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    (Original post by abcdemilyxx)
    same here, just got to go over transcription factors and the lobes in the brain and i'm all done :yep: need an A so it'll hopefully be enough.
    transcription factors?! and lobes are pretty easy..
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    How are local electric currents generated........the book points arrows from the +ve charge to the -ve ,but does that mean the Na+ is attrated to -ve ions or what...??? Please help!
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    (Original post by shuvo_roy)
    Can be used to switch on neurons which control aggression;
    Can be used to switch off neurons for conscious thought, which helps to interrogate prisoners of war and make them speak the truth about enemy secrets;
    the pain thing, etc!
    a bit like...



    :rofl:

    That's how I remember it anyways :erm:
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    (Original post by shuvo_roy)
    How are local electric currents generated........the book points arrows from the +ve charge to the -ve ,but does that mean the Na+ is attrated to -ve ions or what...??? Please help!
    Do you mean the action potential ie. depolarisation/repolarisation ??
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    (Original post by orangeism)
    thanks so much for this!

    and not to sound pushy or anything but do u happen to know how to answer this:

    1. describe the symptoms of parkinson's disease and Explain how the "chaotic activity" in the subthalamic nucleus of patients with parkinson's leads to such symptoms?

    seems like there's more ques on the "dancing worms" part of the article than "stressed out" and "pain and gender"... hmm
    no worries,
    Sysmptons are easy and pretty obvious as PD is related to the 'movement disorders'.
    therefore, limb shaking, everything related to the motor sensory. Sleeping difficulties, behavior problems etc.

    The main function of the STN is not mentioned, and I haven't found any either.
    It is present in the base of the forebrain and strongly connected with the cerebral cortex, thalamus and other areas. So must be associated with a variety of functions, like motor control and learning.
    That's all I can say - Might be due to insufficient Dopamine, causing STN to dysfunction. BUT PLEASE DO CHECK
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    thanks for that samydude. yeah i couldn't find a function for STN either. hope they dont ask anything on that tomorrow..

    and any help with this question, anyone?

    Normal cells do not respond to light stimulus except the rhodopsin & iodopsin containing rods and cone cells; how could the scientists engineer neuronal cells that are sensitive to light?

    thanks!
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    (Original post by Pedus)
    transcription factors?! and lobes are pretty easy..

    it's in the drugs bit of topic 7, how they bind to parts of a certain gene to produce more or less of it to enhance performance.

    lol i hope so, i haven't even looked at them!
    my teacher rushed through the course to try to finish on time so i've had to play catch up
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    Ok people, this might be my last post.

    Let me give you everything i have -

    a) Dancing Worms -
    All to do with Topic 8 (Grey Matter) - Nervous system = Electrical.
    Some key ideas (straight from the article) -

    "At least one brain imaging study has shown that electrical stimulation of the STN can accidentally turn on nearby nerve fibres that connect to the limbic system, a network of brain areas
    that controls mood." (p3 para.3)

    “By shining light, you can then activate only one type of neuron at a time, while leaving the others alone.” (last line of p3)

    "Unlike P2X2, ChR2 is inherently sensitive to light, which meant researchers could probably use it in animals’ brains without having to inject them with a light-sensitive compound first." (p4 para. 6)

    "Unfortunately, unlike worms and fly larvae, humans and rats have opaque heads, so getting light into their brains presents a challenge."
    ...a member of Deisseroth’s team, has created a device that delivers light to the brain using hair-thin optical fibres."


    All about genetics, be sure you know gene therapy inside out.


