dasitmane

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dasitmane last won the day on May 6 2016

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About dasitmane

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  1. No, the article clearly shows that the excitotoxity is a result from 5htp2a receptor activation. did you even read the study?
  2. https://www.ncbi.nlm.nih.gov/pubmed/22983118 more proof that hallucinogens cause neuronal excitotoxic apoptosis. Also note at the end that when the receptors are blocked it aids in the prevention and even halting of apoptosis. So antagonists should be a treatment in emergency cases of hallucinogen treatment, in ERs that is. The neurotoxicity of hallucinogenic amphetamines in primary cultures of hippocampal neurons. Capela JP1, da Costa Araújo S, Costa VM, Ruscher K, Fernandes E, Bastos Mde L, Dirnagl U, Meisel A, Carvalho F. Author information Abstract 3,4-Methylenedioxymethamphetamine (MDMA or "Ecstasy") and 2,5-dimethoxy-4-iodoamphetamine hydrochloride (DOI) are hallucinogenic amphetamines with addictive properties. The hippocampus is involved in learning and memory and seems particularly vulnerable to amphetamine's neurotoxicity. We evaluated the neurotoxicity of DOI and MDMA in primary neuronal cultures of hippocampus obtained from Wistar rat embryos (E-17 to E-19). Mature neurons after 10 days in culture were exposed for 24 or 48 h either to MDMA (100-800 μM) or DOI (10-100 μM). Both the lactate dehydrogenase (LDH) release and the tetrazolium-based (MTT) assays revealed a concentration- and time-dependent neuronal death and mitochondrial dysfunction after exposure to both drugs. Both drugs promoted a significant increase in caspase-8 and caspase-3 activities. At concentrations that produced similar levels of neuronal death, DOI promoted a higher increase in the activity of both caspases than MDMA. In the mitochondrial fraction of neurons exposed 24h to DOI or MDMA, we found a significant increase in the 67 kDa band of apoptosis inducing factor (AIF) by Western blot. Moreover, 24h exposure to DOI promoted an increase in cytochrome c in the cytoplasmatic fraction of neurons. Pre-treatment with an antibody raised against the 5-HT(2A)-receptor (an irreversible antagonist) greatly attenuated neuronal death promoted by 48 h exposure to DOI or MDMA. In conclusion, hallucinogenic amphetamines promoted programmed neuronal death involving both the mitochondria machinery and the extrinsic cell death key regulators. Death was dependent, at least in part, on the stimulation of the 5-HT(2A)-receptors.
  3. More evidence for glutamate related overexcitoxicity.
  4. The neurotoxicity of hallucinogenic amphetamines in primary cultures of hippocampal neurons. Capela JP1, da Costa Araújo S, Costa VM, Ruscher K, Fernandes E, Bastos Mde L, Dirnagl U, Meisel A, Carvalho F. Author information Abstract 3,4-Methylenedioxymethamphetamine (MDMA or "Ecstasy") and 2,5-dimethoxy-4-iodoamphetamine hydrochloride (DOI) are hallucinogenic amphetamines with addictive properties. The hippocampus is involved in learning and memory and seems particularly vulnerable to amphetamine's neurotoxicity. We evaluated the neurotoxicity of DOI and MDMA in primary neuronal cultures of hippocampus obtained from Wistar rat embryos (E-17 to E-19). Mature neurons after 10 days in culture were exposed for 24 or 48 h either to MDMA (100-800 μM) or DOI (10-100 μM). Both the lactate dehydrogenase (LDH) release and the tetrazolium-based (MTT) assays revealed a concentration- and time-dependent neuronal death and mitochondrial dysfunction after exposure to both drugs. Both drugs promoted a significant increase in caspase-8 and caspase-3 activities. At concentrations that produced similar levels of neuronal death, DOI promoted a higher increase in the activity of both caspases than MDMA. In the mitochondrial fraction of neurons exposed 24h to DOI or MDMA, we found a significant increase in the 67 kDa band of apoptosis inducing factor (AIF) by Western blot. Moreover, 24h exposure to DOI promoted an increase in cytochrome c in the cytoplasmatic fraction of neurons. Pre-treatment with an antibody raised against the 5-HT(2A)-receptor (an irreversible antagonist) greatly attenuated neuronal death promoted by 48 h exposure to DOI or MDMA. In conclusion, hallucinogenic amphetamines promoted programmed neuronal death involving both the mitochondria machinery and the extrinsic cell death key regulators. Death was dependent, at least in part, on the stimulation of the 5-HT(2A)-receptors. This basically proves that apoptosis from hallucinogenic overdose is a key factor.
  5. Sounds like you are a bit paranoid. Its not impossible, but it will take time to see if you have it. Based on what you are describing if you do have it its very mild. If youre paraplegia is caused by brain abnormalities rather than spinal it could make you more susceptible. Basically give it some time and see what happens. Basically though, DO NOT do hallucinogens again. They definitely do serious damage to the brain.
