[osake]

From all the textbooks I have read, and from what my teachers have told me, in light rhodopsin gets bleached, opsin binds to membrane which causes sodium ion channels to close, so membrane becomes hyperpolarised. This results in no inhibitory neurotransmitters being released. If no neurotransmitters are released how does the rod cell send impulses to the bipolar cell when there is light? Because in all my textbooks it goes on to say that the bipolar neurones become depolarised, but how can depolarisation occur without neurotransmitters?

Another thing that confused me is, in the dark, the neurotransmitters are released, so the bipolar neurone cannot become depolarised, so how the hell do we see in the dark if no action potential occurs in the bipolar neurone during the dark?

[asaaal]

(Original post by osake)
From all the textbooks I have read, and from what my teachers have told me, in light rhodopsin gets bleached, opsin binds to membrane which causes sodium ion channels to close, so membrane becomes hyperpolarised. This results in no inhibitory neurotransmitters being released. If no neurotransmitters are released how does the rod cell send impulses to the bipolar cell when there is light? Because in all my textbooks it goes on to say that the bipolar neurones become depolarised, but how can depolarisation occur without neurotransmitters?

Another thing that confused me is, in the dark, the neurotransmitters are released, so the bipolar neurone cannot become depolarised, so how the hell do we see in the dark if no action potential occurs in the bipolar neurone during the dark?

Is this for OCR?

[osake]

(Original post by asaaal)
Is this for OCR?

Nope, edexcel

[Eloades11]

(Original post by osake)
From all the textbooks I have read, and from what my teachers have told me, in light rhodopsin gets bleached, opsin binds to membrane which causes sodium ion channels to close, so membrane becomes hyperpolarised. This results in no inhibitory neurotransmitters being released. If no neurotransmitters are released how does the rod cell send impulses to the bipolar cell when there is light? Because in all my textbooks it goes on to say that the bipolar neurones become depolarised, but how can depolarisation occur without neurotransmitters?

Another thing that confused me is, in the dark, the neurotransmitters are released, so the bipolar neurone cannot become depolarised, so how the hell do we see in the dark if no action potential occurs in the bipolar neurone during the dark?

As you have already said, in the dark there is a constant release of neurotransmitters. Action potentials in the rod cells work in the opposite to neurones. This means that when there is light detected, neurotransmitter release is inhibited causing hyperpolarisation, this sends the signals to the optic nerve.

[Friar Chris]

Hehehe this was one of my favourite bits of neuro...


In the absence of light stimulation, Sodium channels in photoreceptors are kept open by the action of cyclic guanosine monophosphate (cGMP), because cGMP is produced by the enzyme guanylate cyclase that is constitutively active in the photoreceptor cell.

Rhodopsin of a rod cell exists in its normal, inactive state bound to 11-cis retinene (carrots are a good source of this compound, hence the old wives' tale). When light energy stimulates the rhodopsin, this causes a change in its conformation that isomerises 11-cis retinene to trans-retinene. By chemistry bla bla, trans-retinene activates a g-coupled protein called Transducin, which in turn causes activation of cGMP phosphodiesterase enzymes, that cleave cGMP to GMP. The reduced [cGMP] resulting means that sodium channels close as they are not held open by cGMP, therefore causing hyperpolarisation and thus reduced neurotransmitter secretion.

The neurotransmitter involved is usually glutamate, which is excitatory in most parts of the nervous system, but is inhibitory in the retina.



Simplified:

Rod cell is highly permeable to sodium when not activated
This is because an enzyme called guanylate cyclase is constantly producing cGMP
cGMP causes sodium channels to open


Light > Rhodopsin
This causes rhodopsin to isomerise 11-cis retinene to trans-retinene.
Trans-retinene activates a protein called transducin.
Transducin activates phosphodiesterases that cleave cGMP, therefore reducing its concentration in the rod cell.
Less cGMP means less sodium channels open.
>> Hyperpolarisation.

[osake]

(Original post by Eloades11)
As you have already said, in the dark there is a constant release of neurotransmitters. Action potentials in the rod cells work in the opposite to neurones. This means that when there is light detected, neurotransmitter release is inhibited causing hyperpolarisation, this sends the signals to the optic nerve.

But for a neurone to send a signal to another neurone doesn't neurotransmitters need to diffuse across the synapse to the other neurone? If neurotransmitter release is inhibited how is the neurone communicating with the optic nerve?