k is far more effective than psilocin as an antidepressant. psilocin is better for making progress in your life so you have less reasons to be depressed. it's a therapy adjunct. what ketamine does is far more pharmacological and immediate.
Some companies are going to test non-psychoactive tryptamines. The aim is to target an audience fearing a psychedelic experience and they seem to involve a lot of money into it so my forecast is that it might work at least a bit. Because of that, I'm now wondering if we aren't exaggerating the psychological effects of Psilocin and the "mystical experience" that comes with it, but at this time it's impossible to tell. Patiently waiting for the results of these studies.
From what I hear, ketamine blocks chandelier cells (GABA related iirc) meanwhile psychedelics stimulate pyramidal cells to out-pace what the chandelier cells can manage. Which is how bad trips can happen because chandelier cells are trying to regulate the pyramidal cells relative to user behavior. I am not a neuroscientist, but I read parts of studies I found interesting. In psychedelics glutamate only increases in only one or two areas. But in the hippocampus glutamate excess is associated to glutamate storms which are associated to depression stroke anxiety insomnia(and consequently first instance psychosis). Because glutamate causes excess calcium uptake which can cycle into cell deaths. The increased density of the hippocampus is therefore associated to decreased risk of stroke anxiety and depression and possibly even insomnia. Which means those could cause from low density, and the physical density change improves neurotransmitter use or prevents accumulations of glutamate or the like from having less space for them to idle into, which could prevent the cells from excess glutamate production which might happen to compensate from glutamate missing its target. I am not 100% certain tho. So basically: 1. Chandelier cells inhibit pyramidal cell dendrite growth 2. Ketamine blocks the inhibition, psychedelics stimulate pyramidal cell dendrite growth 3. Increased growth causes less accumulation of glutamate into pocket areas of low density of the hippocampus 4. It processes glutamate better and because of this prevents glutamate storms and neurotoxicity.
@@cheekybastard99 Basically the sense of control part of the brain tries to 'contain' the growth of other parts of the brain, but on psychedelics cannot, so this leads to a sense of loss of control which leads to a bad trip. So the goal is to let go of control.
Ketamine is something I'm new to and am relatively resistant to in the antidepressant mode. I'm wondering if this could have something to do with having been on a coma-inducing dose of Propofol for approximately 3 weeks? Curious of your opinion! Thank you for the video and for sharing your knowledge.
Not much is known about ketamine use in these two patient populations. My first intuition would be to avoid ketamine in Alzheimer's patients, but there have been some ideas that ketamine could have procognitive. Even less is known about psilocybin.
k is far more effective than psilocin as an antidepressant. psilocin is better for making progress in your life so you have less reasons to be depressed. it's a therapy adjunct. what ketamine does is far more pharmacological and immediate.
Agreed, can verify first hand
I ordered mine from @fran_sbull on instagram, you can get yours too, man got shrooms,dmt,lsd and other psychedelics products.
Some companies are going to test non-psychoactive tryptamines. The aim is to target an audience fearing a psychedelic experience and they seem to involve a lot of money into it so my forecast is that it might work at least a bit. Because of that, I'm now wondering if we aren't exaggerating the psychological effects of Psilocin and the "mystical experience" that comes with it, but at this time it's impossible to tell.
Patiently waiting for the results of these studies.
@@joecallegari8782 Can you elaborate?
From what I hear, ketamine blocks chandelier cells (GABA related iirc) meanwhile psychedelics stimulate pyramidal cells to out-pace what the chandelier cells can manage. Which is how bad trips can happen because chandelier cells are trying to regulate the pyramidal cells relative to user behavior. I am not a neuroscientist, but I read parts of studies I found interesting. In psychedelics glutamate only increases in only one or two areas. But in the hippocampus glutamate excess is associated to glutamate storms which are associated to depression stroke anxiety insomnia(and consequently first instance psychosis). Because glutamate causes excess calcium uptake which can cycle into cell deaths. The increased density of the hippocampus is therefore associated to decreased risk of stroke anxiety and depression and possibly even insomnia. Which means those could cause from low density, and the physical density change improves neurotransmitter use or prevents accumulations of glutamate or the like from having less space for them to idle into, which could prevent the cells from excess glutamate production which might happen to compensate from glutamate missing its target. I am not 100% certain tho.
So basically:
1. Chandelier cells inhibit pyramidal cell dendrite growth
2. Ketamine blocks the inhibition, psychedelics stimulate pyramidal cell dendrite growth
3. Increased growth causes less accumulation of glutamate into pocket areas of low density of the hippocampus
4. It processes glutamate better and because of this prevents glutamate storms and neurotoxicity.
This is really interesting, can you explain this like I'm 10yrs old?
@@cheekybastard99 Basically the sense of control part of the brain tries to 'contain' the growth of other parts of the brain, but on psychedelics cannot, so this leads to a sense of loss of control which leads to a bad trip. So the goal is to let go of control.
@@mimszanadunstedt441 thank you
for the algorhythm
We need more actual pharmacology on youtube
Agreed!
When used in a therapeutic setting, the combo of mdma and ketamine have profound potential in the important work of mental health
Ketamine is something I'm new to and am relatively resistant to in the antidepressant mode. I'm wondering if this could have something to do with having been on a coma-inducing dose of Propofol for approximately 3 weeks? Curious of your opinion! Thank you for the video and for sharing your knowledge.
hello. There news about Psilocybin binds to TrkB receptors? would you talk about it?
Working on it.
psyvhedelivs work Also through TrkB activation. New findings suggest that ssris also excert their antidepressant effects through trkB activation
As someone who studies rapid-acting antidepressants and TrkB related molecular mechanisms, I am not convinced.
What about its affect on the brains of Parkinson’s, dementia and Alzheimer’s?
Not much is known about ketamine use in these two patient populations. My first intuition would be to avoid ketamine in Alzheimer's patients, but there have been some ideas that ketamine could have procognitive. Even less is known about psilocybin.
There are studies ongoing: www.neurologylive.com/view/fda-approves-ind-ketamine-parkinson-disease-dyskinesia
My girl ketamina Valentina
Круглосуточно в Киеве орут сирены воздушной тревоги, мирные жители Украины живут в страхе не зная когда их могут убить