) Lysosomes and synaptic vesicles
C) Endoplasmic reticulum and cell nucleus
D) Endoplasmic/sarcoplasmic reticulum and mitochondria
E) Mitochondria and lysosomes

Question 12

There are _______ classes or families of calcium ATPases.

A) 2
B) 3
C) 4
D) 5
E) 10

Question 13

Why is the recovery of intracellular calcium concentration after calcium influx not influenced by membrane potential?

A) Because the transport cycle of the plasma cell membrane calcium ATPase is electrogenic
B) Because the plasma cell membrane calcium ATPase has a high affinity for calcium
C) Because calcium binding to the plasma cell membrane calcium ATPase is voltage-dependent
D) Because the transport cycle of the plasma cell membrane calcium ATPase is electroneutral
E) Because the plasma cell membrane calcium ATPase has a low transport capacity

Question 14

How does the calcium transport cycle via the calcium ATPase begin?

A) It begins with the attachment of two calcium ions to cytoplasmic binding sites.
B) It begins with the attachment of two protons to extracellular binding sites.
C) It begins with the hydrolysis of ATP.
D) It begins with opening of a channel pore.
E) It begins with calcium binding to the extracellular side of the calcium ATPase.

Question 15

What is the stoichiometry of the NCX transport system?

A) Two potassium ions outward for every three sodium ions entering the cell (3 Na⁺:2K⁺)
B) Two calcium ions outward for every two protons entering the cell (2 H⁺:2 Ca²⁺)
C) One calcium ion outward for every three sodium ions entering the cell (3 Na⁺:1 Ca²⁺)
D) One ion X outward for every one sodium and one calcium ions entering the cell (1Na⁺:1 Ca²⁺:1 X)
E) Na⁺ and Ca²⁺ are not transported in a fixed ratio through the NCX transport system

Question 16

How does reducing the extracellular sodium concentration increase the intracellular calcium concentration?

A) By increasing passive calcium influx through the cell membrane
B) By reducing the activity of the NCX transport system
C) By hyperpolarizing the resting membrane potential
D) By inverting the electrochemical gradient for calcium
E) By inhibiting the activity of the Na⁺/K⁺ ATPase

Question 17

How can ion exchange mechanisms be made to run backwards?

A) By altering one or more of the ion gradient involved in the exchange
B) By inhibiting ATP hydrolysis
C) By hyperpolarizing the resting membrane potential
D) By replacing extracellular sodium with lithium
E) By removing calcium from the extracellular solution

Question 18

How can you calculate the energy dissipated by sodium entry through the NCX transport system?

A) By dividing the sum of all charges moved across the NCX transport system by their driving force
B) By subtracting the resting membrane potential from the equilibrium potential for sodium
C) By calculating the equilibrium potential for sodium
D) By analyzing the 3D crystal structure of the NCX transport system
E) By multiplying the charge moved across the membrane by the driving force for this movement

Question 19

When does the NCX stop moving ions across the membrane?

A) When the energy dissipated by sodium entry equals that associated with movement of calcium ions
B) When the resting membrane potential equals the reversal potential for calcium
C) When the driving force for sodium is different than 0 mV
D) When there is no net driving force for calcium
E) When there is not ATP

Question 20

How does the NCKX system differ from the NCX system?

A) The NCX system is only expressed in the outer segment of vertebrate retinal rod cells.
B) The NCKX system is only expressed in muscle fibers.
C) The NCKX system is expressed in the plasma cell membrane, whereas the NCX system is expressed in the sarcoplasmic and endoplasmic reticulum and in mitochondria.
D) In addition to transporting sodium and calcium, NCKX transports potassium.
E) The NCKX system is a primary active transport mechanism, whereas the NCX system is a secondary active transport mechanism.

Question 21

What is the stoichiometry of the NCKX transport system?

