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Mental Images

A

adm1

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Sep 14, 2009
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14
How is the brain functioning when you see visual hallucinations?

How are visual hallucinations formed? Not causes

Everything u know...articles, e-books , anything please...
 
Traditional psychedelics such as LSD, psilocybin and phenethelymines bind with the 5-HT2A serotonin receptor, which has some sort of effect on the brain's visual and cognitive cortexes.

Disassociates like PCP and DXM clog the NMDA receptor, which is vital to the brain's ability to regulate transmissions between neurons. External stimuli is blocked, and one's brain creates images to replace what is not being seen.
 
rolodex propaganda said:
Traditional psychedelics such as LSD, psilocybin and phenethelymines bind with the 5-HT2A serotonin receptor, which has some sort of effect on the brain's visual and cognitive cortexes.

Disassociates like PCP and DXM clog the NMDA receptor, which is vital to the brain's ability to regulate transmissions between neurons. External stimuli is blocked, and one's brain creates images to replace what is not being seen.
Click to expand...

+1 QFT

I'd also like to add that hypnogogic and hypnopompic hallucinations (which I'm more interested in as of late) can be caused by muscle atonia caused by signal blockade (i think at the cerebellum or brainstem level) as the brain begins to transition into REM sleep.

Also, alcohol/benzo/GABA agonist withdrawal traditionally can cause frightening visual imagery. in the case of alcohol I might chalk it up to the NMDA activity alcohol has, but that wouldnt fully account for the hallucinations seen during say, xanax or chloral withdrawal.

presumably there are multiple mechanisms that can cause this phenomenon and thus far we have mentioned just a couple.
 
http://en.wikipedia.org/wiki/Form_constant


but that wouldnt fully account for the hallucinations seen during say, xanax or chloral withdrawal.
Click to expand...

Exctation of all GABA controlled neurons- which is a lot. Benzo's reduce excititory transmssion (lke 5ht, NE, Dopamine, acetyle-choline); opposte effect is acheved when in wthdrawal. Also, the increase effects of adrenaline would play a role.
 
No wonder the DTs are so fucked up. Which are not limited to alcohol: GHB withdrawals paint a similar picture.
Is it the adrenergic action that makes GHB withdrawals a health hazard to your heart? This seems to be much much heavier when the abuser has increased the doses to battle tolerance, if you keep going higher and higher then quit cold turkey you can get a heart attack. I assume that adrenaline is the culprit it seems likely.
I also theorize that it had something to do with my recent panic attack.

I didn't know alcohol had NMDA activity, does that account for the derealization the DTs can give you? I once had such an experience after short but heavy drinking. Got a hangover that became really scary while I stayed in the room of a Chech hostel while my friends continued our fortnight vacation binge.

Sorry to steer this thread off-topic by the way.

Wanna add that cannabis has given me very random mental imagery especially after a period of abstinence / without tolerance. It's like I get 10 mental images per second and they all depict some persons portrait or an object, like a deck of memory cards flashing before my eyes. I got this as well when smoking DMT on 4-FMP only there were 100 images per second then. It was quite strange and quite different from a normal clean DMT trip!
 
I believe the mechanism is inhibition of EGO factor-alpha and widespread agonism of the subconscious receptors in the brain.
 
Are you sure that receptors are pharmacologically distinguishable between conscious and subconscious? I thought that was more of a 'software' or pattern/brainwave type of deal than a wetware (hardware) deal.
 
Oh right =D

I was obviously unfamiliar with that, but I read EGO as an abbreviation, with factor alpha it definitely sounded like a protein receptor complex or something... like GPCR.
For instance, ketamine is a very complex psychoactive, who knows on what it all acts that we dont know of yet? I don't. Thats for damn sure.

mmm you rascal
 
I wouldn't limit this to just the 5ht2a receptor, as most psychedelics, save Br-DFLY, DOI, & TCB-2 (if its even psychedelic... I suspect it would likely be, but don't know for sure), are at least somewhat non-specific in their affinity for 5ht receptor sites. While 2a sites in the prefrontal cortex likely play a large role in the visual aspects of the classical psychedelics, other 5ht sites likely have some effect as well.
 
nexus gives me A LOTof visuals, morphing, bright colours, and geometric patters with eyes closed
 
Enriched expression of serotonin 1B and 2A receptor genes in macaque visual cortex and their bidirectional modulatory effects on neuronal responses.

Cereb Cortex. 2009 Aug;19(8):1915-28.

To study the molecular mechanism how cortical areas are specialized in adult primates, we searched for area-specific genes in macaque monkeys and found striking enrichment of serotonin (5-hydroxytryptamine, 5-HT) 1B receptor mRNA, and to a lesser extent, of 5-HT2A receptor mRNA, in the primary visual area (V1). In situ hybridization analyses revealed that both mRNA species were highly concentrated in the geniculorecipient layers IVA and IVC, where they were coexpressed in the same neurons. Monocular inactivation by tetrodotoxin injection resulted in a strong and rapid (<3 h) downregulation of these mRNAs, suggesting the retinal activity dependency of their expression. Consistent with the high expression level in V1, clear modulatory effects of 5-HT1B and 5-HT2A receptor agonists on the responses of V1 neurons were observed in in vivo electrophysiological experiments. The modulatory effect of the 5-HT1B agonist was dependent on the firing rate of the recorded neurons: The effect tended to be facilitative for neurons with a high firing rate, and suppressive for those with a low firing rate. The 5-HT2A agonist showed opposite effects. These results suggest that this serotonergic system controls the visual response in V1 for optimization of information processing toward the incoming visual inputs.

http://www.ncbi.nlm.nih.gov/pubmed/19056862
 
I believe that lsd causes your brain to produce (or mimics?) extra dopamine, serotonin, and epinephrine, all of which regulate your pyramidal cells which produce your conscious experiences. This is why things have brighter colors, your attention changes, etc.
On top of this, it also causes extra glutamate to be release, which is the chemical that sensory input causes. This is what causes hallucinations.

source: lecture about lsd and why it's so potent (I can't find it atm, but it's on youtube)
 
I was reading some interesting conjecture on the way visuals are produced by psychedelics in the brain, specifically 5-HT2a receptor agonists. I'm not sure if I would believe this without seeing proper research based on his hypothesis. But I looked at many of his sources and what he describes actually seems to fit a lot of the things I've considered and felt about the effects of psychedelics. I think this might really represent only a part of the effect of these psychedelics but honestly we know so little for sure about the finer details - most research has so far only painted a rough scheme of what the drugs do.
http://www.tripzine.com/listing.php?smlid=697
 
Deus said:
I believe that lsd causes your brain to produce (or mimics?) extra dopamine, serotonin, and epinephrine, all of which regulate your pyramidal cells which produce your conscious experiences. This is why things have brighter colors, your attention changes, etc.
On top of this, it also causes extra glutamate to be release, which is the chemical that sensory input causes. This is what causes hallucinations.

source: lecture about lsd and why it's so potent (I can't find it atm, but it's on youtube)
Click to expand...

LSD basically "mimicks" serotonin at the 5HT2a receptor. Glutamate is an excititory neurotransmitter; most psychedelics increase glutaminergic actitvty, leading to more frequent or random signal processing in the brain. Glutamate doesn't cause hallucinations, nor do pyramidal cells produce conciouness. The latter are a type of cellular structure throughout the brain, and are probably nvolved in conciouness; the former basically excites neurons in the visual cortex and pre-frontal lobe, causng them to misfire, or repeatedly fire- ths could be the cause of random patterning, as well as thought looping.
 
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