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Posts posted by mindperformer
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I pickle the flowers every year, they taste delicious in vinegar, you could also use the vinegar itself in which you pickled it.
Also I extracted the scent from the flowers with:liquid paraffin for 1 day (enfleurage), then extracted the liquid paraffin with 80% alcohol for 2 weeks (shaking well) and concentrated it to the absolute.
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Oxypinnatanine was (as yet) only found in Hemerocallis fulva, which grows wild, here in Vienna on danube island (a long island in the river danube).
But maybe nobody searched for it in Hemerocallis citrina.
An interesting study of Hemerocallis citrina from 2012:
Ethanol extracts from Hemerocallis citrina attenuate the decreases of brain-derived neurotrophic factor, TrkB levels in rat induced by corticosterone administration
Li-Tao Yi , Huo-Chen Li , Jing Li , Ying Zhou
ETHNOPHARMACOLOGICAL RELEVANCE: Hemerocallis citrina, a traditional herbal medicine, has been used for the improvement of behavioral and emotional status in Eastern-Asia countries. AIM OF THE STUDY: Our previous studies have demonstrated that the ethanol extracts of H. citrina flowers (HCE) reversed the behavioral alterations and monoamine neurotransmitter dysfunctions in stressed mice. However, the relation of its antidepressant-like action with neurotrophic molecular expressions remains unknown. MATERIALS AND METHODS: To clarify this, we explored the effect of HCE (32.5, 65, 130mg/kg, p.o.) on the behavior, brain-derived neurotrophic factor (BDNF) and its receptor (TrkB) in depression-like rats induced by exogenous administration of the stress hormone corticosterone (40mg/kg, s.c.). RESULTS: It was observed that repeated administration of corticosterone induced an elevation on the serum corticosterone levels, which caused the abnormalities observed in the sucrose preference test and forced swimming test (FST). Administration of HCE (65 and 130mg/kg) reversed the changes above and up-regulated the BDNF and TrkB receptor protein expressions in the brain region of frontal cortex and hippocampus. CONCLUSION: These findings confirm that HCE produce an antidepressant-like effect in corticosterone-induced depression-like model of rats and this effect is at least partly mediated by BDNF-TrkB signaling in the frontal cortex and hippocampus.
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Interesting plant, irie that somebody is exploring it.
I have Hemerocallis citrina on the balcony year-round, it tolerates over -15°C in winter and has lovely smelling flowers the whole summer.
To my experience the scent of the flowers could be described as (descending dominance):
floral (like lilies but softer) - sweet - fresh-citrus (lime) - butter-creamy - fruity (banana) - oceanic
I also associate the scent with bathing.
The leaves taste slightly like garlic and, like old chinese herbal books state, can make you "see ghosts" if eaten fresh and in large quantities.
The term "hallucinogenic" may be a translation error.
I only ate them in smaller quantities and could only notice a slightly sedating effect.
A japanese study from 2012 found a sedative substance in Hemerocallis fulva: Oxypinnatanine (a kind of amino acid).
quote:
By the electroencephalographic measurement after intraperitoneally administration and oral administration of oxypinnatanine in mice, the increase in amount of sleep was observed...
Also another study found that oxypinnatanine (30 mg/kg) increased the total time of NREM sleep by 84%.
More interresting compounds in Hemerocallis fulva:
icariside D2 (anticarcinogenic),
sallidroside (also in Rhodiola rosea, along with
rosavin, as one of the potential compounds responsible for the putative antidepressant and anxiolytic actions.
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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.
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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:
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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)
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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.
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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.
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4 hours ago, Xperiment said:Sorry to dumb this thread down, but does this change in 5-HT2A receptors stay around after SSRI medication has ceased?
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.
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@ 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.
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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
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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
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@ 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.
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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.
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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.
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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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Hi Day Tripper,
could be a Sophora microphylla phenotype with dark seeds like on this site: http://inetgardens.com/kowhai-culture.htm
The flowers and leaves look similar
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Thanks for identificational hints Roberto.
I think there is a great possibility that you are right...
I found this study: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4272316/
I think your displayed seeds labelled "Titze" are from the "Titze line" and cultivated for years in the nursery of Pablo Titze in Talagante, Chile, it is the most common line of allegedly Sophora toromiro in Chile.
In contrast to the "original" S. toromiro from Heyerdahl's seed-collection (now the population at the Botanical Garden Göteborg), the Titze-line seems rather different in morphology.
The Titze may be a hybrid with C. macrocarpa and C. cassiodies.
It is also the Toromiro-line wof the Instituto Forestal ((INFOR), Chile for a future reintroduction attempt.
But: My specimen never flowered, so comparison with this study is difficult.
Regarding to the leaflets I can's see similarities to Titze, so I will add a foto from my plants which is now 6 years old.
Unfortunately I'm fighting against spider mites.
