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any biology ppl know about rhodopsin
im doin the aqa a2 biology exam on thrsday but i just cant see any logic to the following:
rod cells contain a pigment called rhodopsin and are sensitive to the intensity of light. they respond by the following reaction
light
rhodopsin - opsin + retinal
opsin open ion channels in the membrane which results in an action potential so u can see (vision).
in bright light though the rod cells cannot function coz rhodopsin is constantly being broken down.
wouldnt this mean though that if it is constantly broken down then opsin will keep making an action potential therefore enabling good vision frm the rod cells?
rod cells contain a pigment called rhodopsin and are sensitive to the intensity of light. they respond by the following reaction
light
rhodopsin - opsin + retinal
opsin open ion channels in the membrane which results in an action potential so u can see (vision).
in bright light though the rod cells cannot function coz rhodopsin is constantly being broken down.
wouldnt this mean though that if it is constantly broken down then opsin will keep making an action potential therefore enabling good vision frm the rod cells?
emmz
there must be some1 who does biology 
yes, but they dont help unless you pay them in some way.
thats how it seems to worK; help = pay
sorry, emmz, je n'ai pas de doing biology.
emmz
im doin the aqa a2 biology exam on thrsday but i just cant see any logic to the following:
rod cells contain a pigment called rhodopsin and are sensitive to the intensity of light. they respond by the following reaction
light
rhodopsin - opsin + retinal
opsin open ion channels in the membrane which results in an action potential so u can see (vision).
in bright light though the rod cells cannot function coz rhodopsin is constantly being broken down.
wouldnt this mean though that if it is constantly broken down then opsin will keep making an action potential therefore enabling good vision frm the rod cells?
rod cells contain a pigment called rhodopsin and are sensitive to the intensity of light. they respond by the following reaction
light
rhodopsin - opsin + retinal
opsin open ion channels in the membrane which results in an action potential so u can see (vision).
in bright light though the rod cells cannot function coz rhodopsin is constantly being broken down.
wouldnt this mean though that if it is constantly broken down then opsin will keep making an action potential therefore enabling good vision frm the rod cells?
I'm not certain about this........ but I think......
rod cells have a limited amount of rhodopsin. So in bright light, its ALL broken down. This means that there is no more breaking down and so no more action potentials from this. Then the cones take over the main line of vision... does this sound right?
Sweetpeaz
I'm not certain about this........ but I think......
rod cells have a limited amount of rhodopsin. So in bright light, its ALL broken down. This means that there is no more breaking down and so no more action potentials from this. Then the cones take over the main line of vision... does this sound right?
rod cells have a limited amount of rhodopsin. So in bright light, its ALL broken down. This means that there is no more breaking down and so no more action potentials from this. Then the cones take over the main line of vision... does this sound right?
yea thanx it probly is right but who knows lol. are u doin the bio exam r u just intelligent.
This thread is in two forums!
Anyway, a few questions:
Are you doing AQA Biology specification A?
Is this from a previous paper?
If it is, then you can download the marking scheme from the AQA web site.
I'm doing this exam as well - started revision today. Good luck anyway.
J.
Anyway, a few questions:
Are you doing AQA Biology specification A?
Is this from a previous paper?
If it is, then you can download the marking scheme from the AQA web site.
I'm doing this exam as well - started revision today. Good luck anyway.
J.
(here goes..., BYB4 explanation...)
It basically works the other way around to most nerve impulses/synapses/receptors, which is annoying & the reason they include it
Rod cells are connected to bipolar cells connected to optic nerve etc.
Dark: Rhodopsin stable, so no impluse where there shouldn't be etc
In the dark Rod cells are constantly depolarised (gated Na chanels open all the time). This causes a constant release of the transmitter at the synapse to bipolar cell (transmitter = glutamate). This transmitter inhibits the depolarisation of the bipolar cell so it doesn't produce its own transmitter and therefore no impulse via optiv nerve.
Light:Rhoposin unstable so opsin & cis/trans retinal formed.
Opsin causes the Rod cells gated Na chanels to close but they continue to be pumped out (by active transport) therefore Rod cell is hyperpolarised (very -ive inside, very +ive outside). It therefore releases no glutamate. No glutamate on bipolar receptors means there is nothing inhibiting its depolarisation so it depolarises and releases its transmitters and impulse sent via optic nerve!
