AQA A biology - nervous impulses

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amylouise
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for inhibitory synapses, it says that the neurotrasmitter binds to a different receptor on the post synaptic membrane, and this causes pottassium ions to diffuse out and cause hyperpolarisation. This therefore makes depolarisation harder to that an action potential cannot be made.

I can grasp this, but I don't understand the movement of the pottassium ions, because they've moving AGAINST their electrochemical gradient!! The potential difference between inside the neurone and outside the neurone is imbalanced, and I read that the movement of pottassium ions would be prevented because of this charge imbalance.

Also, in order for Rods to cause a generator potential, hyperpolarisation must occur, meaning the pottasium ions move out. As a result the rod cell releases less neurotransmitter onto the relay neurone. How the hell does this make us see??? I thought that the movement of sodium ions caused generator and action potentials - how is it that pottassium ions are doing it here??
Inhibitory synapses work on the idea of neurotransmitters binding to a different site & then causing hyperpolarisation, but for Rod, hyperpolaristation is supposed to prevent neurotransmitter release. This is the complete reverse!

Please help someone!
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The potassium ions are not moving against their electrochemocal gradient. The sodium/potassium pump actively transports potassium ions into the rod cell, they then diffuse out normally. The trans-retinal causes the membrane to become more permeable to potassium ions - meaning that they diffuse out quicker and more so, therefore the cell becomes hyperpolarised. This hyperpolaristaion causes less neurotransmitter to be released onto the bipolar neurone which can then generate an action potential - as this is an inhibitory synapse and it is no longer being inhibited.


Does this answer your question?? I don't think we have to know about inhibitory synapses in general too well. Just be able to recognise one and understand how rod cells work.

You feeling nervous about this exam? I know I am... reckon I have learned all I can but somehow it just doesn't feel enough.
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amylouise
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I know that potassium ions are not diffusing against a concentration gradient. But, because the outside of the cell is positive, their movement is restricted because of this positive charge. (Potassium ions are positively charged)

What you said about inhibitory synapses was good, I understand that now. Thanks.
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amylouise
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actually, it doesn't make complete sense.
I thought hyperpolarisation was the movement on potassium ions INTO the cell, not out of it. If they move out, the cell is effectively being depolarised.
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MadNatSci
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Perhaps it will help a bit if you think in terms of charge rather than ions? Hyperpolarisation is when the membrane potential of the cell becomes more negative; depolarisation when it becomes more positive. So when potassium ions leave, the cell is becoming less negative relative to the outside - ie it's being hyperpolarised.

Also remember that this is all relative. The outside of the cell is positive relative to the inside; this doesn't mean that it's actually positively charged, just less negative than inside the cell. Hope that makes sense...
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Thats what I tried to say! I understand it that polarisation of the axon occurs when it is more negative compared with outside. Therefore the increased movement of potassium ions out of the axon will increase its negativity compared to outside (the outside is thus becoming less negative) and thus the neurone becomes hyperpolarised.

Depolaristaion occurs when sodium ions diffuse into the neurone, but potassium ions are not diffusing out, therefore it becomes more positively charged (or less negative - however you look at it). Polarisation is maintained because the sodium ions are being transported out but cannot diffuse back in, and the potassium ions are being transported in but can diffuse back out -
therefore there is an accumulation of possitvely charged ions on the outside of the neurone which is thus polarised.
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Ben.S.
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(Original post by amylouise)
for inhibitory synapses, it says that the neurotrasmitter binds to a different receptor on the post synaptic membrane, and this causes pottassium ions to diffuse out and cause hyperpolarisation. This therefore makes depolarisation harder to that an action potential cannot be made.

I can grasp this, but I don't understand the movement of the pottassium ions, because they've moving AGAINST their electrochemical gradient!! The potential difference between inside the neurone and outside the neurone is imbalanced, and I read that the movement of pottassium ions would be prevented because of this charge imbalance.

Also, in order for Rods to cause a generator potential, hyperpolarisation must occur, meaning the pottasium ions move out. As a result the rod cell releases less neurotransmitter onto the relay neurone. How the hell does this make us see??? I thought that the movement of sodium ions caused generator and action potentials - how is it that pottassium ions are doing it here??
Inhibitory synapses work on the idea of neurotransmitters binding to a different site & then causing hyperpolarisation, but for Rod, hyperpolaristation is supposed to prevent neurotransmitter release. This is the complete reverse!

Please help someone!
Forget about potassium for rods (not completely, obviously!) - hyperpolarisation is brought about by the closing of ligand-gated sodium channels which are open in the dark. In the dark, a current (the dark current) flows through the rod cell, carried in by sodium ions in one segment and out by potassium in another. Closing of sodium channels causes a reduction in the influx of positiovely charged ions (potassium ions continue to exit to some degree, but it is the sodium which is important) and hyperpolarisation.

Ben
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