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    (Original post by ConnorB)
    Can someone explain what effect Parkinsons has on the brain and why L-Dopa is prescribed to patients with the condition? (5/6 marker? )
    5 to 6 mark !! ill try...

    the levels of dopamine reduce in basal ganglia area of the brain so impulses cannot be fired to motor neurones originating from this area of brain, this result in tremors in hands and difficulty in motion . L dopa is a precursor of dopamine and also it can cross the blood brain barrier and enter the brain effectively, once inside the brain it is converted to dopamine thus escalating the levels of dopamine in basal gnaglia and healing the disease.
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    (Original post by pandoraclaire)
    there is a thread about the pre release on here, i have collected all of the questions people have put up and started to answer them. If you want i could put some of the practice questions people have put up so far on this thread? It covers quite a few things =/
    HEYY HII! Can u post up the questions here? i reeeeeeaaaallly need them noww.pleaseeeeee im having a major nervous breakdown D:
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    (Original post by iesians)
    5 to 6 mark !! ill try...

    the levels of dopamine reduce in basal ganglia area of the brain so impulses cannot be fired to motor neurones originating from this area of brain, this result in tremors in hands and difficulty in motion . L dopa is a precursor of dopamine and also it can cross the blood brain barrier and enter the brain effectively, once inside the brain it is converted to dopamine thus escalating the levels of dopamine in basal gnaglia and healing the disease.
    Very Good

    I'd also of said that it is converted to dopamine through the enzyme dope-decarboxlyase and that more nerve impulses are transmitted across synapses in the parts of the brain that controls movement (Cerebellum)

    But you probably would have got the marks anyway
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    Can someone explain what effect Parkinsons has on the brain and why L-Dopa is prescribed to patients with the condition? (5/6 marker? )
    Parkinson's disease: neurons in frontal cortex and spinal cord become inactive as dopamine neurotransmitter is not released. Motor function affected and a result symptoms such as depression, poor balance and movement and difficulty in speech are observed. Treatments include L-dopa, Dopamine agonists, MOAB inhibitors, gene therapy and stem therapy. L-dopa is a precursor of dopamine and so is converted into dopamine after crossing the blood brain barrier. Their structure is very similar. Dopamine cannot pass the blood brain barrier because of size. It relieves the symptoms (L-dopa) and mimics the activity of dopamine.
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    (Original post by ConnorB)
    Very Good

    I'd also of said that it is converted to dopamine through the enzyme dope-decarboxlyase and that more nerve impulses are transmitted across synapses in the parts of the brain that controls movement (Cerebellum)

    But you probably would have got the marks anyway
    WTHH im totally clueless about that enzyme !!?!?!:eek:
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    (Original post by ConnorB)
    Can someone explain what effect Parkinsons has on the brain and why L-Dopa is prescribed to patients with the condition? (5/6 marker? )
    With those who have Parkinson's the basal ganglia neurones die which are responsible making dopamine which is released into the motor cortex, as a result, the person has problems with movemement and characteristic symptoms include muscle stiffness, walking difficulties, tremours due to a dopamine deficiency. L dopa is prescribed rather than dopamine because it is small enough to cross from the blood into the brain and then made into dopamine, reducing the symptoms.

    oh gosh, I need to revise :/
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    WTHH im totally clueless about that enzyme !!?!?!
    You don't have to remember the name lol
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    And how does MDMA affect synaptic Transmission (3)
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    Can someone explain the Krebs Cycle to me please?
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    (Original post by ConnorB)
    And how does MDMA affect synaptic Transmission (3)
    ummm is MDMA ecstasy ??! lol
    if yes then
    it is a selective serotonin reuptake inhibitor, so it halts the reuptake of serotonin back in pre synaptic membrane thus mantaining a high conc of serotonin in synapse resulting in constant firing of action potential in post synaptic neurone.
    it may also trigger the release of more serotonin.
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    (Original post by iesians)
    i think deoxygenated absorbs radio signals ! and oxygenated does not thats why active areas are lighter
    So they are lighter because the signal is not being absorbed?
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    And how does MDMA affect synaptic Transmission (3)
    I think it mimics the activity of the neurotransmitter. Prevents neurotransmitter uptake/breakdown, more of it remains in synaptic cleft. Binds to post synaptic membrane, Na+ channels open, membrane depolarized. Results in action potentials.

    Promotes serotonin synthesis too and is more readily taken up. Affects pathways responsible for mood, sleep, perception and appetite. Interacts with reward pathways. Milder release of dopamine too so has addictive properties. Is considered a stimulant and causes one to become psychoactive. Increases heart rate through sympathetic pathway. Causes one to feel dehydrated, is a anti-diuretic so kidneys do not produce urine and cells lysed by osmosis. could lead to death.
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    (Original post by VickyDoodle)
    Can someone explain the Krebs Cycle to me please?
    acetyl group combines with oxaloacetate and the cycle starts, in this cycle the compounds are constantly oxidised and carbon is removed form chains, the released carbon escapes as carbon dioxide. the H ions released from oxidation of intermediates reduces NAD and FAD , in the end an oxaloacetate molecule is regenerated and so can once again combine with acetyl group and start the cycle again.
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    (Original post by ConnorB)
    And how does MDMA affect synaptic Transmission (3)
    MDMA binds to a molecule on the presynaptic membrane preventing the reuptake/reabsorption of the neurotransmitters. This means that a high concentration of neurotransmitters remains in the synapse causing action potentials being continually generated on the postsynaptic membrane.
    MDMA can also reverse the transport mechanism of pumps resulting in a further increase in seretonin.
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    (Original post by fudgesundae)
    So they are lighter because the signal is not being absorbed?
    100%
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    (Original post by ConnorB)
    Can someone explain what effect Parkinsons has on the brain and why L-Dopa is prescribed to patients with the condition? (5/6 marker? )
    1. The dopamine secreting neurones in Basal Ganglia die
    2. Therefore significantly less of the neurotransmitter dopamine is released and so the muscle cortex receives less dopamine leading to a lack of control of muscles.
    3. Symptoms of the disease include depression, poor speech, difficulties walking, muscle spasms.
    4. L-dopa is a precursor of dopamine, which cannot be given straight to the patient as it cannot travel from the bloodstream to the brain.
    5. L-dopa can and so when it enters the brain it is converted into dopamine.
    6. This increases the concentration of dopamine in the neurones and so dopamine can bind to receptors and the symptoms of the disease decrease.

    Would this get me 6 marks?
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    (Original post by ConnorB)
    And how does MDMA affect synaptic Transmission (3)
    It binds to serotonin reuptake molecules on the pre synaptic membrane, preventing them from taking up serotonin from the synaptic cleft. Hence the concentration of serotonin in the cleft increases and so the person experiences feelings of extreme happiness.
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    (Original post by iesians)
    100%
    ok thanks
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    Would this get me 6 marks?
    should do.
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    what is the structural difference b/w tendons and ligaments ??! (3 marks)
 
 
 
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