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The Corroboree

mindperformer

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About mindperformer

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    Senior Psychonaut

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    Male
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    Austria
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    Ethnobotany, pharmacology, elements and element-minerals, nature, quantum physics, "culinarily plants"...

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    Vienna

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  1. yes, this was also the conclusion of R. Carhart-Harris and for me its also very plausible that a more primary consciousness with high entropy was a psychological atavism, early in the evolution of the human brain. It may has to do with the neolithic revolution in the levante, especially mesopotamia with its structured system, the first cities, officials and bookkeeping by cuneiform writing, then also the industrial revolution and so on, so we were forced by the environment to change to a sweet spot with lower entropy.
  2. mindperformer

    Fossil leaves

    I was lucky to find petrified leaves (in a rather hard stone) on a small mountain called 'Roter Berg' in the outskirts of Vienna, the red radiolarites from this mountain were prehistorically used for making spearheads and blades. In some soil layers there were found ammonites too. The plant remains are dated 8,9-9 Million years old and stem from the Pannonium (11,608 - 7,246 million years before present). They may present Lythraceae. Here the microscopic pictures:
  3. The ergoline derivatives are only found in fungi world (one exception is the poorly researched and ergoline- containing plant Securidaca longipedunculata, in which no endophytic fungus was found, not yet). Psychoactive plants with Ergolines: In morning glorys (Ipomoea) there were endophytic fungi found: Periglandula ipomoeae In ololiuqui (Turbina syn. Rivea corymbosa) it is the endophytic fungus Periglandula turbinae In Piri-Piri (Cyperus articulatus) some populations are infected with Balansia cyperi Sleepy grass (Achnatherum robustum syn. Stipa robusta) is infected with Neotyphodium funkii Bog Bilberry (Vaccinium uliginosum) is infected with Monilinia megalospora Claviceps purpurea infects many grains LSA (Ergine) is reported as beeing sedative and weakly hallucinogenic Methylergometrine is vasoconstrictive and 2mg have are LSD- like action according to Ott From my other thread on this plants: Some active constituents: Ergine: (LSA)-Dopamine Antagonism (sedative profile) and only weak 5-HT2A/C-agonism Isoergine: 5-HT2A/C partial agonism Methergine (Methylergometrine): 5-HT2A/C partial agonism and describes as hallucinogenic by J. Ott Ergometrine (Ergonovine): Partial HT2A/C agonism Lysergene: HT2A Partial agonism/full antagonism Festuclavine: HT2A Partial agonism/full antagonism Agroclavine: HT2A Partial agonism/full antagonism Elymoclavine: HT2A Partial agonism/full antagonism, Dopamine Agonism Chanoclavine: D1/2-Dopamine and 5-HT2A/C Agonism Lysergic acid: α-hydroxyethylamide Lysergol: HT2A Partial agonism/full antagonism, HTF1 agonism, Ergotamine: partial 5-HT2A agonism Ergovaline: partial 5-HT2A agonism Isolysergic acid Lysergene: HT2A Partial agonism/full antagonism Setoclavine Isosetoclavine Isolysergol Lysergic acid hydroxyethylamide (LSH) also occurs in the Convolvulaceae and may play a role in their weak psychedelic effects Does somebody know about studies on the distribution of this fungi and their response to environmental and growing conditions of the plants? With sleepy grass Jim DeKorne speculated that the endophytic fungus is distributed by seeds, which are already infected, but he also mentioned that not all populations of sleepy grass were active. I have sleepy grass seeds, stored for 15 years in a small pouch and the endophytic fungus visibly has completely taken over the whole seeds. Ololiuqui (Turbina syn. Rivea corymbosa): Periglandula is connecting with the tissue of ololiuqui leaves by their trichomes. There can be visible darker spots on the downside of the leaves. This should mean that the plant is infected and prudicing the alkaloids (ololiuqui contains them in the leaves and transports them when fruiting to the seeds, storing them in the seeds)
  4. The (functional selective) partial 5-HT2A- agonistic psychedelics are causing the antidepressant activity by enhancing connectiveness in the brain, but decreasing the strong coupling between the DMN (default-mode network) and the MTL (medial temporal lobe), by activating the pyramidal neurons by 5-HT2A- mGlu2- receptor-dimers, by specific activation of it's Phospholipase D- pathway. All in all in the theory of consciousness (R. Carhart-Harris) the psychedelic state is a state of high entropy ('disorder', see primary consciousness), so more connection possibilities are possible (formlessness). Versus: Depressive and sedative states, seizure, inflexibility are states of low entropy (high order, petrification). The sweet spot for 'normal' waking consciousness (constrained, precise, confident cognition, not easily surprised) is between this two extremes but more on the side of low entropy. See D. Nichols and R. Carhart-Harris.