Its complicated, expecially when they don't make it clear which cells they are refering to, (which AQA seems to do way to often!) but I'm pretty sure this is correct. Just remember its back to front until it reaches the bipolar cell when it goes normal again!
Any more problems (or if I've confused you further...) just ask!
It basically works the other way around to most nerve impulses/synapses/receptors, which is annoying & the reason they include it
Rod cells are connected to bipolar cells connected to optic nerve etc.
Dark: Rhodopsin stable, so no impluse where there shouldn't be etc
In the dark Rod cells are constantly depolarised (gated Na chanels open all the time). This causes a constant release of the transmitter at the synapse to bipolar cell (transmitter = glutamate). This transmitter inhibits the depolarisation of the bipolar cell so it doesn't produce its own transmitter and therefore no impulse via optiv nerve.
Light:Rhoposin unstable so opsin & cis/trans retinal formed.
Opsin causes the Rod cells gated Na chanels to close but they continue to be pumped out (by active transport) therefore Rod cell is hyperpolarised (very -ive inside, very +ive outside). It therefore releases no glutamate. No glutamate on bipolar receptors means there is nothing inhibiting its depolarisation so it depolarises and releases its transmitters and impulse sent via optic nerve!
Its complicated, expecially when they don't make it clear which cells they are refering to, (which AQA seems to do way to often!) but I'm pretty sure this is correct. Just remember its back to front until it reaches the bipolar cell when it goes normal again!
Any more problems (or if I've confused you further...) just ask!
emmz
im doin the aqa a2 biology exam on thrsday but i just cant see any logic to the following:
rod cells contain a pigment called rhodopsin and are sensitive to the intensity of light. they respond by the following reaction
light
rhodopsin - opsin + retinal
opsin open ion channels in the membrane which results in an action potential so u can see (vision).
in bright light though the rod cells cannot function coz rhodopsin is constantly being broken down.
wouldnt this mean though that if it is constantly broken down then opsin will keep making an action potential therefore enabling good vision frm the rod cells?
rod cells contain a pigment called rhodopsin and are sensitive to the intensity of light. they respond by the following reaction
light
rhodopsin - opsin + retinal
opsin open ion channels in the membrane which results in an action potential so u can see (vision).
in bright light though the rod cells cannot function coz rhodopsin is constantly being broken down.
wouldnt this mean though that if it is constantly broken down then opsin will keep making an action potential therefore enabling good vision frm the rod cells?
When rhodopsin is exposed to light it undergoes a process called bleaching. This is the process where by it is broken down into opsin and retinal (called bleaching because the usual purple colour of rods becomes opaqe..hence the alternative name for rhodopsin: visial purple) It is during this proces that a conformational change in rhodopsin's structure causes the ap to be generated. After this photoisomerisation cascade (through 5 steps... its not just the case that it goes straight to retinal and opsin...it just happens that these are the constituent parts for the molecule) rhodopsin is reformed this process occurs via reduction followed by oxidation/isomerisation IN THE DARK. Therefore 'opsin' will not be continually causing signals to be sent, to the brain because no rhodopsin is being broken down. This is why it takes us a while to be able to see properly when we go from a light place to a dark place... we were said to be light adapted. You should also know about dark adaption
hornblower
This thread is in two forums!
Anyway, a few questions:
Are you doing AQA Biology specification A?
Is this from a previous paper?
If it is, then you can download the marking scheme from the AQA web site.
I'm doing this exam as well - started revision today. Good luck anyway.
J.
Anyway, a few questions:
Are you doing AQA Biology specification A?
Is this from a previous paper?
If it is, then you can download the marking scheme from the AQA web site.
I'm doing this exam as well - started revision today. Good luck anyway.
J.
er no im doin the spec b. when is the spec a exam? gud luck wiv it
Katie J
(here goes..., BYB4 explanation...)
It basically works the other way around to most nerve impulses/synapses/receptors, which is annoying & the reason they include it
Rod cells are connected to bipolar cells connected to optic nerve etc.
Dark: Rhodopsin stable, so no impluse where there shouldn't be etc
In the dark Rod cells are constantly depolarised (gated Na chanels open all the time). This causes a constant release of the transmitter at the synapse to bipolar cell (transmitter = glutamate). This transmitter
inhibits the depolarisation of the bipolar cell so it doesn't produce its own transmitter and therefore no impulse via optiv nerve.
Light:Rhoposin unstable so opsin & cis/trans retinal formed.
