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any idea how visuals work?

Migrated topic.
rawmo

rawmo

Rising Star
Hey there,

i'm trying to track down some info on how psychelics [e.g. DMT] affect the visual pathways in the brain. [how they think they work and affect our vision in such distinct ways]
e.g.
any knowledge that has been worked out re the style of visuals created, the physiology, brain patterns (MRI stuff?] and all that.

any links or info appreciated : )
 
It's obviously magic. @_@
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yeah, that's exactly what i thought ; )

other than that i remember someone saying something along the lines that science and magic can be indistinguishable...
 
rawmo said:
Hey there,

i'm trying to track down some info on how psychelics [e.g. DMT] affect the visual pathways in the brain. [how they think they work and affect our vision in such distinct ways]
e.g.
any knowledge that has been worked out re the style of visuals created, the physiology, brain patterns (MRI stuff?] and all that.

any links or info appreciated : )
Click to expand...

This is a great video but will take a long time to download:

http://www.torrentreactor.net/torre...-mind-Recent-advances-of-psychedelic-research

It's from a conference on the pharmacology of psychadelics. Talks from all kinda folks from animal research to fMRI.
 
One thing I'd like to point out:

I spent a few hours in the chapel of sacred mirrors once. Just gazing at Alex Grey's amazing art up close. The meditations were profound.
After a while I sat there in the middle and closed my eyes
and everything I had just looked at was there, except it was interwoven, and flowing beautifully.

My brain/consciousness took the data from all of his art and compiled it into these epic, curling, visions.
 
rawmo said:
Hey there,

i'm trying to track down some info on how psychelics [e.g. DMT] affect the visual pathways in the brain. [how they think they work and affect our vision in such distinct ways]
e.g.
any knowledge that has been worked out re the style of visuals created, the physiology, brain patterns (MRI stuff?] and all that.

any links or info appreciated : )
Click to expand...
I think benzyme once attached a cool scientific poster proposing some mechanisms of how visuals work. I re-attach it here for reference.
 

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that poster was well interesting. who made it? got any more?

ps for complicated stuff like this I love all the pictures and arrows, much nicer than reading a massive essay for my simple brain
 
^^See the references on the bottom right hand of the poster. They should lead to much more information. I recommend looking on a database like google scholar or pubmed the titles of those papers. Then look for people who have cited then to find more recent papers. If you are having trouble finding full text for an interesting article let me know and I can see if I have access to it.
 
slidewinder said:
One thing I'd like to point out:

I spent a few hours in the chapel of sacred mirrors once. Just gazing at Alex Grey's amazing art up close. The meditations were profound.
After a while I sat there in the middle and closed my eyes
and everything I had just looked at was there, except it was interwoven, and flowing beautifully.

My brain/consciousness took the data from all of his art and compiled it into these epic, curling, visions.
Click to expand...

Sweet! :lol:
 
James Kent made signal theory. There are problems with signal theory although it is at least a start. For starters the role of 5-HT2a in the visual effects is questionable. Also ST is admittedly completely unable to explain the more complex types of visuals but it is an interesting start regarding some of the mild "open eye" visuals. It is known that many of the visuals result from activity at higher levels cortical circuits rather than early regions such as the retina, thalamus (LGN), or V1. Additionally it is likely that specific cortical regions are involved in each "class" or "form" of visual effects. Imaging studies are going to be required to sort this all out. Additionaly lesion studies will also be required to associate specific cortical regions with categories of visual effects.

Also there is evidence suggesting that receptors other than 5-HT2a, and other 5-HT receptors are responsible for the visuals (Wallach's endogenous hallucinogen article:Erowid.org: Erowid Reference 7404 : Endogenous hallucinogens as ligands of the trace amine receptors: A possible role in sensory perception : Wallach JV). Several compounds with 5-HT2a activity that are considered hallucinogens lack visuals. In fact many compounds lack visuals but are still hallucinogens (5-Meo-DMT, DET, MIPT, AMT....) there are also 5-HT2a agonist that are not hallucinogenic at all. This is a fascinating area unfortunately little is known.

There is not much information on this. It is very fascinating and a group in germany has recently published a few articles using imaging studies during DMT and Ketamine experiences (type DMT and ketamine into google scholars and a few should come up). SWIM left his bag in the office with the articles but will post the titles later on. Science does not even know where normal waking visual experience comes form let a lone hallucinogen induced visuals. However hallucinogens are a unique tool to study the processes in the CNS involved in subjective experience.
 
bufoman said:
James Kent made signal theory. There are problems with signal theory although it is at least a start. For starters the role of 5-HT2a in the visual effects is questionable. Also ST is admittedly completely unable to explain the more complex types of visuals but it is an interesting start regarding some of the mild "open eye" visuals. It is known that many of the visuals result from activity at higher levels cortical circuits rather than early regions such as the retina, thalamus (LGN), or V1. Additionally it is likely that specific cortical regions are involved in each "class" or "form" of visual effects. Imaging studies are going to be required to sort this all out. Additionaly lesion studies will also be required to associate specific cortical regions with categories of visual effects.

Also there is evidence suggesting that receptors other than 5-HT2a, and other 5-HT receptors are responsible for the visuals (Wallach's endogenous hallucinogen article:Erowid.org: Erowid Reference 7404 : Endogenous hallucinogens as ligands of the trace amine receptors: A possible role in sensory perception : Wallach JV). Several compounds with 5-HT2a activity that are considered hallucinogens lack visuals. In fact many compounds lack visuals but are still hallucinogens (5-Meo-DMT, DET, MIPT, AMT....) there are also 5-HT2a agonist that are not hallucinogenic at all. This is a fascinating area unfortunately little is known.

