Latest Neural Research: Changing Channels | ADHD Information

I came across this today, and thought it might be somewhat relevant... I look forward to reading people's thoughts and theories on this one!

http://www.livescience.com/humanbiology/050325_brain_channel s.htmlThat's really interesting.  That may be the brain's mechanism for maintaining homeostasis, tolerating drug effects (like when a drug stops working), etc.  Even if it is just a matter of cell survival by avoiding excitoxicity, that doesn't mean this process doesn't result in more elaborate functions, too.  Evolution's been fine-tuning for a long time now.  Most of our 'higher' functions do boil down to one component or another trying to ensure its own survival.  Heck, GENES seem to have a survival drive (see Richard Dawkins' The Selfish Gene) and some pretty intricate things arise from their actions (e.g., everything that lives). 

I know that a neuron can add more excitatory channels (e.g., the glutamatergic AMPA receptor), but I didn't know that it could switch channels like that.  Does that mean a normally excitatory cell could become an inhibitory cell?  That has some pretty huge implications.  ... for LOTS of diseases that involve excitotxicity, like epilepsy.  Maybe the seizure prone brain lacks this mechanism in some cells and therefore cannot prevent excitotoxicity?

You know when you feel really overwhelmed or overstimulated and then you feel stuck?  like you couldn't think what to do next if your life depended on it?  I wonder...  ok, as usual I'm getting carried away.

I'm trying to see the implications of this mech for AD(H)D, but I always get confused with how inhibition works in this case... When my brain freezes up and I can't make it work, I feel like my inhibitory response is working overtime... but when I won't shut up or exercise bad judgement, I feel like my inhib response has totally forsaken me... which is it?  It's really hard to draw a 'systems' conjecture about a mechanism when it operates at the molecular level.

I have to admit a lot of doubt about that final statement: 'If doctors could swap the calcium-allowing channels in these cells for the kind that keeps calcium out, it might be possible to prevent the cells from dying.' ... If dr.s could really do that, it would keep the signal from being sent at all. The action potential is an all-or-nothing event.  If enough calcium (/sodium) doesn't enter the cell to bring the current above threshold, the neuron just doesn't fire and the cell downstream of it never hears a thing.  What they need to do is attenuate the Ca2+ influx and to do that (using the newly discovered mechanism), they would need to sitch only a certain proportion of excitatory channels for inhibitory ones and that proportion would depend on the patient.  They would need really smart nanobots for that (nanobots that could assay the amount of both kinds of protein on every neuron in the path and 'replace' them or antagonize them or whatever.. and of course it's not like there's one protein for positive ion admitting channels and another for chloride channels.  the nanobots would have to be able to distinguish between several types of glutamate receptor proteins and several GABA receptor proteins.... hmmm.  Nanobots are around the corner though.  As are cybernetic implants..