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NEUR 310 > Ion Channels and Receptors > Flashcards

Ion Channels and Receptors Flashcards

1
Q

How many voltage-gated potassium channel subunits assemble to form a functional channel?

A

Four.

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2
Q

Which segments of the voltage-gated potassium channel subunits form pore loops?

A

S5 and S6.

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3
Q

What is the selectivity filter when we refer to voltage-gated ion channels?

A

The for loop module: four for loops converging to create a narrow opening for which internal faces are lined with GYGVT residues (conferring electrostatic interaction with charged ions).

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4
Q

How is the selectivity filter of voltage-gated potassium channels filtering out negatively-charged ions such as chloride?

A

GYGVT residues of the for loop module contain negatively oxygen atoms charged facing the opening.

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5
Q

Why don’t cations smaller than potassium leak through the selectivity pore?

A

The hydration shell of ions is removed when passing through the pore. In order for the transaction to be energetically favourable, the passing ion must interact with carboxyl oxygens lining the pore. If cations are too small (not large enough), they will not be able to interact with the carboxyl oxygens, rendering their transaction unfavourable and thus very unlikely.

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6
Q

What structural characteristic of voltage-gated ion channels prevents them from getting stucked with an ion jamming?

A

The selectivity filter is simultaneously occupied by two cations. Therefore, electrostatic repulsions between the two ions facilitate their passing into the pore.

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7
Q

How can a change in membrane potential cause an ion channel to open?

A

Channels contain gating charges that move according to voltage. The movement of the sensors trigger a conformational change that lets ions flow in/out.

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8
Q

What segment of voltage-gated potassium channels forms the voltage-sensor?

A

S4. Every 3 amino acid of S4 is positively charged.

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9
Q

When we talk about a voltage gradient, where is that gradient spatially located exactly?

A

Across the membrane.

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10
Q

What is the functional utility of S1-3?

A

Create a chamber around S4 for it to move translationally into.

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11
Q

How is the movement of S4 changing the structural conformation of voltage-gated potassium channels?

A

It is pulling the S5-S6 segments of the pore module onto the internal faces of the cytoplasmic end of the module.

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12
Q

What happens to channel activity if the N-terminus tail is deleted?

A

Inactivation is eliminated, but activation and conduction preserved

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13
Q

Which structure of voltage-gated potassium channels is the “ball” in the ball & chain model?

A

N-terminus tail.

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14
Q

How can voltage-gated potassium channels acquire different specificities?

A

With different intracellular domains.

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15
Q

Which sodium channel subtypes are expressed in the adult CNS?

A

Nav1.1
Nav1.2
Nav1.6

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16
Q

Nav1.1 have been associated with which channelopathy? What is the principal cause of its dysfunction?

A

Severe myoclonic epilepsy of infancy (SMEI). Mutation in SCN1A.

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17
Q

What is the principal difference between partial and generalized epilepsy?

A

Partial epilepsies start at a specific brain location and spread over the brain. Generalized epilepsies are not spatially constrained, they happen everywhere all at once.

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18
Q

What is counter-intuitive about the dysfunction of Nav1.1 and its ability to trigger hyper-excitability?

A

The loss of a sodium channel would be thought to hinder the excitability potential.

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19
Q

What analogy can be used to describe a seizure?

A

Electrical excitation storm.

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20
Q

True or false: SMEI mutations are inherited?

A

False: they are spontaneous mutations.

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21
Q

If only one allele is coding for a truncated version of Nav1.1, is the other “healthy” allele sufficient to confer a normal phenotype?

A

No.

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22
Q

How can a mutation in a sodium channel (Nav1.1) mediating excitation be responsible for the overexcitation underpinning epilepsy?

A

Mutations in Nav1.1 are targeted to inhibitory bipolar neurons ->loss of inhibition and excitation balance = overexcitability.

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23
Q

What is being varied and what is being recorded in current-clamp? Voltage-clamp?

A

Current-clamp: used to study change in membrane potential
-measure V
-vary I
Voltage-clamp: used to study the properties of channels
-measure I
-vary V

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24
Q

What kind of experiment was designed to probe the neural underpinnings of SCN1A KO mice?

A

Acute neuronal dissociation of bipolar and pyramidal neurons.

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25
Q

What sodium channels are intimately involved in pain syndromes?

A

Nav1.7 PNS neurons
(Nav1.8 DRG neurons)
(Nav1.9 DRG neurons)

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26
Q

What is inherited erythromyelalgia?

A

Disorder characterized by episodes of redness and pain in the feet and hands. It can often be triggered by warmth or mild exercise.

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27
Q

IE is caused by mutations in which sodium channel? What is the main consequences of the mutations?

A

Nav1.7 ->channel activates at more negative potentials (threshold is lowered)

28
Q

What mutations are required for congenital inability to experience pain?

A

Two bad copies of Nav1.7 making this sodium channel type completely dysfunctional.

29
Q

True or false: AP can propagate on the cell body.

A

True.

30
Q

For what essential synaptic process is backpropagation important?

A

Synaptic plasticity because backpropagation enables synapses to get information about the output activity of the neuron.

31
Q

Spike timing dependent plasticity is dependent on two main events, what are they?

A

Presynaptic neurotransmitter release and postsynaptic depolarization (EPSP - AP).

32
Q

What receptors are particularly important to regulate spike timing dependent plasticity?