    Will post about the other two articles ...
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    (Original post by abcdemilyxx)
    it's in the drugs bit of topic 7, how they bind to parts of a certain gene to produce more or less of it to enhance performance.

    lol i hope so, i haven't even looked at them!
    my teacher rushed through the course to try to finish on time so i've had to play catch up
    yea exactly the same.. some bits im reading now, it feels like im learning this from scratch.

    ah ok, will look at that later.
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    (Original post by Pedus)
    yea exactly the same.. some bits im reading now, it feels like im learning this from scratch.

    ah ok, will look at that later.

    we'll be alright :yep:

    chances are the paper will just be all how science works anyway, silly edexcel.
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    (Original post by samydude)
    Might be due to insufficient Dopamine, causing STN to dysfunction. BUT PLEASE DO CHECK
    student book says that lack of dopamine -> control of motor functions gradually lost. i'm assuming that motor control is lost due to the fact that less dopamine present in the brain means less activity in the brain. but the article mentions that it's the chaotic activity in STN that leads to parkinson's..?

    gulp.. HELP! any idea why the article says chaotic activity? or am i understanding this all wrong
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    I m getting so confused After readinf all the answers posted by people and thanx so much to Sidrah and skotch and doughboy for helping...
    just finished reading the whole thread after 2 hours
    phew
    now time to read wat i downloaded all this way
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    (Original post by orangeism)
    thanks for that samydude. yeah i couldn't find a function for STN either. hope they dont ask anything on that tomorrow..

    and any help with this question, anyone?

    Normal cells do not respond to light stimulus except the rhodopsin & iodopsin containing rods and cone cells; how could the scientists engineer neuronal cells that are sensitive to light?

    thanks!
    Remember, Rhodopsin and Iodopsin are both Secondary Receptors. Meaning they're specialized for sensing light. The question is crappy, I say.
    If they had to engineer neuronal cells, they would have to attach rhodopsin or Iodopsin to the neuronal cells to function as sensing light.

    Can it be possible to use a hormone/photochrome to trigger the impulse or neurone ... hmm :confused:
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    (Original post by orangeism)
    thanks for that samydude. yeah i couldn't find a function for STN either. hope they dont ask anything on that tomorrow..

    and any help with this question, anyone?

    Normal cells do not respond to light stimulus except the rhodopsin & iodopsin containing rods and cone cells; how could the scientists engineer neuronal cells that are sensitive to light?

    thanks!
    ChR2 are extracted from single-celled pond algae which is inherently sensitive to blue light!
    NpHR is isolated from desert-dwelling microbe, which is sensitive to yellow light!

    So, genitically engineering cells to produce these proteins can make the cells light sensitive!
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    (Original post by Pedus)
    Do you mean the action potential ie. depolarisation/repolarisation ??
    Page 206 of the green book by Ann Fullick.

    When stimulated, the Na+ move into the axon, thus depolarising the membrane, and local electric currents are generated in the membrane......how's that?
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    (Original post by orangeism)
    student book says that lack of dopamine -> control of motor functions gradually lost. i'm assuming that motor control is lost due to the fact that less dopamine present in the brain means less activity in the brain. but the article mentions that it's the chaotic activity in STN that leads to parkinson's..?

    gulp.. HELP! any idea why the article says chaotic activity? or am i understanding this all wrong
    Ok, Dopamine is a neurotransmitter.
    When there is no Dopamine i.e no neurotransmitter, there will be no transfer of an impulse. Therefore the pre-synaptic knob will be filled with Na+ as it tries to pass the cleft. Thus an increase in action potential in the PRE-SYNAPTIC KNOB. We say it as 'High frequency oscillatory activity' thus going 'nuts'. :eek3:
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    (Original post by samydude)
    Ok, Dopamine is a neurotransmitter.
    When there is no Dopamine i.e no neurotransmitter, there will be no transfer of an impulse. Therefore the pre-synaptic knob will be filled with Na+ as it tries to pass the cleft. Thus an increase in action potential in the PRE-SYNAPTIC KNOB. We say it as 'High frequency oscillatory activity' thus going 'nuts'. :eek3:
    I agree Completely :yep: :yep: :woo: :woo: :cool:
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    Anyone got the answers to the topic tests in the green book of ann fullick... you could say even after all the waffel not providing answer for the questions is a rip off as the chem and phys ones do provide answers
    cant wait till the 29th when all my exams are over
    phew!!!:eek3: :eek: :confused:
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    realised we don't need to understand how the resting potential arises....just how its restored after depolarisation grrrrr cost me 2 hours last week
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    isnt it caused by a difference in the potential of inner and outer membrane and the inner is negative compared to the outside??
 
 
 
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