There is not much information on this. It is very fascinating and a group in germany has recently published a few articles using imaging studies during DMT and Ketamine experiences (type DMT and ketamine into google scholars and a few should come up). SWIM left his bag in the office with the articles but will post the titles later on. Science does not even know where normal waking visual experience comes form let a lone hallucinogen induced visuals. However hallucinogens are a unique tool to study the processes in the CNS involved in subjective experience.
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Nichols has some interesting insight on the mechanisms
see p. 24 (in Adobe Acrobat/Reader)
 

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Wallach's recent 2009 article however shines some reasonable doubt on any 5-HT2a model of hallucinations. 5-HT2a agonists exist that are powerful hallucinogens yet lack any visuals (5-MeO-DMT, MIPT, AMT, DET). Furthermore 5-HT1a opposing activity can not explain the attenuation in visuals. Many 5-HT2a agonist exist that are not even hallucinogenic although agonist directed trafficking may explain this. I think the major visuals result from an as yet uncharacterized mechanism possibly an endogenous hallucinogen site. It seem that direct activity on higher level cortical circuits is likely involved. This would explain the level of intricacy and complexity. If endogenous hallucinogens are involved in higher level cortical processes which is very possible than this may be were administered HA get a portion of their effects from.
 
bufoman said:
Wallach's recent 2009 article however shines some reasonable doubt on any 5-HT2a model of hallucinations. 5-HT2a agonists exist that are powerful hallucinogens yet lack any visuals (5-MeO-DMT, MIPT, AMT, DET). Furthermore 5-HT1a opposing activity can not explain the attenuation in visuals. Many 5-HT2a agonist exist that are not even hallucinogenic although agonist directed trafficking may explain this. I think the major visuals result from an as yet uncharacterized mechanism possibly an endogenous hallucinogen site. It seem that direct activity on higher level cortical circuits is likely involved. This would explain the level of intricacy and complexity. If endogenous hallucinogens are involved in higher level cortical processes which is very possible than this may be were administered HA get a portion of their effects from.
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And how about the hypothetical scenario in which non-hallucinogenic 5-HT2a agonist psychoactives are also antagonists of other receptors, therefore by definition of their action they "block" the visuals?

Or how about the activity of psychedelics on 5-HT2c or other 5-HT2 receptors?It is not unlikely that even minor activity of some psychoactive compounds on other serotonin receptors creates a synergy necessary to overcome a threshold and induce downstream hallucinogenic activity.

For the moment SWIM remains a bit sceptical about the details of psychoactives - receptor association studies. In their majority they are performed in vitro in either tissue cultures usually artificially expressing the receptor(s) to-be-tested. Not that we haven't learned a lot, but the exact mechanisms and fine details of their action (that usually makes the difference) are by large unknown to us.
 
I agree I am skeptical as well. The attenuating effect has been proposed for 5-HT1a as 5-HT1a activity opooses 5-HT2a activity in the cortex. Wallach covers this theory and shows that compounds exist with do not fit this model. I think all he implies is that all current models are flawed. Bufotenine for example has significant activity at 5-HT1a (more than 5-MeO-) as does Psilocin and DPT these compounds have visual effects. Also AMT has little activity at 5-HT1a yet still lacks visuals, as does MIPT. 5-HT2c activity does not correlate with visuals either.

5-HT2a seem far more likely involved in the hallucinogen experience but probably not the visuals.

There is no evidence to support 5-HT2a aside from antagonist studies however these antagonists may bind to receptors other than 5-HT2a however they do not bind to other known 5-HT sites (this excludes other 5-HT receptors).

However for example these antagonists (ritanserin, ketanserin) may bind to trace amine receptor as well as other unknown sites. The active sites of the TAAR and 5-HT2 are almost identical. Interesting some non-visual hallucinogens, 5-MeO, bind to TAAR only weakly... while it may not be TAAR1 it shows that these receptors can have selectivity by modifying a few key AA in the active site.

It may be that these unknown sites that the antagonists target are responsible for the visual effects. I think it is to early to conclude however one should still may hypothesis that can be tested.
 
Yup. And let us not forget the recent discovery of dmt as a ligand of sigma-1 receptors. There is an ever more recent review hypothesis presenting "a hypothetical signaling scheme that might be triggered by the binding of DMT to sigma-1 receptors".


Sci Signal. 2009 Mar 10;2(61)
When the endogenous hallucinogenic trace amine N,N-dimethyltryptamine meets the sigma-1 receptor.
Su TP, Hayashi T, Vaupel DB.


N,N-dimethyltryptamine (DMT) is a hallucinogen found endogenously in human brain that is commonly recognized to target the 5-hydroxytryptamine 2A receptor or the trace amine-associated receptor to exert its psychedelic effect. DMT has been recently shown to bind sigma-1 receptors, which are ligand-regulated molecular chaperones whose function includes inhibiting various voltage-sensitive ion channels. Thus, it is possible that the psychedelic action of DMT might be mediated in part through sigma-1 receptors. Here, we present a hypothetical signaling scheme that might be triggered by the binding of DMT to sigma-1 receptors.
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too bad my institude does not have a subscription for this article. Maybe someone can help^^?
 
Lets not forget that in vitro binding affinity cannot alone be used to predict how active or inactive a substance is in vivo. Although I'll agree that the 5-HT visual idea is lacking in many many areas there is certainly more going on here.

I think the ST is making a good start at developing a theory of visuals. The receptors might be wrong but that will be figured out the more this gets studied.
 
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