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The Large and Nifty Not-quite-advanced Drug Chemistry, Pharmacology and More Thread

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It's not that counter-intuitive: methylphenidate appears neuroprotective insofar as it limits methamphetamine's efficacy (and indeed, they examined proposed mechanisms at DAT and VMAT2). Less intuitive, however, are the proposed effects on genetic expression related to vesicular formation. It's here that I think my knowledge incomplete.

ebola
 
Have any other "dragon-fly" compounds been investigate? Chloro, fluro, ethyl etc?
If not, whats the reason for this?

also, has "bromo-dfly"s phenthylamine analogue been looked into? Aside from 2C-B-FLY.
 
Hyperthesis, epinephrine doesn't cross the blood-brain barrier, so it is not directly psychoactive. It has powerful effects on the peripheral/autonomic nervous sytems, which can influence mental state secondarily. Also, you're right about glucose influencing moods, but germanely to this discussion, it only influences mood below the normal/necessarylevel, but not above it. Hyperglycemia is not acutely psychoactive and is not a performance enhancer to any great extent.

Neurotoxicity of amphetamine, methamphetamine, MDMA, and MDA at anything less than heroic doses has not been shown in humans to the best of my knowledge. It has been shown in rodent models for sure for many of these, but also usually with extreme doses, multiple acute doses, or chronically.
 
Neurotoxicity of amphetamine, methamphetamine, MDMA, and MDA at anything less than heroic doses has not been shown in humans to the best of my knowledge.
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Since it's extremely difficult to simulate chronic, low-level dosing, it's extremely difficult to demonstrate neurotoxicity directly generalizable to humans. It's for this reason that it was difficult to establish amphetamine as relatively benign in low doses and methamphetamine neurotoxic at commonly encountered recreational doses (and this is why the conclusions about entactogens remains unclear).

ebola

edit: upon giving your post a more thorough reading, you appear to know all this.
 
nuke said:
In rats it doesn't take much, I think 1mg/kg

http://www.ncbi.nlm.nih.gov/pubmed/12452543
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With a cursory look, 1 mg / kg was a dose used to measure long-term behavioral consequences from a prior neurotoxic dose (5 mg / kg, 3 times, separated by 3 hours). This study doesn't seem to be the best from which to generalize neurotoxicity (particularly given their operationalization of neurotoxicity). Nonetheless, people do get that tweaked in a sitting sometimes (you crazy motherfuckers :p).

ebola
 
Ah, thanks for going over the methods for me then. Usually the dose for neurotoxicity is 5mg/kg-10mg/kg it seems like
 
Should we expect the threshold for neurotoxicity to scale with the threshold for efficacy? In lieu of more specific indicators, I guess so. Now, the question is, is this the threshold for neurotoxicity to be set at clear physiological damage in an individual, clear enduring behavioral deficits in an individual, or statistical trends discernible in populations exposed to neurotoxic conditions?

ebola
 
ebola? said:
Should we expect the threshold for neurotoxicity to scale with the threshold for efficacy? In lieu of more specific indicators, I guess so.
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Unfortunately, the answer could be no.

Baggott and Mendelson said:
In general, smaller species excrete drugs more quickly and form metabolites in greater amounts than larger species. This is due to many factors including the proportionally larger livers and kidneys and faster blood circulation times in smaller mammals (Lin 1998; Mordenti,1989). As a result of such factors, the time it takes to lower the plasma levels of MDMA by half is about 1.5 hours in a rat (Cho, 1990) and about 8 hours in a human (Mas, 1999). This suggests that small species may require higher doses to achieve drug exposures comparable to those seen in larger species.
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So 5 mg/kg in rats / 6.2 = 0.8 mg/kg for surface area, then taking blood circulation times into account 0.8 mg/kg / (8/1.5) = 0.15 mg/kg for humans, that's only 10.5 mg in 70 kg person. This estimate might be low considering there is overlap between the body surface area conversion factor and the blood circulation time conversion factor.

Also, it is very possible that dextroamphetamine is more harmful to dopaminergic neurons than methamphetamine is, as it activates these neurons in more parts of the brain. A friend of mine ran into a toxicity study that found dextroamphetamine caused dopamine deficits in three regions of the brain compared to methamphetamine causing deficits in one region.
 
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For what purpose? Obviously not drug synthesis, that's against the rules.
 
Munroe said:
Have any other "dragon-fly" compounds been investigate? Chloro, fluro, ethyl etc?
If not, whats the reason for this?

also, has "dfly"s phenthylamine analogues been looked into? Aside from 2C-B-FLY.
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Quoted cause I managed to post at an inopportune moment
 
which receptors are responsible for the release of chemicals such as serotonin dopamine, norepinephrine, and so on if so inclined, thank you in advance!

-KK

Also one can exclude the 5ht receptors as i have found that they release a broad list of chemicals, and furthermore if this is a task in it's own to name the receptors because alot of receptors are responsible for these chemical releases not just one i apologize but for example what receptor is responsible for dopaminergic activity while on opiates, thanks.
 
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I just want to confirm that what I think will happen will happen before I do it:

If one slowly adds a solution of hydrochloric acid (pool cleaner) to aMT freebase until all the aMT is dissolved, then evaporates off the water, what is left is aMT HCl, correct? There's no excess HCl or need to calculate moles because excess HCl evaporates into the atmosphere, right?
 
Which drugs cause a peripheral blockade of adrenoreceptors?
 
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