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Introduction To Pharmacology And Physiology > The action potential > Flashcards

The action potential Flashcards

1
Q

Membrane potential is measured as the potential of the extracellular solution relative to the inside of the cell, is this correct?

A

No! Membrane potential is measured as the potential inside the cell relative to the extracellular solution

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2
Q

What unit are membrane potentials measured in?

A

Millivolts mV

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3
Q

Which cells have membrane potentials at rest and are they positive or negative?

A

All animal cells do- they are negative

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4
Q

What two factors are important for the generation of the membrane potential?

A

Asymmetric distribution of ions across the plasma membrane

Selective ion channels in the plasma membrane

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5
Q

Electrical gradient has more effect on direction of ion flow than concentration gradient, is this correct?

A

No, ions will always move down their concentration gradient first and then down their electrical gradient.

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6
Q

What is equilibrium potential for an ion?

A

The membrane potential if it solely relied on that ion.

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7
Q

What is the nernst equation?

A

A way for working out equilibrium potential-

E=61/charge on ion multiplied by log (concentration of ion on outside/concentration of ion on inside)

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8
Q

What is depolarisation?

A

A decrease in the size of the membrane potential from its normal value so cell becomes less negative

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9
Q

What is hyperpolarization?

A

An increase in the size of the membrane potential from its normal value so the cell become more negative

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10
Q

What will increasing membrane permeability for a particular ion do to the membrane potential in regards to the equilibrium potential of that ion?

A

It will move the membrane potential towards the equilibrium potential of that ion.

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11
Q

What are changes in the membrane potential caused by?

A

Changes in membrane permeability due to changes in activity of ion channels.

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12
Q

What is conductance?

A

The contribution of each ion to the membrane potential will depend on how permeable the membrane is to that ion.

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13
Q

Which equation can we use that takes into account imperfect selectivity of each ion? What must you remember to do?

A

The GHK equation, turn the logarithmic fraction for chloride ions upside down.

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14
Q

What are the different ways a cell can be gated?

A

Ligand gating
Voltage gating
Mechanical gating-membrane deformation causes opening or closing of channels

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15
Q

How is mechanical gating used in the inner ear?

A

K+ channels close in the cuticular plate, this causes the membrane to depolarise. This causes calcium ion channels to open.
Vesicles containing neurotransmitter fuse with the basement membrane close to the afferent nerve
Neurotransmitter binds to receptor on post synaptic plate and generates action potential that goes to CNS for interpretation

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16
Q

What is the receptor protein in fast synaptic transmission?

A

An ion channel- neurotransmitter binding causes the channel to open.

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17
Q

How do inhibitory synapses work? What are some common inhibitory neurotransmitters?

A

Opening of ligand gated channels which cause hyperpolarization
Common neurotransmitters include-glycine, GABA

18
Q

Which two ways can slow synaptic transmission work?

A

Direct G protein gating

Gating via an intracellular messenger

19
Q

How does direct G protein gating work and what are its benefits?

A

Binding of signal chemical to GPCR causes release of G protein which then moves along the inside of the membrane and binds to channel- hydrolyses ATP and opens channel

This is localised and quite rapid

20
Q

How does gating via an intracellular messenger work and what are its benefits?

A

G protein activation causes enzyme activation which initiates signalling cascade which activates intracellular messenger or protein kinase which opens channel.

This happens throughout the cell as it is not confined to the plasmalemma
The signal can be amplified by cascade
However is slow as more intermediates

21
Q

What are the different stages of the action potential in cardiac muscles?

A

1-rapid influx of Na+ through open fast na+ channels
2-transient K+ channels open and K+ efflux returns membrane potential to 0mV

  1. Influx of calcium through L type calcium channels is electrically balanced by K+ efflux through delayed rectifier K+ channels
  2. Calcium ion channels close but delayed rectifier K+ channels remain open and return membrane potential to -90mV
22
Q

What are the properties of cardiac ion channels?

A

Selectivity-only permeable to a single type of ion
Voltage sensitive- a specific MP range is required for particular channel to be in open configuration
Time dependent- some ion channels are configured to close a fraction of a second after opening (become inactivated and can only be opened again when the MP is returned to resting levels.

23
Q

What is the part of the axon at which membrane potentials ‘sum up’ to possibly create an action potential?

A

The axon hillock

24
Q

Why is there such a rapid increase in membrane potential during the action potential?

A

Positive feedback loop for sodium
Sodium influx causes membrane depolarisation which causes more sodium channels to open which causes more influx so more depolarisation.

25
Q

Why does the membrane potential stop rising?

A

All sodium channels have become inactivated.

26
Q

What is the difference between the absolute refractory period and the relative refractory period?

A

Absolute- no action potentials can be stimulated- all sodium channels inactive
relative- an AP can be produced if the stimulus is large enough, some sodium channels have started to recover

27
Q

What is the structural difference between sodium and potassium channels?

A

Both have four subunits each made up of 6 transmembrane regions. Sodium transport proteins contain an inactivation particle which blocks the pore and inactivates the channel. Sodium channels are also made of only one alpha subunit. Potassium channels are made up of four alpha subunits.

28
Q

What is the local current theory?

A

Injection of current into an axon will cause the resulting charge to spread along the axon and cause an immediate local change in the membrane potential- this spreads according to an inverse exponential graph

29
Q

What is capacitance?

A

The ability to store charge and is a property of the lipid bilayer

30
Q

What controls the membrane resistance?

A

The number of ion channels open.

31
Q

What effect will a high capacitance have on voltage change?

A

Voltage will change more slowly in response to current injection

32
Q

What effect will a higher resistance have on how far the change in voltage spreads along the axon?

A

It will spread further- this is why myelination increases distance each action potential ‘covers’

33
Q

What do i need to know about voltage gated calcium channels?

A

Similar to sodium channels- different depending what organ they are in
Activate more slowly than sodium channels
Also activate and inactivate
Inactivation in calcium ion dependent.

34
Q

How is neurotransmitter released from the presynaptic neurone?

A 
Calciu enters through channels when stimulated by depolarisation
Calcium binds to synaptotagmin
Vesicles brought close to membrane
Snare complex makes a fusion pore
Transmitter released through pore
35
Q

What happens when neurotransmitter binds to receptors on the post synaptic membrane?

A

Brief depolarisation will activate adjacent sodium voltage gated channels due to local spread of charge.

36
Q

How are ligand gated ion channels on the post synaptic membrane different?

A

They allow both sodium and potassium through. However more sodium will move in because the membrane potential is further away from the Ena. Than from the Ek

37
Q

How does tubocurarine work?

A

Competitive inhibitor of Ach binding sites on ligand gated ion channels so less opening- less depolarisation of post synaptic neurone

38
Q

How does succinylcholine work?

A

Brief depolarisation activates then deactivates vg sodium channels. Because SC not degraded by Ach esterase it stays in receptors and continues to cause depolarisation so voltage gated sodium channels stay inactivated.

39
Q

What is mayasthenia gravis?

A

Autoimmune disease targeting nACh receptors
Patients suffer profound weakness
Weakness increases with exercise
Caused by antibodies directed against nAChr on post synaptic membrane of skeletal musclethis leads to loss of functional nAChR by complement mediated lysis and receptor degradation
Endplate potenitals are reduced in amplitude therefore leading to muscle weakness and fatigue

40
Q

How does a muscarinic Ach receptor operate differently from a nicotinic receptor?

A

Produces a slower depolarisation because they are coupled to G proteins which trigger a cascade of events in the cell.

Introduction To Pharmacology And Physiology (3 decks)

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