5-HT2A receptor and Asperger.

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Not surprising considering the fact that AS is a neurological disease. I wonder if there are abnormal dopamine and epinephrine release in aspies as well? That might explain the fact that ADHD/ADD often goes hand in hand with ASD.

Best thing to do is get a (TMA) Tissue Mineral Analysis test, that way you don't waste money on stuff that you don't need and end up going Dangers in either way...

http://www.futurepundit.com/archives/002127.html
http://news-info.wustl.edu/tips/page/normal/864.html

This links talkes about "depressed people have fewer 5-HT2A serotonin receptors"

Yes but they is different types of depression, traumatic / emotional / chemical , trying to attack the 2 first ones with a drug would be just a mood lifter, my doctor has dropped bothering with drugs as I have refused to go on multi ones....

The thought pattern would be more likely the source of the start of depression as you need something to trigger depression, chemical will work on people that has gone out of whack but not with people who are depressed from outside sources, plus drugs don't work on they own, as its just a mood-stabilizer, if you don't take away what is coursing it to trigger it won't help...

I think they need to put more research into this as I find it stupid just to stick drugs at someone, and not try other methods if they don't work after a month or so, along side it...

Really this way of looking at things really needs to change, as everything left right and centre will be thrown out but the truth… Always someone who reopens it and puts more effort into it who figures it out… Would it not be cheaper to put 100% into it than focus on 1 thing...


I must be in the 30%...

http://www.erowid.org/chemicals/ssris/ssris_info1.shtml

The chart want format right so you will have to use the above link if you the one guy out there interested in my posts

IC50 for 5-HT reuptake for 5HT2A

Clomiprimine 36
Fluoxetine 100
Sertraline 45000
Paroxetine 62,000
Fluvoxamine 3,200
Citalopram 3,100

I've used fluoxetine, sertraline, paroxetine. The 5HT2A reuptake is
related to the sexual side effects (delayed oragsm usually). The above numbers confirm my own testing. Fluoxetine has low sexual side effects in men comapred to the other ssri's. Interesting I did feel more social on sertaline and paxil which got ,me thinking there maybe something to the 5HT2A receptors and social anxiety.

http://psy.psychiatryonline.org/cgi/con ... 5/3/217/T1

Don't know what venlafaxine xl, is called in america, hate that every country has a different name... nearly..

And I was on 300mgs with nothing but my mouth getting dryer... Click on the doc to make it bigger then expand if you don't have auto large on...

Only pattern I see is the person been under the dilution of this pill will help them, does weight, height, come into it on why the numbers are so different, why some do and some don't... Some get worse... going the wrong way? did they try reversing it on the ones who got worse...

look at number 8, 15 person

I had very positive effects from occasional(4X a year)use of LSD.Very spiritual and at peace with myself and the world....very NOT like my normal state of thinking/feeling.Cant say how long it lasted but at least a few weeks.I also really liked Robotussien....Only took 4ozs to make me feel at peace.Had to give up both out of fear of long term effects.

I recently tried Wellbutrin to help quit smoking and it seemed to be very helpful until I broke out in a rash and had to stop taking it....my hands itched so badly I had to take time off from work....it was horrid.

I still think there is a link between my depression and my IBS.....if 85% of serotonin is created in the "gut" it has to have some effect that my gut is "hyper-active" or "stalled".

This is very interesting information. I like studying the chemistry of the brain and all the receptors that mediate the effects of all these chemicals. It would be interesting to understand the implications of the reduced binding in social communication-impaired autistics, but it seems we don't understand nearly enough about the precise functions of the individual receptors.

That chart of drug potencies at the various brain targets is interesting. I had seen some of that information before (such as the relative 5HTRI vs. NARI vs. DARI potencies of the various drugs), since I recently wrote a paper where I modeled the three-dimensional structures of the proteins involved in reuptake and tried to rationalize the activities based on chemical structures.

Unfortunately, the data you presented came from binding (as opposed to functional) experiments, so the effect of the drugs (agonist or antagonist) at the 5-HT2A receptor cannot be inferred from it. I would assume that clomipramine is an antagonist, by considering its chemical structure and the fact that I know it is an antagonist at most of the other receptors listed.

Overall, for clomipramine it's really difficult saying what of its effect is due to 5-HT2A binding, considering the similar potencies at many targets. In addition to serotonin and norepinephrine uptake inhibition, there's a H1 blocking effect that causes drowsiness, an alpha blocking effect that causes blood pressure changes, and particularly importantly an antimuscarinic (ACh) effect that causes dry mouth and constipation.

Back in elementary school, there was a period in which psychiatrists put me on lots of antidepressants because they had no idea what was wrong, and the tricyclics (which include clomipramine) were still the first thing people tried at that time. I was on one of those drugs for all of about a month, over which I lost a lot of weight, before the constipation got so bad that there was no option other than to discontinue it. Among psychoactive drugs, my negative impression of the tricyclic antidepressants is matched only by that for the phenothiazine antipsychotics, which I luckily have never had to take and hopefully never will. Both classes tend to block neurotransmitter receptors very non-selectively, almost guaranteeing that they will cause more problems through their unwanted effects than their intended effects solve.

Later I was put on SSRIs, and fluoxetine made me giggly all the time (in fact my mom credits it with having started my ongoing bipolar-ness due to this hypomanic effect, even though I discontinued it long ago). The others just seemed to make me not sleep well. I haven't been on any antidepressants for years.