A) One calcium and one potassium ion outward for every four sodium ions entering the cell (4 Na⁺:1 Ca²⁺:1K⁺)
B) Three potassium ions outward for every three sodium ions and one calcium entering the cell (3 Na⁺:1 Ca²⁺:3K⁺)
C) Two calcium ions outward for every two protons and one potassium entering the cell (2 H⁺:2 Ca²⁺:1K⁺)
D) One ion X outward for every one sodium, one potassium and one calcium ions entering the cell (1Na⁺:1 Ca²⁺:1K⁺:1 X)
E) Na⁺, K⁺ and Ca²⁺ are not transported in a fixed ratio through the NCX transport system

Question 22

Why is the regulation of intracellular chloride important in neurons?

A) Because it can change the threshold for action potential initiation
B) Because it determines the magnitude of synaptic excitation
C) Because it determines the polarity of synaptic inhibition
D) Because it controls the production of ATP
E) Because it has implications for calcium homeostasis

Question 23

What supplies the energy required for the inward chloride transport across the plasma cell membrane?

A) The movement of potassium down its concentration gradient
B) The movement of sodium down its concentration gradient
C) ATP hydrolysis
D) The Na⁺/K⁺ ATPase
E) The sodium-calcium exchanger

Question 24

What supplies the energy required for outward chloride transport across the plasma cell membrane?

A) The movement of potassium down its concentration gradient
B) The movement of sodium down its concentration gradient
C) ATP hydrolysis
D) The Na⁺/K⁺ ATPase
E) The sodium-calcium exchanger

Question 25

Which transporters are blocked by furosemide and bumetanide?

A) The chloride-bicarbonate exchanger
B) The NCX and NKCX systems
C) Vesicular transporters for the neurotransmitter glutamate
D) Plasma cell membrane transporters for the neurotransmitter glutamate
E) The inward chloride and outward potassium-chloride transporters

Question 26

What is the main function of chloride-bicarbonate exchangers?

A) Regulate cell volume
B) Maintain cells at their resting membrane potential
C) Regulate intracellular pH
D) Determine the polarity of synaptic inhibition
E) Determine the polarity of synaptic excitation

Question 27

Where are neurotransmitters synthesized?

A) Nucleus
B) Endoplasmic and sarcoplasmic reticulum
C) Cytoplasm
D) Mitochondria
E) Golgi apparatus

Question 28

Where are neurotransmitters stored?

A) Synaptic vesicles
B) Glial cells
C) Dendrites
D) Soma
E) Axon initial segment

Question 29

Each of these is a vesicular neurotransmitter transporter except

A) VMAT.
B) VAChT.
C) VGAT.
D) GAT.
E) VGLUT.

Question 30

Which ion, in addition to protons, is cotransported into synaptic vesicles together with glutamate?

A) Sodium
B) Chloride
C) Potassium
D) Calcium
E) GABA

Question 31

What is one of the main functional deficits of VGLUT3 knockout mice?

A) Deafness
B) Blindness
C) Ataxia
D) Epilepsy
E) Migraine

Question 32

Which of the following is a GABA transporter mostly expressed in neurons?

A) GAT1
B) GAT3
C) GLAST
D) DAT
E) NET

Question 33

How is ACh recycled into presynaptic terminals?

A) Through the activity of VChAT
B) Through monoamine transporters
C) Through glutamate transporters
D) Through GABA transporters
E) ACh is not recycled into presynaptic terminals.

Question 34

How does reversed glutamate uptake affect brain function after brain damage by stroke or trauma?

A) By preventing glutamate receptor activation
B) By promoting glutamate uptake in presynaptic terminals
C) By promoting glial cell death
D) By triggering excitotoxicity in the damaged area
E) Glutamate transporters can only transport glutamate towards the cell cytoplasm, not into the extracellular space.

Question 35

What unique feature distinguishes GLYT2 glycine transporters from other members of the SLC6 family?

A) It is only expressed in neurons.
B) It is only expressed in presynaptic terminals.
C) Its transport stoichiometry is three sodium to one chloride to one glycine.
D) It is only expressed in postsynaptic terminals.
E) It is only expressed extrasynaptically.

Question 36

What are two purposes served by the recovery of neurotransmitters?

