I found this, it increases noradrenaline.
https://onlinelibrary.wiley.com/doi/pdf/10.1002/hup.259
I take it orally.
https://onlinelibrary.wiley.com/doi/pdf/10.1002/hup.259
I take it orally.
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I found this, it increases noradrenaline.
https://onlinelibrary.wiley.com/doi/pdf/10.1002/hup.259
I take it orally.
I found this, it increases noradrenaline.
https://onlinelibrary.wiley.com/doi/pdf/10.1002/hup.259
I take it orally.
I think metergoline is an antagonist across the entire 5-HT2 and as such would stop an LSD trip.
"You can see gas exchange in plants.." cool!@haidut
Something that has been confounding me about LSD. I don't feel like the "trip" per se is from serotonin agonism, but rather serotonin antagonism. As Alduous Huxley once said LSD removes the filters of perception or something along those lines and that is my experience. Doesn't make sense to me that serotonin agonism would lead to all of these beautiful/profound experiences. LSD mostly feels like heightened dopaminergic function to me and not something that is truly "psychedelic". Colors are more vibrant, my senses are sharper, sight, sound, taste, smell. You can see gas exchange in plants, your intuition is strong, and I once could see air hitting the wings of a plane as it was landing from a great distance. I do not feel like these were hallucinations per se, but rather my metabolic rate had been raised to a point that I was able to perceive things that normal 2018 stress does not allow. We know that the ergots especially LSD are a mixed bag, but their net effect is usually dopamine agonism. So, yes, I have had cypro cut a "trip" in the traditional sense. But, rather than cutting a trip in the beautiful profound sense, I think it is just blocking the stress response you can get from highly dopaminergic substances. It's kind of like what happens when you have too much coffee without food. I always make sure I have access to orange juice if I know I'm taking LSD, it keeps it from getting too stressful. Just my two cents :)
@haidut
Something that has been confounding me about LSD. I don't feel like the "trip" per se is from serotonin agonism, but rather serotonin antagonism. As Alduous Huxley once said LSD removes the filters of perception or something along those lines and that is my experience. Doesn't make sense to me that serotonin agonism would lead to all of these beautiful/profound experiences. LSD mostly feels like heightened dopaminergic function to me and not something that is truly "psychedelic". Colors are more vibrant, my senses are sharper, sight, sound, taste, smell. You can see gas exchange in plants, your intuition is strong, and I once could see air hitting the wings of a plane as it was landing from a great distance. I do not feel like these were hallucinations per se, but rather my metabolic rate had been raised to a point that I was able to perceive things that normal 2018 stress does not allow. We know that the ergots especially LSD are a mixed bag, but their net effect is usually dopamine agonism. So, yes, I have had cypro cut a "trip" in the traditional sense. But, rather than cutting a trip in the beautiful profound sense, I think it is just blocking the stress response you can get from highly dopaminergic substances. It's kind of like what happens when you have too much coffee without food. I always make sure I have access to orange juice if I know I'm taking LSD, it keeps it from getting too stressful. Just my two cents :)
Are you sure the air hitting the wings wasnt condensation created by the extreme momentary compression of water vapor in the air caused by the deployment of the flaps?
"You can see gas exchange in plants.." cool!
Is what you described from oral or topical?I mentioned this earlier in the thread, but after habituating myself to a couple daily drops of Metergoline I've taken a couple larger doses (8-12 drops) and have definitely experienced a trippiness similar to -but much milder than- using mushrooms or even MDMA (never used LSD so not sure on that). There's a relaxed receptivity, more and "deeper" appreciation of sensations, and a minimal amount of rumination, narration, and/or inner dialogue and thoughts, all combining for a sort of childlike wonder and curiosity. However I didn't experience any visual hallucinations. I do think I'd like to try a very large dose of this sometime though...
I agree.Yah, it was a very emotional experience. I think that humans in the past were likely to have these states of consciousness more frequently, but the chronic environmental stressors we are exposed to probably dwindles a lot of our senses.
OralIs what you described from oral or topical?