Opsin causes the Rod cells gated Na chanels to close but they continue to be pumped out (by active transport) therefore Rod cell is hyperpolarised (very -ive inside, very +ive outside). It therefore releases no glutamate. No glutamate on bipolar receptors means there is nothing inhibiting its depolarisation so it depolarises and releases its transmitters and impulse sent via optic nerve!
Its complicated, expecially when they don't make it clear which cells they are refering to, (which AQA seems to do way to often!) but I'm pretty sure this is correct. Just remember its back to front until it reaches the bipolar cell when it goes normal again!
Any more problems (or if I've confused you further...) just ask!
It basically works the other way around to most nerve impulses/synapses/receptors, which is annoying & the reason they include it
Rod cells are connected to bipolar cells connected to optic nerve etc.
Dark: Rhodopsin stable, so no impluse where there shouldn't be etc
In the dark Rod cells are constantly depolarised (gated Na chanels open all the time). This causes a constant release of the transmitter at the synapse to bipolar cell (transmitter = glutamate). This transmitter
inhibits the depolarisation of the bipolar cell so it doesn't produce its own transmitter and therefore no impulse via optiv nerve.
Light:Rhoposin unstable so opsin & cis/trans retinal formed.
Opsin causes the Rod cells gated Na chanels to close but they continue to be pumped out (by active transport) therefore Rod cell is hyperpolarised (very -ive inside, very +ive outside). It therefore releases no glutamate. No glutamate on bipolar receptors means there is nothing inhibiting its depolarisation so it depolarises and releases its transmitters and impulse sent via optic nerve!
Its complicated, expecially when they don't make it clear which cells they are refering to, (which AQA seems to do way to often!) but I'm pretty sure this is correct. Just remember its back to front until it reaches the bipolar cell when it goes normal again!
Any more problems (or if I've confused you further...) just ask!
wow thanx for that. but two questions:
if in the dark the receptors of the cell are inhibited and no impulses r sent, then how can rods see in the dark or dim light? coz i thought their purpose was to send impulses in the dark and see
last question - u said it works the other way round to most impulses. how?
thanx againemmz
wow thanx for that. but two questions:
if in the dark the receptors of the cell are inhibited and no impulses r sent, then how can rods see in the dark or dim light? coz i thought their purpose was to send impulses in the dark and see
last question - u said it works the other way round to most impulses. how?
thanx again
if in the dark the receptors of the cell are inhibited and no impulses r sent, then how can rods see in the dark or dim light? coz i thought their purpose was to send impulses in the dark and see
last question - u said it works the other way round to most impulses. how?
thanx againmany rod cells are connected to a single bipolar neurone, so their individual generator potentials add up (summation) to generate an action potential (or hyperpolarisation). however the fact that many rod cells share one bipolar neuron amongst themselves results in their poor visual acuity (in comparison to cone cells).
As for the opposite impulse, usually cells (i.e. neurones) depolarise when stimulated above a threshold value, whereby they become positively charged, however hyperpolarisation occurs in rod cells, whereby they become more negatively charged (the permeability to sodium ions reduces instead of increasing, as it does with an action potential in a neurone).
Hope that helps
Boygenious, you put that far better than I could (& in better detail!), can only add that normally transmitter release results in an impulse all the way to the brain (or spinal cord etc...) in the case of rod cells, transmitter inhibits the impulse. (alternatively; other transmitters released when stimulated, not continually when not stimulated)
Katie J
Boygenious, you put that far better than I could (& in better detail!), can only add that normally transmitter release results in an impulse all the way to the brain (or spinal cord etc...) in the case of rod cells, transmitter inhibits the impulse. (alternatively; other transmitters released when stimulated, not continually when not stimulated)
i think it's glutamate, it's not really in my syllabus though, so i'm not too sure
Related discussions
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- 4 a levels
- Does anyone go to Newvic sixth form?
- advice about resitting
- PPL at oxford
- can i become a psychiatrist without an alevel in biology?
- Are CGP guides for A-level Biology and Chemistry supportive?
- how do i know medicine/or any other career is right for me?
- Sixth form choice (London)
- Are Maths, Physics and Chemistry good subjects for A-Levels?
- Are my gcse results good enough for Oxford
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- Edexcel A-level Biology A (Salters-Nuffield) Paper 2 - 14th June 2024 [Exam Chat]
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