For comparison, the original species from Göteborg: https://hiveminer.com/Tags/toromiro
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@ ☽Ţ ҉ĥϋηϠ₡яღ☯ॐ€ðяئॐ♡Pϟiℓℴϟℴ:
The safety strongly depends on what you want to do with scents. As also some naturals can be hyperallergenic, don't spray them on the skin, except they are made for this purpose. Spray your scents on the clothes or in the hair.
The essential oils with the highest safety:
German Chamomile, blue (Matricaria chamomilla syn. Matricaria recutita, also for sensitive skin),
Italian Everlast (Helichrysum italicum, also for wounds, one of the best for regeneration),
Gallic Rose (Rosa gallica, the best comes from the Georgian Caucasus),
Lavender in small concentrations (the best is Wild Lavender from 1.800m altitude in the french alps)
Rosewood (= Bois De Rose, distilled from the wood of a rainforest-tree, also buy oils from sustainable cultivations, contains mainly the allrounder Linalool)
Sandalwood in small concentrations (also only from cultivation)
Palmarosa (distilled from a grass, which contains mainly the allrounder Geraniol)
Jasmine in very small concentrations
Geranium
Basil (with low Eugenol-content)
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@ doxneed2c-me:
I don't take Isopropanol for tinctures because it has its own strong smell, only sometimes for dry concretes, when evaporating all of the solvents.
Around 50% of all my extractions are tinctures with 80% grain-alcohol from the supermarket. You need at least 80% for extracting essential oils and other lipophile compounds (to which ~ 99% of all odorant molecules belong).
Grain alcohol has much less odor than spirit of wine or denatured alcohol.
Sometimes a simple tincture could not extract some unstable scents or fragile flowers.
In this case I make an enfleurage:
1.) mazerate the material (flowers for example) for 3-12 hours, sometimes longer (depends on the material) in
pure liquid paraffin, this is a total unreactive, scentless and perfect solvent for enfleurages.
2.) squeeze the liquid paraffin out of the material (with a stuff or curtain-textile)
3.) Add about half of the amount 80% grain-alcohol, shake it and leave it standing for at least 1 week, shaking sometimes
4.) Separate the two fractions: first separate / siphon the alcohol with a wash bottle (like this: http://www.rapidonline.com/science/rd-wash-bottle-with-cap-500ml-14-2024) and then filtrate it through a coffee filter ...I also tried separatory funnels but they don't work perfect when separating the
down-layer of liquid paraffin. With the wash-bottle you can siphon directly and completely the alcohol-layer.
If the smell of the tincture or the alcoholic solution from the enfleurage is too weak you can make an absolute:
Put the greater part (7/10-8/10) in a wide pyrex-bowl and let it evaporate on e.g. a heating mat until only a very small amount liquid is left, now you have the absolute
then combine it with the rest of the tincture for preservation and to keep it in a pourable solution.
However sometimes a distillation is more suitable, like with lemongrass, because the enzymes degrade the scent in an extraction very fast.
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the indolics (some of the few alkaloids with an odour because they are small and volatile):
Indole itself smells at 10%: animalic - floral (jasmine) - phenolic (plastics) - faecal - gasoline
DMT smells similar but less animalic but more floral and phenolic
AMT smells much more faecal and phenolic
Iboga: look at the second last post
the indolics share some similarities (also in a chemical sense) with the Anthranilates:
Methylanthranilate, the most common, smells sweet - heavy-tropical-berry (concord grape) - musty-earthy - juicy - floral - phenolic/plastics (like DMT but less faecal and more fruity)
Dimethylanthranilate smells sweet - fruity - anthranilate-like - clean-floral
Anthranilates are the major odor-compounds of the aroma of concord-grapes, wild grapevine, Cestrum nocturnum- flowers, Saponaria officinalis- flowers, orange flower (neroli), Viburnum x burkwoodii- flower, Mahonia bealei- flowers, Schisandra chinensis- flower, Hesperis matronalis- flower, Wood-strawberries,
Nigella damascena-seeds (contain Methyl 3-methoxyanthranilate), and others
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some may ask, "why the woody stems and not the leaves of coca,
and why the leaves of Papaver setigerum and not the pods?"
answer: because the latter of both are
1. too precious for a scent-only-extract
2. illegal in some countries
By the way: Papaver setigerum is not the ancestor of opium poppy (although this is stated on some pages in the internet).
According to newest research P. setigerum is the nearest relative of P. somniferum and both had a wild ancestor in the western mediterranean (France, Italy), which is now extinct.
P. setigerum is more close to the wild ancestor and P. somniferum is a cultivar since over 4.000 years.
However, the species cultivated by the cypriots 4.000 years ago (and exported by them to egypt) is P. setigerum, which is now also a common wild plant in cyprus.
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Hemerocallis
in Ethnobotany
Posted
The study I posted found an upregulation of BDNF (brain derived neurotrophic factor) and TrkB (tropomyosin receptor kinase , which means it is neurotrophic, which means it supports the survival and growth of nerve cells!