Membrane Potentials Flashcards

1
Q

What are the 3 different types of membrane potentials?

A
  1. Action potential: transmit signal over long distance
  2. Graded potential:
    decide when an action potential should be fired
  3. Resting membrane potential: keeps cell ready to respond
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2
Q

What maintains the resting membrane potential?

A

Leaky Potassium ion channels & electro-chemical concentration gradients

  • Leaky potassium ion channels will let potassium move out of the cell down its concentration gradient, this movement causes an electrical gradient which causes the charge to decrease
  • Equilibrium potential is the membrane potential at which the electrical gradient is eactly equal and opposite to the concentration gradient
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3
Q

What is the Nernst equation?

A

Predicts the equilibrium potential for a single ion species

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4
Q

What happens if you have too much potassium?

A
  1. Reduction to concentration gradient
  2. Smaller electrical gradient at equilibrium
  3. Reduced resting membrane potential so the cell depolarises quicker
  4. Therefore, neurons fire more readily
  5. Heart effected = ventricular fibrillation
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5
Q

What’s potassium’s equilibrium?

A

-90mV

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6
Q

What’s the Goldman equation?

A

Predicts the equilibrium potential generated by several ions

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7
Q

What’s depolarisation?

A

Change in the membrane potential from a negative value towards 0mV

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8
Q

What’s repolarisation?

A

Movement of the membrane potential away from a positive value and toward the resting potential (-70mV)

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9
Q

What’s Hyperpolarisation?

A

Movement of the membrane potential away from the normal resting potential and farther from 0mV

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10
Q

What’s an Action Potential?

A

Electrical impulse that is propagated along the surface of an axon and does not diminish as it moves away from its source - travels along the axon to one or more synapses

  • Function to send electrical signal over a long distance
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11
Q

What’s the All-or-None Principle?

A

A given threshold either triggers a typical action potential or none at all

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12
Q

What are the properties of an action potential?

A
  • Stimulus strength is proportional to membrane potential’s ability to surpass threshold potential + create action potential
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13
Q

If the stimulus strength is high does this create stronger action potentials?

A
  • No
  • A strong stimulus will just increase the number of action potentials generated = a larger stimulus might stimulate 2+ action potentials and so on
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14
Q

What’s a Graded/Local Potential?

A

Changes in the membrane potential that cannot spread far from the site of stimulation - any stimulus that opens a gated channel produces a graded potential

  1. Na ions enter the cell and are attracted to the negative charges along the inner surface of the membrane, shifting the membrane potential more positive/towards 0mV (depolarisation)
  2. As plasma membrane depolarises, Na ions are released from its outer surface, these ions along with extracellular Na ions then move toward the open channels, replacing ions that have already entered the cell = Local Current
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15
Q

What’s the key concept regarding graded potentials?

A

The maximum change in membrane potential is proportional to the size of the stimulus; which determines the number of open Na channels

The more open channels the more Na ions enter the cell, the greater the membrane area effect + the greater the degree of depolarisation

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16
Q

How are action potentials generated?

A
  1. A stimulus causes Na ion channels to open, with a strong stimulus causing multiple to open

(resting potential -70mV)

  1. This causes an influx of Na ions to enter the axon and the cells charge becomes more positive (depolarises)
  2. Due to the stimulus strength, the change in charge causes adjacent Na channels to open and increases the depolarisation
  3. Eventually, the membrane potential reaches THRESHOLD (-60mV)
  4. The plasma membrane is now more permeable to Na - driven by a large electrochemical gradient, rapid depolarisation occurs
  5. Membrane potential is now around +30mV (near Na’s equilibrium) and Na channels now close and K channels open - allowing K to leave causing repolarisation
  6. K channels being to close when the membranes potential reaches the normal resting potential - there is a slight lag in closing which causes hyperpolarisation (-90mV)
  7. K channels finally close and the resting potential increases to -70mV
17
Q

What and when is the refractory period?

A

From the time an action potential begins until the normal resting membrane potential has stabilised - the plasma membrane does not respond normally to additional depolarising stimuli

18
Q

How can the rate of depolarisation/conduction velocity across the excitable membrane be increased?

A

Myelination

19
Q

What is myelin?

A
  • Formed by Schwann cells in Peripheral Nervous System
  • Formed by Oligodendrocytes in Central Nervous System

Create the myelin sheath

Gaps in the myelin = Nodes of Ranvier

Insulates the axon

20
Q

What’s the function of Myelin?

A
  • Insulates axons
  • It consists of folds of membrane from Schwann or Oligodendrocytes
  • Electrical insulation and increases the speed at which an action potential travels along the axon
  • Na channels are only present at the nodes of ranvier - allows AP to spread like a local current to the next segment with little decrement/AP only evoked at N.o.R
  • Myelination increases membrane resistance + decreases membrnae capacitance
  • Causes Saltatory conduction
21
Q

What’s Saltatory Conduction?

A
  • Saltatory propagation in the CNS/PNS carries action potentials along an axon much more rapidly than does continuous propagation
  • This cannot occur in unmyelinated axons
  • Only the nodes of Ranvier can respond to depolarisation
    1. Action potential appears at the initial segment of a myelinated axon
    2. Local current skips the internodes and depolarises the closest node to threshold
    3. Due to the nodes being separated along the axon, the AP jumps from node to node rather than moving along in a series of tiny steps
  • Uses significantly less energy because less surface area is involved and fewer Na ions must be pumped out of the cytoplasm
22
Q

What’s de-myelination?

A

Progressive destruction of myelin sheaths in both CNS/PNS

= Loss of sensation and motor control – leaves effected region numb and paralysed

  • Prevents the depolarisation of axons to their threshold
23
Q

What conditions are linked to de-myelination?

A

Diphtheria: Bacterial infection, diphtheria toxin damages Schwann cells and destroys myelin sheaths in PNS – sensory and motor problems leading to fatal paralysis

MS: Recurrent de-myelination of axons in the optic nerve, brain and spinal cord – partial loss of vision, problems with speech, balance, general motor coordination

  • 1/3 of cases the disorder is progressive and typically effects women more than men
24
Q

What’s Guillain-Barre syndrome?

A
  • Autoimmune disorder characterised by de-myelination of peripheral nerves – weakness or tingling of legs that spreads to arms = leads to paralysis
  • When breathing is affected, patients placed on a ventilator
  • Virus triggers syndrome as onset is usually after a few days or weeks after respiratory or gastrointestinal infection
  • Most patients fully recover but some have residual weakness
25
Q

What are the compound action potentials?

A
  • Mammals possess a number of small and large unmyelinated and myelinated axons – compound together to evoke an action potential
26
Q

Classification of Axons: What are the 3 groups?

A
  1. Type A fibres
  2. Type B fibres
  3. Type C fibres
27
Q

What are Type A fibres?

A
  • The largest myelinated axons, with diameteers from 4 - 20μm
  • Carry action potentials at speeds of (Aa) 70-120m/s, (Ab) 30 -70m/s, (Ag) 15 - 30m/s, (Ad) 12 -30m/s
  • Most sensitive to anoxia (absence of oxygen)
  • Proprioception and motoneurones
  • Least sensitive to local anaesthetic
  • Carry sensory information about position, balance, and delicate touch and pressure sensations form the skin surface to CNS - motor neurones that control skeletal muscles also send their commands over large, myelinated Type A axons