----This investigation was designed as a randomized, placebo-controlled, double-masked, crossover study in NZW rabbits with normal intraocular pressure (IOP) to investigate dopaminergic effects on IOP. SKF 38393, a selective D1-receptor agonist, increased, and SDZ PSD-958, a selective D1-receptor antagonist, decreased IOP, respectively. The selective D2-receptor agonist quinpirole decreased IOP, whereas the selective D2 receptor antagonist metoclopramide had no significant effect. Combinations of quinpirole with SDZ PSD-958 decreased IOP in an additive manner. SDZ GLC-756, a mixed D1-receptor antagonist/D2-receptor agonist, decreased IOP in a dose-dependent manner with a maximum effect greater than the maximum effects produced either by the D1-receptor antagonist SDZ PSD-958 and the D2-receptor agonist quinpirole. The effect of SDZ GLC-756 could only be partially blocked by the selective D2-receptor antagonist metoclopramide suggesting that both D1-receptor blockade and D2-receptor stimulation participate in its IOP-lowering effect. Tonography suggests that SDZ GLC-756 has no significant effect on outflow facility. Furthermore, the results suggest that both D1 and D2 receptors each play an independent role in the regulation of IOP in rabbits. Thus, simultaneous blockade of D1 receptors and stimulation of D2 receptors may provide a new pharmacological approach for the treatment of ocular hypertension frequently associated with glaucoma.
Effects of dopamine D-1 and D-2 receptors on intraocular pressure in conscious rabbits | Request PDF. Available from: https://www.researchgate.net/public..._on_intraocular_pressure_in_conscious_rabbits [accessed Aug 26 2018].
The data presented suggest a role for 5-HT in the control of IOP. Previously demonstrated receptors on the iris-ciliary body and the effect of the 5-HT1-agonist 5-CT suggest that the rise in IOP may be caused partly or entirely by an increase in aqueous secretion mediated by 5-HT1-like receptors. Whether or not 5-HT has a role in altering aqueous outflow resistance remains to be seen. An effect of serotonin on other aspects of aqueous dynamics or on the extraocular muscles to cause a change in IOP cannot be excluded.
Topical application of serotonin or the 5-HTX-agonist 5-CT intraocular pressure in rabbits | Request PDF. Available from: https://www.researchgate.net/public...-agonist_5-CT_intraocular_pressure_in_rabbits [accessed Aug 26 2018].
Abstract
Published investigations of serotonin-1A (5-hydroxytryptamine1A; 5-HT1A) receptor agonists and serotonin-2A (5-hydroxytryptamine2A; 5-HT2A) receptor antagonists in nonprimate species provide conflicting results with regard to their intraocular pressure-lowering efficacy. Thus, their therapeutic utility in the treatment of human glaucoma has been confusing. We evaluated the effect of selected 5-HT1A agonists and 5-HT2A receptor antagonists on intraocular pressure in a nonhuman primate model, the conscious cynomolgus monkey with laser-induced ocular hypertension. Neither selective 5-HT1A agonists [e.g., R-8-hydroxy-2-(di-n-propylamino)tetralin and flesinoxan] nor selective 5-HT2 receptor antagonists [e.g., R-(+)-alpha-(2,3-dimethoxyphenyl)-1-[2-(4-fluorophenyl)ethyl]-4-piperidinemethanol (M-100907) and 6-chloro-2,3-dihydro-5-methyl-N-[6-[(2-methyl-3-pyridinyl)oxy]-3-pyridinyl]-1H-indole-1-carboxamide (SB-242084)] lowered intraocular pressure in the primate model following topical ocular administration. However, compounds that function as agonists at both the 5-HT1A and 5-HT2 receptors were found to effectively lower intraocular pressure in the model: 5-hydroxy-alpha-methyltryptamine, 5-methoxy-alpha-methyltryptamine, 5-hydroxy-N,N-dimethyltryptamine (bufotenine), and 5-methoxy-N,N-dimethyltryptamine. Furthermore, the selective 5-HT2 receptor agonist R-(-)-1-(4-iodo-2,5-dimethoxyphenyl)-2-aminopropane lowered intraocular pressure in the primate model, demonstrating a pharmacological response associated with activation of the 5-HT2 receptor. These observations suggest that compounds that function as efficient agonists at 5-HT2 receptors should be considered as potential agents for the control of intraocular pressure in the treatment of ocular hypertension and glaucoma in humans.