  5. It is unknown why (besides the 5-HT1A- downregulation) also the 5-HT2A- downregulation by SSRIs (and antagonism with fluoxetine) plays a role in the antidepressant effect of SSRIs (see also R. Carhart-Harris on this topic). Because other 5-HT2A- antagonists like atypical antipsychotics augment the therapeutic effects of SSRIs. Again this could also be explained by the fact that although the level of 5-HT2A- receptor density is downregulated after long-term SSRI treatment (according to most studies), their affinity for Serotonin is upregulated. An as we all know there are many studies on the permanent antidepressant effect of serotonergic psychedelics which are selective 5-HT2A- Agonists.
  6. No this long-term- SSRI- change of the 5-HT2A- receptor does not stay / is not permanent. The neuronal changes (also the reason for the SSRI discontinuation syndrome) after discontinuing SSRIs stay for 1-2 weeks, dependent on the SSRI used because sertraline and fluoxetine (but not paroxetine) have active metabolites with half-lives around 2–3 and 7–15 days respectively. The studies on the level of 5-HT2A- receptor density after 3 weeks SSRI treatment are paradox, some found an decrease and some an decrease, however all in all it is the receptor-binding-affinity specific for serotonin which is upregulated, like the level of Serotonin itself is also upregulated. Additionally some SSRIs like Fluoxetine have 5-HT2A- antagonistic activity. In the first 0-3 weeks SSRI treatment the situation is completely different, the presynaptic 5-HT1A-autoreceptors downregulate the serotonin- level. This lower serotonin- level means that Serotonin has a lower competitiveness to suppress psychedelic tryptamines from the receptor, so the tryptamines are potentiated in the first 0-3 weeks SSRI treatment.
  7. @ Alchemica: I also investigated Galphimia glauca there seem to be many studies, attesting sedative, anxiolytic, anti-allergenic and antidepressant activity. It is distributed in Central America and is also used traditionally. Galphimin B is sedative and anxiolytic and it is highly possible that it is an Antagonist of the 5-HT1A- receptor. But: It also acts on 5-HT2A- receptors, highly likely also as Antagonist, whis is also one of the main mechanisms (besides Dopamine- antagonism) of anti-psychotics (neuroleptics), this makes it not so useable for me personally.
  8. There were some experiments with this plant reacting to music, it changes its movement dependent on the music played, although it wasn't possible to find a specific pattern, see youtube videos
  9. Because the name of the thread is Emotional plants, there is one plant which fits exactly: The Telegraph plant (Codariocalyx motorius syn. Desmodium gyrans): It is ne of the few plants capable of rapid movement of its leaves. The small lateral leaflets , they rotate constantly in a period of 3-5 minutes (visible to the naked eye), dependent on the temperature. The big leaflets also move but much slower, they have a sleeping position in the night. It is medium difficult to germinate and a littlebit difficult as young plant but stable and easy to grow when its getting older, most important is high humidity and at least room temperature. The leaves, sprout and root contain DMT and 5-MeO-DMT. In the leaves they found the alkaloids: DMT: 0.0041 % DMT-N-oxide: 0.0090 % Bufotenine: 0.0034 % 5-MeO-NMT: 0.0049 % 5-MeO-DMT: 0.0018 % and Flavonoids (major compounds): Luteolin and its glycoside, Apigenin-7-O-glucuronide, Scutellarein-6-O-glucuronide So it is a rather strange coincidence that the only constant moving plant visible to the naked eye is also producing this psychedelics / neurotransmitters. The Tryptamines may play a role like Serotonin found in plants: Phytoserotonin also plays a role in the following aspects of plant function: Growth regulation Xylem sap exudation Flowering Ion permeability Plant morphogenesis Regulation of ripening
  10. @ Alchemica: thanks for the like, I can recommend the studies from R. Carhart-Harris and D. Nichols, they are the newest explanations of the action of Psychedelics on the 5-HT2A and 5-HT1A receptors. The lectures from R. Carhart-Harris can also be found on youtube.
  11. Potency of Cathinone and Cathine vs. Ephedrine and Amphetamine: This can be explained by the different affinity for Dopamine-, Norepinephrine- and Serotonin- releasing:
  12. The Cathinone and Cathine have very uneven distribution in the plant:
  13. I forgot the very interesting SSRI- interaction with hallucinogens. I know someone who tried mushrooms on SSRI medication and felt nothing. This phenomenon is poorly explored. There are many reports of people on SSRI- medications who have no effects from LSD, Psilocin and other Tryptamines but yet they had effects from phenylethylamines like Mescaline. Again Tryptamines could be regarded as partial Agonists with high functional selectivity and Phenethylamines are full agonits. Under SSRI- medication longer than 3 weeks, the presynaptic 5-HT1A- receptors (reduce Serotonin levels) are back-regulated, for the 5-HT2A- receptors the situation under SSRIs is more complicated. It seems that the population density of them is down-regulated and the downstream effectors are also changed (GIRK- channels), but the receptor-affinity for Serotonin is up-regulated, so they don't have the right constitution for Tryptamines anymore. Phenylethalamines like Mescaline and DOM bypass this shift in receptor constitution and still hav hallucinogenic action while under SSRI treatment. I had my own experience where I took the SSRI Citalopram for only 2 days, when LSD was very much potentiated. According to some studies in the first 3 weeks SSRI treatment there is no dysregulation of 5-HT2A- receptors, instead hallucinogens are potentiated.
  14. I made some calculations based on the Cathine / Cathinone content and also searched the literature for dosages of leaves, which were hard to find. I came to the conclusion that you need 100 - 200 g fresh Kath- leaves for one dose. Dried leaves have a 3,3 times lower weight than fresh leaves. Calculating with the effective Cathinone- dose for 60 kg body weight whould be 310 g fresh leaves for an action which is comparable with Amphetamine. To factor also the Cathine content into the calculation (which only has a tenth of the efficacy of Cathinone), it has a 3-times higher content in the fresh leaves, in dried leaves the Cathine- content is even higher because of the conversion on Cathinone to Cathine during the drying process. Because 100 g Kath leaves contain 83 - 120 mg Cathine and an active dose of Cathine is 16 - 53 mg. So it can be concluded that: although there can be felt minimal effects from 10-15g Kath leaves, for medium strength effects there must be consumed at least 50 - 100 g leaves.
  15. The functional selectivity of the Ligands (partial vs. full Agonists, silent vs. active Antagonists, inverse Agonists etc.) seems to play a major role. There are many transcription factors / downstream effectors of the receptor which could be activated or not by 5-HT1A- Ligands, also there are interactions with 5-HT2A-Agonists like the Tryptamines (partial agonists) and Phenylethylamines (mainly full agonists). These interaction are based on the co-expression of 5-HT1A and 5-HT2A- receptors in mPFC (medial PreFrontal Cortex, self-consciousness, addiction,...) pyramidal neurons. 5-HT2A- receptors excite and 5-HT1A receptors inhibit the activity of pyramidal neurons. The overall influence of mPFC neurons on serotonergic function is excitatory. As there are many downstream effectors there are also differences between the partial agonists but generally some compounds are considered full agonists (efficacy relative to endogenous agonists like Serotonin). Full 5-HT1A- agonists are: 8-OH-DPAT, Annonaine, Nornuciferine, Asimilobine and Flibanserine Partial 5-HT1A- agonists: Vilazodone, Buspirone, Rauwolscine, 5-MeO-DMT, LSD, 10-Shoagol (in dried ginger), 1-Dehydro-6-gingerdione (in ginger), Cannabidiol (CBD, weak agonist), DPT, AMT, Bufotenin, MDMA, Psilocybine, Psilocin and Quetiapin. Some 5-HT1A agonists can effect the release of adrenaline, dopamine and acetylcholine, the last two meinly in the prefrontal cortex. They are anxiolytic, antidepressant, antiemetic, analgetic, reduce eggression, enhance sociability, reduce impulsiveness and addiction-related craving, extend the REM-dream phase. A main part of the actions of 5-HT1A- agonists is based on reinforced Oxytocin- and Beta-Endorphine- release and promotion of BDNF- production. However only high dosages of Agonists seem to have relevant effects because the presynaptic autoreceptors lessen the effects. (MDMA acts as Serotonin- and Oxytocin- releaser, because of its 5-HT1A- action). As you already mentioned 5-HT1A- Antagonists reinforce hallucinogenic effects of psychedelics and many agonists buffer 5-HT2A- mediated hallucinogenic effects. DMT and LSD, despite their high potency, are also partial agonists on the 5-HT1A- R., and DMT behaves as full agonist in the adenylate cyclase (a second messenger) assay. Furthermore these receptors are edited at the level of mRNA to produce spatially restricted isoforms, each with a different activity. Inverse 5-HT1A- Antagonists: Spiperone Neutral / silent 5-HT1A- Antagonists: WAY 100,635 and UH-301 (both enforce hallucinogenic action of 5-HT2A- partial agonists) I think 5-HT1A agonism plays a role in the lacking of tolerance of DMT and the low side-effect profile of DMT, Psilocin and LSD vs. more risky Bromo-Dragonfly and most Phenylethylamines, but there are also differences in functional selectivity of 5-HT2A- R. involved (PLC vs. PLA-2 and PLD). Most promising natural 5-HT1A- ligands: Julibroside and Quercitrin in Albizia julibrissin. This plant triggers the LSD- effect as mentioned in the DMT Nexus- forum
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