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    hi, can sum1 explain how a synapse works, i get all of it until how when the transmitter substance e.g acetylcholine is released, and diffuses through the synaptic cleft and binds onto the receptors on the postsynaptic membrane, but what happens nxt? can sum1 kindly explain...thanx
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    ahh i love the synapse ok get ready.. When a nerve impulse (action potential) arrive at the pre synaptic knob, it causes an influx of calcium ions into the pre synaptic membrane. This results in the movement of neurotransmitter containing vesicles (the neurotransmitter being acetylcholine) to bind and fuse with the presynaptic membrance and release their contents by exocytosis. acetylcholine then diffuses across the synaptic cleft (or synapse) and the transmitter then binds with the receptors on the post synaptic membrance which results in an influx of sodium ions into the post synaptic knob results in the propagation of an action potential . Enzymes in the synaptic cleft break down the transmitters substance at the receptors to prevent over stimulation. Forgotten what its broken up into doh!. The products of the breaking down of acetylcholine by the enzymes diffuse back into the pre synaptic knob and ATP from mitochondria is used to resynthesise acetylcholine for use again hope this helps.
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    ACh is broken down into acetate and choline by acetylcholinesterases

    /edit: and it is only choline which is reabsorbed (and then recycled to form ACH with the aide of Acetyl CoA)
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    (Original post by iceman_jondoe)
    This results in the movement of neurotransmitter containing vesicles (the neurotransmitter being acetylcholine)
    Jut to prevent confusion, it is not always ACh which is the neurotransmitter, there are many other possibilities
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    kool...thanx guys!!
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    was this not in the edexcel exam paper this year!
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    MY FAVOURITE!!

    actions potential cannot jump across synapses, they pass along transmitter substances eg acetylcholine.

    bascially, action potenial (AP) arrives at pre-syn membrane which causes uptake of calcium ions.

    ca ions cause vesicles containing acetylcholine to fuse with pre-syn membrane.

    achetylcholine (ACH)is released and diffuses across the synpatic cleft

    ACH molecules bind with receptors in the post-syn causing them to open sodium channels

    sodium ions flood in through the open channels in the post-syn memmbrane. this depolarises the memmbrane and initiates an AP.

    hope this helps
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    ^^ surely that's exactly what iceman_jondoe said two days ago!
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    and ur point is?
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    (Original post by ogechi)
    and ur point is?
    Why post it, especially after the OP had read it?? :rolleyes:
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    I had a question regarding the roles of a synapse - I just want to make sure I have the right idea:

    A Synapse causes various reactions to a possible stimulus. It does this by interconnecting pathways along which information is passed to the nervous system. So, information is passed to the nervous sytem. In the brain, each neurone has thousands of synapses with other neurones. Some of these synapses will release a neurotransmitter which will actually cause an action potential to be created in the postsynaptic membrane, and hence causing the a reaction in the muscles, for example. Other synapses will release a neurotransmitter which will actually prevent the depolarization of the postsynpatic membrane, hence inhibiting it. What causes which neurotransmitter should be released, depends on the summed effect of the number and frequency of action potentials arriving at the inhibitory and stimulatory synapses of this particular neurone in the brain.

    is that right or did I understand it wrong?

    Thank you for any help! I did try and look for this on the web, but everything that showed confused me even more :blush:
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    sounds good to me!
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    great! Thank you!
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    I was under the impression that each neurone released a unique neurotransmitter at the synapse, and this couldn't be changed by altering the frequency of action potentials.
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    i think each neurone releases more than one neurotransmitter, and the amount of each released depends on the frequency of stimulation.
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    (Original post by j00ni)
    I was under the impression that each neurone released a unique neurotransmitter at the synapse, and this couldn't be changed by altering the frequency of action potentials.
    Some release more than one, though you won't get one releasing, say GABA and ACh. There are co-transmitters which may be released along with the main one, though. But yes, the type of neuron also affects which NT will be released.
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    (Original post by Helenia)
    Some release more than one, though you won't get one releasing, say GABA and ACh. There are co-transmitters which may be released along with the main one, though. But yes, the type of neuron also affects which NT will be released.
    Oh, ok, what I was getting at though is that surely one synaptic know wouldn't release both stimulator and inhibitory NTs
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    ^ Was just thinking the same thing.
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    (Original post by j00ni)
    Oh, ok, what I was getting at though is that surely one synaptic know wouldn't release both stimulator and inhibitory NTs
    No, I don't think it would. However, although I'm not sure you need to know this for A-Level, some, like ACh, can be both excitatory or inhibitory depending on which receptor they bind to. For example, if a low frequency stimulus causes a small burst of ACh release, it will only be able to get across the synaptic cleft and bind to the receptors there before it is hydrolysed. However, if a higher frequency stimulus causes a larger ACh release, some of this may escape the synaptic cleft and bind to extrasynaptic receptors which may cause different (inhibitory) effects in the cell. So it's possible, though that's much more about fine tuning and regulating the system than causing totally opposing effects.
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    (Original post by Helenia)
    No, I don't think it would. However, although I'm not sure you need to know this for A-Level, some, like ACh, can be both excitatory or inhibitory depending on which receptor they bind to. For example, if a low frequency stimulus causes a small burst of ACh release, it will only be able to get across the synaptic cleft and bind to the receptors there before it is hydrolysed. However, if a higher frequency stimulus causes a larger ACh release, some of this may escape the synaptic cleft and bind to extrasynaptic receptors which may cause different (inhibitory) effects in the cell. So it's possible, though that's much more about fine tuning and regulating the system than causing totally opposing effects.
    What do you mean by that exactly, where? I haven't come across this
 
 
 

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