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Post by Deleted on Nov 13, 2014 11:02:09 GMT
"A darting mouse may hold an important clue in the development of Attention Deficit Hyperactivity Disorder (ADHD), autism and bipolar disorder, according to a study by a Vanderbilt University-led research team recently published in the Proceedings of the National Academy of Sciences......" Credit www.medicalnewstoday.comMore here
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Post by supine on Nov 13, 2014 16:01:51 GMT
It's interesting that they might have found some markers indicating ADHD type behaviours, but I'm a little concerned how it is they don't understand how the drugs are working currently, since they were described to me as dopamine reuptake inhibitors and that they prevent the brain re-absorbing dopamine which is used for cross brain communications. From the article.. "Blakely wonders whether stimulants like Adderall and Ritalin quell hyperactive and impulsive behaviors in some children with ADHD by reducing inappropriate dopamine leak" Which kind of gives me the impression that the drugs are acting to lower dopamine levels in the brain, I'm confused now, all these double negatives twist my melon (maaaan) And from the wiki on dopamine reuptake inhibitors: "Reuptake inhibition is achieved when extracellular dopamine not absorbed by the post-synaptic neuron is blocked from re-entering the pre-synaptic neuron. This, in turn, leads to increased extracellular concentrations of dopamine and therefore an increase in dopaminergic neurotransmission" (my emphasis)
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Post by JJ on Nov 14, 2014 10:12:43 GMT
Doesn't make sense to me either
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Post by Deleted on Nov 14, 2014 13:21:46 GMT
The theory is that there is not enough dopamine (or other neurotransmitter) in the synaptic cleft to allow consistent transmission of pulses along the nerve. You need a certain concentration - it's a bit like having fuel that is too wet to burn, at a certain % of moisture the fire can start. When a nerve fires we dump neurotansmitters into the synaptic cleft to be detected by the 'other side' - when enough detector sites are triggered the impulse continues. Too much neurotransmitter is thrown into the cleft and the system works by absorbing them at a certain rate - 'reuptake', otherwise there would be the spare amount building up when it isn't wanted. There is a constant 'leak' of neurotransmitter which keeps the system 'primed' so the amount of neurotransmitter required to trigger the next cell is fairly small. The theory is that either we aren't producing enough neurotransmitter or the reuptake sites are working WAY too fast (too many?) and hoovering it up so the required level isn't there. Treatment is, therefore, stimulating the production or slowing the reuptake of the targeted neurotransmitter. A reuptake inhibitor is a molecule that is sufficiently similar to the target molecule to be able to sit in its reuptake site - like different pieces of Lego can fit together even though they're different sizes/shapes, but the parts don't click together if you have something too different (like Duplo wont connect with regular Lego). Now the site is 'blocked' it can't hoover up the active neurotransmitter. Too much medication can cause too much neurotransmitter to be available - which you feel as jitteryness (too much firing of the nerve). "Reuptake inhibition is achieved when extracellular dopamine not absorbed by the post-synaptic neuron is blocked from re-entering the pre-synaptic neuron. This, in turn, leads to increased extracellular concentrations of dopamine and therefore an increase in dopaminergic neurotransmission" They mention 'extracellular' - we usually call it a synaptic cleft - it's the area between two nerve cells. The pulse arrives from the presynaptic side and if there is sufficient neurotransmitter the message leaps across to the post synaptic side, towards its destination. The postsynaptic side has sites where the neurotransmitter is detected (exact 'Lego' sites) - the presynaptic side has the reuptake sites, which recycles the molecule so it can be thrown into the cleft next time there is a signal. It's unbelievably fast - electricity triggers chemicals, which triggers electricity to be produced in the next cell (there are many cells between where the system starts and terminates) all in milliseconds - it can work, reload, and work again like a machine gun. Here's a pretty picture Let's hope I explained something that was unclear - I always worry I'm being patronising It's a balancing act - too little neurotransmitter and 'good' signals will not pass along the nerve, too much and 'false' signals can start
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Post by carly31 on Nov 14, 2014 14:31:46 GMT
PHWOAAAAARRR!Here's a pretty picture
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Post by JJ on Nov 15, 2014 1:00:10 GMT
Not patronising @planetdave - a good explanation. But I still don't understand, for the same reason I think that supine doesn't - if we have leaky re uptake inhibitors, then we'll have excess dopamine. But the meds increase our dopamine. And we need dopamine for impulse control. So why would the leaky re uptake inhibitors / excess dopamine be a cause for lack of impulse control?
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Post by Deleted on Nov 15, 2014 2:37:45 GMT
Hmm
I don't think they're explaining it well.
There is 'leakage' - it's a constant stream of neurotransmitters into the synaptic (extracellular) cleft.
The reuptake sites work fine (maybe too well) - there has to be a reason why we're short of neurotransmitters.
It boils down too either neurotransmitter production is low or reuptake is high - both result in insufficient neurotransmitter being available for the system to work properly.
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Post by supine on Nov 16, 2014 15:14:16 GMT
Thanks for the explanation @planetdave
The comment I quoted appears to suggest that hyperactivity is caused by too much leakage of dopamine, so I think my confusion came about because I thought ADHD meant there was too little dopamine to carry signals - but I now think that ADHD is either too much, or too little, dopamine. Does that sound right?
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Post by Deleted on Nov 17, 2014 1:39:15 GMT
ADHD is having too little neurotransmitter to make the nervous system reliable - too much medication could cause excessive amounts of neurotransmitter to build up - we usually experience that as 'jitteryness' (it's nerves getting hyper sensitive and firing off when there isn't a 'true' signal to transmit, they go off like a fireworks factory in a thunderstorm). There has to be a syndrome that is the opposite to ADHD (Schizophrenia?) ie where either excess dopamine is produced or not reabsorbed quickly enough (you can't 'unblock' reuptake sites but you could block receptor sites to bring it into the Goldilocks zone).
Try not to get hung up on dopamine - it's the most famous of the neurotransmitters involved in ADHD but there is an extensive list of them and they all need to be in balance.
It's incredible that any nervous system works at all, it's completely bonkers in complexity and the requirements to maintain minerals, fats and proteins in precise coordination.
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Post by shiveringsky on Nov 17, 2014 20:00:54 GMT
So the problem is the pretty pink blobs shoot off too much dopamine? Or the bit on the yellow which has had a bite taken out of it cant absorb it? (Or Im just making it even less clear... sorry. Genuinely want to follow this.)
I really half wish the issue was dating mice. Though it would bring up the confusion of 'when did i do that?'
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