A

NMDA receptors.

33
Q

Can backpropagation relieve the magnesium blockade of NDMA receptors?

A

Yes, allowing depolarization.

34
Q

What is a functional role of thalamic neurons regarding the transition to sleep?

A

Contribute to formation of delta waves (large amplitude, slow oscillations) -> transition from wakefulness to slow wave sleep.

35
Q

What electrophysiological property determines whether a thalamic neuron is in bursting mode vs transmission mode?

A

The resting membrane potential.

36
Q

What two types of ion channels are responsible for the bursting mode of thalamic neurons?

A
  1. T-type calcium channels
  2. HCN (Ih)
37
Q

What is the t of t-type calcium channels standing for?

A

Transient -> deactivate rapidly.

38
Q

T-type channels activate in the low or high ranges of membrane potentials?

A

Low (very negative).

39
Q

True or false: T-type channels also deactivate at quite high negative membrane potentials.

A

True.

40
Q

Bursting mode is happening at low or high potentials? Transmission mode?

A

Bursting: low
Transmission: high

41
Q

When HCN (Ih) channels open, what cations are they letting flow inside of the cell?

A

Na+

42
Q

At which membrane potentials are HCN channels opening?

A

Hyperpolarized potentials.

43
Q

Explain how the activity of t-type calcium channels and HCN sodium channels generate bursting firing?

A

At hyperpolarization, Ih is activated = slow depolarization
Slight depol. removes It inactivation -> when membrane potential is pulled into the peak activation range of It -> burst of Ca2+ spikes interlocked with fast Na+ spikes
Since membrane potential gets rapidly into positive values, It inactivates -> spiking stops
Membrane then repolarizes, eventually activating Ih again and restarting the cycle

44
Q

How are acetylcholine, norepinephrine and histamine modulating thalamic activity?

A

Close leak potassium channel ->depol ->transmission mode.

45
Q

What brain region is mediating sleep spindles?

A

Reticular thalamic nucleus.

46
Q

What are the inputs to the reticular thalamus? What are its outputs?

A

Excitatory inputs from thalamus and cortex.
Inhibitory outputs to thalamus.

47
Q

Oscillations of the reticular thalamus is mediated by which type of channel? What is activating this channel?

A

K+ channel (promoting hyperpolarization) activated by intracellular Ca+.

48
Q

In the bursting cycle of thalamic neurons, name the currents contributing to each phase of the cycle?

A

Slow depol: current from t-type calcium channels
Depol. (AP): currents from Na, K, Ca
Hyperpol.: current from K+ channels Ca+-gated (when Ca+ builds up intracellularly, these K+ channels open and hyperpolarize the cell).

49
Q

What are the four categories of glutamate receptors?

A

AMPA
NMDA
Kainate
Orphan

50
Q

Is it AMPA or NDMA receptors that are tetramers?

A

Both.

51
Q

What are the 4 possible subunit types to an AMPA receptor? AMPA receptors in the adult brain are usually composed from which subunits

A

GluA1-A4
Usually from GluA1 and GluA2

52
Q

How are AMPA receptors acquiring their impermeability to Ca?

A

Post-transcriptional modification to GluaA2 mRNA by RNA-specific adenosine deaminase, substituting Q-to-R amino acids at QRN site in the pore.

53
Q

What kind of activity are AMPA receptors specialized to mediate?

A

Fast EPSPs.

54
Q

What are the 5 possible subunit types to an NMDA receptor? NMDA receptors in the adult brain are usually composed from which subunits

A

GluN1
GluN2A-B-C-D
GluN1 subunits are necessary for the receptor to be functional, in the adult brain they are usually complemented with GluN2A (GluN2B too if extrasynaptic)

55
Q

True or false: when open, NDMAR are permeable to Ca.

A

True, important for synaptic plasticity.

56
Q

What the necessary conditions for NMDA receptors to open?

A

Binding of glycine to GluN1
Binding of glutamate to GluN2
Depolarization postsynaptically

57
Q

What is determining the current time course of NMDA receptors?

A

Types of GluN2 subunits.

58
Q

What are the main domains of glutamate receptor subunits?

A

Amino terminal domain (ATD) (extracellular space)
Ligand-binding domain: D1 and D2
Transmembrane domains (TMD) :M1, M3 and M4 = transmembrane segments + M2 = pore loop

59
Q

What is the functional interaction between D1, D2, an agonist, and the channel pore?

A

D1 and D2 from an extracellular clamshell-like structure in which agonsits can bind, causing a conformational change (closing the clamshell) that opens the pore (by pulling)

60
Q

What are competitive antagonists doing to the clamshell?

A

Binding without allowing the clamshell to close.

61
Q

How many agonist molecules are most likely needed to open NMDA receptors?

A

4 bc. tetramers

62
Q

To what ion channel family are GABAa receptors and nicotinic acetylcholine receptors belonging to?

A

Cys-loop ion channel family

63
Q

How many subunits are nicotinic acetylcholine receptors composed from?

A

5

64
Q

Neural nicotinic receptors can be of which compositions?

A

Either alpha subunits or alpha and beta

65
Q

Each nicotinic subunit has how many transmembrane segments?

A

4 (TM2 lining the pore)

66
Q

How are nicotinic receptors selecting for cations?

A

Outer and inner openings of pore and ringed with negative charges -> but don’t select for specific cation types

NEUR 310 (12 decks)

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