  6. A Recent Discovery MDMA and MDA cause neurons to release a neurotransmitter called serotonin. Serotonin is important to many types of nerve cells, including cells that receive sensory information and cells that control sleeping and emotions. The released serotonin can over activate serotonin receptors. In animals, MDMA and MDA have been shown to damage and destroy nerve fibers of neurons that contain serotonin. This can be a big problem, because serotonin neurons have a role in so many things, such as mood, sleep, and control of heart rate. Scientists have recently found that the damaged serotonin neurons can regrow their fibers, but the fibers don't grow back normally. The fibers may regrow into brain areas where they don't normally grow, but not into other brain areas where they should be located. The new growth patterns may cause changes in mood, learning, or memory.
  7. Lol thanks Jay. How have you been? Synapse plasticity most likely wouldn't be the case here, its a temporary condition and easily rectifiable. Im still leaning towards neuronal loss, be it whatever the route, and likened to that in lithium overdose.
  8. 6 years Edit: Man some people have had this a long time! I dont get the visual snow, dp/dr, or any visuals. I used to get the snow and dp/dr but they went away. Never had visuals. For me most of mine is manifested by a crippling anxiety, its almost unbearable, and just about anything can trigger it. As long as im not exposed to anything and dont drink too much coffee it typically ok. But to much coffee in the morning can make it bad. And some times it flares up and I dont have an explanation.
  9. Just want to bump this thread. Still trying to make progress.
  10. The cause of HPPD is fairly simple and very detailed in my ongoing thread. Its simply neuronal overexcitation leading to apoptosis. I've posted an endless amount of information showing its the only possible cause. Neurogenesis is the only possible cure for HPPD. Also the guys theory is easily disproved in the fact that if it were caused by immune dysfunction attacking the brain, it would most likely be a progressive disease. Which its not.
  11. Has anyone by chance found any information as to what may be the most definitive cause for this condition. The only 3 specific things that I can think are Neuronal excitotoxic apoptosis Chemical embedment in the synapses that cant be broken down Or some altercation of DNA changing neuronal function
  12. Lol, based on the fact that he said "higher level of consciousness" I dont need to read the whole article to understand that he is an idiot. And who dictates what this forum is about? So who are you to say what its about? And as far as I'm concerned in all the research that I have done I'm easily ahead of the so called professionals in this disease, and based on your history you have made absolutely zero progress in the diagnosis nor treatment there of, so you have absolutely no room to speak. Edit: I actually read a little more of your most ridiculous statements and the fact that you think that psychedelics should be used on mentally ill/handicapped patients shows that you not only know absolutely nothing about neurology, but that you're a belligerent moron, a mere child running with scissors unrelentingly. Please put down the scissors, step away from your keyboard, and slap yourself repeating "I know not what I say" till you understand the reason for the therapy at hand. No pun intended, phaggot.
  13. Really!? The brain on hallucinogens acts different than normal!? HOLY FUKK what a way to waste a chit ton of tax money and time on a worthless research project. Loser fukk researcher should just retire now. What a worthless bitch. How stupid do you have to be to even publish those findings? "Brain doesn't act normal on psychedelics" hahaha nahhhhh I dont believe it. Professor Anil "Hurr Durr" Seth "higher 'level' of consciousness" Lol what a worthless piece of shit.
  14. In some of my free time I learned classical astrology and you can tell a lot about how a persons life will be. I would like to see if maybe some of us who got HPPD have anything in common astrologically. If you would like to contribute please post the exact time and location you were born. The time needs to be down to the minute, location is necessary as well. If you dont know the exact time it can be found on your birth certificate.
  15. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3181663/ Just going to leave this here for future reading. I am finding a lot of information saying that hallucinogens do not cause neuronal loss, but I'm still doubtful. Found in the article posted Recent electrophysiological studies have produced new evidence that both psychedelic hallucinogens and NMDA antagonists activate the serotonergic system and enhance glutamatergic transmission via non-NMDA receptors in the frontal cortex.93,94 Whether this common mechanism contributes to the higher-level cognitive, perceptual, and affective effects of serotonergic hallucinogen and NMDA antagonists warrants further investigation.40 So excitotoxicity via glutamate could be the culprit. Enjoy some music guys. Fast forward to 1:19:30 [