Action Potentials

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  • Created by: SamDavies
  • Created on: 24-04-18 00:37

Membrane Potential

Membrane potential - the voltage across the membrane at any moment. It is generated by selective ion movement across the plasma membrane.

The movement of ions generates a chemical concentration gradient and an electrical gradient

The resting membrane potential of most cells is ~ -70mV to -80mV

ALL permeable ions contribute to resting membrane potential

Nernst Equation - this is used to calculate the electrical potential of a chemical reaction. In its equilibrium state, the Nernst equation should be zero.

Goldman EquationThis is used to determine the equilibrium potential across the cells membrane using all of the ions that can cross the membrane

The membrane is much more permeable to K+ than to Na+, so the resting potential is close to the equilibrium potential of K+ (the potential that would be generated by K+ if it were the only ion in the system).

In glial cells, the resting membrane potential is equal to the K+ equilibrium potential

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Resting Potential

  • Neurone is not passing an impulse
  • Na+ and K+ voltage-gated channels are closed
  • Sodium/potassium ion pumps use ATP to pump 3 Na+ out for every 2 K+ in, but the membrane is more permeable to K+ ions than Na+ ions so many K+ ions “leak” out again
  • Cytoplasm also contains large organic anions
  • The outside of the membrane is positively charged whilst the inside is negatively charged. The cell membrane is said to be polarised
  • Resting potential of -70mv
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Depolarisation

  • When there is a stimulus, Na+ ion channels open and Na+ ions diffuse into the cell.
  • The membrane depolarises – it become less negative with respect to the outside.
  • If the depolarisation is large enough to reach the threshold potential of -50mV, it will open voltage-gated sodium ion channels near the trigger zone.
  • This causes an influx of sodium ions which causes more nearby VGNaC to open, and the depolarisation eventually reaches ­+40mV, which is an action potential. The inside is now positive compared to the outside.
  • The nerve impulse can pass
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Repolarisation

  • The VGNaC close and they enter an inactivated state where they are unable to open at any membrane potential for a brief time
  • Voltage-gated K+ ion channels open and K+ ions move out of the cell
  • The K+ ion leak channels also cause an efflux of K+ ions due to the diffusion and electrical gradients within the neurone
  • K+ ions diffuse out of the cell, bringing the potential difference back to negative compared with the outside – repolarisation.
  • The VGKC automatically start to close at lower membrane potentials, and because the membrane potential is more negative, there is less driving force pushing K+ ions out of the leak channels
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Hyperpolarisation

  • VGKC close more slowly and the extra efflux of K+ ions out of the cell causes the inside to become slightly more negative than during the resting potential stage – hyperpolarisation.
  • Now there is more Na+ inside the cell than outside and more K+ outside the cell than inside. So the sodium/potassium pump actively transports Na+ out of the cell and K+  into the cell
  • The original potential difference is restored, so the cell returns to its resting state.
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Refractory Period

1.    Absolute refractory period

  • When VGNaC close, they are in an inactivated state. So no matter how much excitatory input comes into the neuron, you can't make them re-open and trigger another action potential

2.    Relative refractory period

  • VGNaC have become functional again and can respond to membrane potential changes
  • But the membrane potential is hyperpolarised (below the resting potential). It will take more excitatory input than normal to trigger an action potential

3.   Nerve impulses only travel in one direction

  • Action potentials travel forwards along axons
  • As they move, the resting potential will be re-established behind. Not until this happens can another action potential occur
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Conduction

Faster conduction:

1) Larger diameter of axon - passive flow of current through the axon is quicker with a large diameter because you have less resistance against the membrane of the axon

2) Less channels in axonal membrane - more resistance to flow across the axonal membrane, less leaky. To do this, insulating the membrane with a myelin sheath will help 

Saltatory conduction:

  • The myelin sheath is an insulating layer of fatty material made of Schwann cells surrounding the axon of a neuron which Na+ and K+ ions cannot pass through.
  • Between the Schwann cells are gaps – called the nodes of Ranvier, which contain voltage-gated sodium and potassium ion channels, allowing ionic exchange to occur.
  • The action potential ‘jumps’ from one node to the next – saltatory conduction
  • The myelin sheath means that action potentials can only occur at the gaps between the Schwann cells. This speeds up the transmission of the action potential
  • The signal across the axon will continue to dissipate until it reaches a node of Ranvier, where it is boosted
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Synaptic Transmission

  • A change in potential difference in the presynaptic neurone, caused by the influx of Na+ ions from VGNaC
  • This causes the VGCaC to open, allowing Ca2+ ions to diffuse into the presynaptic neurone 
  • Vesicles containing the neurotransmitter are bound to the presynaptic membrane via proteins called SNARE proteins
  • When they enter, Ca2+ ions bind to the SNARE proteins, helping the fusion of the vesicles to the presynaptic neurone and secretion of the neurotransmitter into the synaptic cleft via exocytosis
  • There are neuroreceptors on the post synaptic membrane. When complementary neurotransmitters bind to them...
    • Na ion channels open (i.e. neurotransmitter-gated Na channel) causing an influx of Na+ ions (if the excitatory postsynaptic potential is large enough, threshold potential can be reached and an action potential created in post synaptic neuron)

OR

  • K ion channels open causing an efflux of K+ ions, decreasing the membrane potential and making it harder for an action potential to intiate (inhibitory response)
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Neurotransmitter Termination

  • To ensure that the synapse does not continue to produce action potentials in the postsynaptic neurone, acetylcholinesterase in the synaptic cleft hydrolyses the acetylcholine into choline and ethanoic acid
  • The choline and ethanoic acid are recycled – they re-enter the synaptic knob by diffusion and are recombined to acetylcholine using ATP from respiration in the mitochondria
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Functions of the Synapse

1.    Transmit information between neurones

2.    Pass impulses in one direction only

3.    Act as junctions

4.    Filter out low level stimuli

5.    Allow adaptation to intense stimulation

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Summation

Summation – when several small potential changes can combine to produce one larger change in potential difference across the membrane

Temporal summation – if a low-level stimulus is persistent, it will generate several successive action potentials in the presynaptic neurone. The release of many vesicles of acetylcholine over a short period of time will enable the postsynaptic generator potentials to combine together to produce an action potential

Spatial summation – summation also occurs when several presynaptic neurones each release small numbers of vesicles into one synapse 

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