A) 1) store neurotransmitter into synaptic vesicles; 2) promote neurotransmitter diffusion into glial cells
B) 1) trigger reversed uptake; 2) restore ionic gradients across the membrane
C) 1) dissipate ionic gradients across the membrane; 2) promote neurotransmitter degradation
D) 1) inhibit further neurotransmitter release; 2) promote excitotoxicity
E) 1) prevent neurotransmitter diffusion out of the synaptic cleft; 2) recover neurotransmitter molecules for release

Question 37

What are the α- and β-subunits of the sodium-potassium ATP responsible for?

A) The α-subunit is responsible for binding sodium ions. The β-subunit is responsible for binding potassium ions.
B) The α-subunit is responsible for the enzymatic activity of the pump and contains all the substrate-binding sites. The β-subunit has several extracellular glycosylation sites and is necessary for pump function.
C) The α-subunit is responsible for binding sodium and potassium ions. The β-subunit is the substrate of phosphorylation.
D) The α-subunit is not necessary for pump function. The β-subunit contains binding sites for sodium, potassium and ATP.
E) The sodium-potassium ATPase consists of a single polypeptide chain without a β-subunit.

Question 38

Which experimental approach has been used to determine the molecular structure of the sarcoplasmic and endoplasmic reticulum calcium ATPase?

A) Electrophysiology
B) Cloning
C) Computer modeling
D) X-ray crystallography
E) Genetic screening

Question 39

Which sodium-calcium exchangers have the shortest amino acidic sequence?

A) NCKX1
B) NCX1
C) NCKX2-4
D) NCX2-3
E) All exchangers have the same amino acid sequence length

Question 40

Which bacterial homologs have been used in crystallography studies to determine key structural features of eukaryotic neurotransmitter transporters?

A) LeuT_Aa and Glt_Ph
B) GAT and GLYT
C) NET and SERT
D) DAT and GAT
E) VMAT and VAChT

Question 41

Which chloride transporter is transiently expressed in the immature brain?

A) KCC2
B) NKCC1
C) NCX
D) NKCX
E) GLAST

Question 42

How do developmental changes in chloride transporter expression affect GABAergic transmission?

A) The developmental switch from NKCC1 to KCC2 allows GABA to become depolarizing.
B) Changes in chloride transporter expression do not alter GABAergic transmission.
C) In the immature brain, GABA transporters can transport both glutamate and GABA. The delayed expression of KCC2 promotes the substrate specificity of GABA transporters.
D) Developmental changes in chloride transporters allow GABAergic transmission to have faster kinetics.
E) The delayed expression of KCC2 allows GABA to evoke membrane hyperpolarization in the mature, not the immature brain.

Question 43

Which of the following transporters is the target of fluoexitine (Prozac), used in the treatment of psychiatric disorders such as depression and anxiety?

A) Monoamine transporters
B) GABA transporters
C) Glutamate transporters
D) Sodium-calcium exchangers
E) Vesicular transporters

Question 44

Summarize the difference between primary active transport and secondary active transport.

Question 45

Given that the sodium-potassium pump is electrogenic, how do you think intracellular injection of sodium would change the membrane potential of a neuron?

Question 46

What makes transporters electrogenic?

Question 47

Where are calcium pumps located in a cell?

Question 48

Which fundamental feature distinguishes plasma membrane from endoplasmic and sarcoplasmic reticulum calcium ATPases?

Question 49

Why is the overall transport capacity of the NCX transport system, despite having a lower affinity for calcium, 50 times greater than that of the calcium ATPase?

Question 50

How can the ion exchange mechanism of the NCX transport system be made to run backward?

Question 51

How can you calculate the energy dissipated by sodium entry via the NCX transport system?

Question 52

How does the NCX transport system in vertebrate retinal rods differ from that expressed in other cell types?

Question 53

Why is the regulation of intracellular chloride concentration important in neurons?

Question 54

Why is GABA depolarizing in the immature brain?

Question 55

What is the main function of chloride-bicarbonate exchangers?

Question 56

Which ionic gradients commonly drive neurotransmitter uptake into synaptic vesicles and in the cell cytoplasm?

Question 57

What are the main structural features of the sodium-potassium ATPase?

Question 58

Why is neurotransmitter uptake physiologically relevant?

Question 59

What is the mechanism of action of fluoexitine (Prozac), used in the treatment of psychiatric disorders such as depression and anxiety?