CNS/PNS Ratios

[Thyme]

Okay, lets see if I can word this right. Im really into pharmacology and stuff, but Im young and havent studied it in school (in depth) yet so my jargon might be off

Im interested in knowing the cns : pns stimulation ratios of stims such as amph, meth, and ephedrine
Also the ratios of cns (and pns) of the drugs in relation to each other

heres a very basic and stupid example:

~~~

like, 100mg ephedrine has the same cns effect as 50mg amph. yet the pns of ephedrine would be 4x as strong

or

for every 10mg ephedrine you get 1 cns but 4 pns, while 5mg amph gives 1 cns but only 2 pns

~~~

See what I mean, I dont even know what unit of measurement to use in regards to pns or cns stimulation, or if there even is one....let alone the ratios of ANY drugs.

I would totally use the search engine or google, IF I EVEN KNEW WHAT WORDS TO USE/LOOK FOR

help a nooblet out?

if you could direct me to a site or quickly type out something that would help me understand, I would greatly appreciate it

thanks,

Thyme

 

[Thyme]

oh and I realize this isnt exactly advanced stuff, but I figured you guys would have a better idea of what Im talking about

sorry if I posted in the wrong place

 

[ebola?]

I'm pretty sure that this type of quantitative comparison/contrast would be impossible.

like, 100mg ephedrine has the same cns effect as 50mg amph.

I wish, lawl. Maybe at the NE transporter.

ebola

 

[Thyme]

I'm pretty sure that this type of quantitative comparison/contrast would be impossible.

hmm, alright.
maybe some anecdotal, un-exact, vague evidence then..

Can anyone here say that (x)mg of Stim(A) gave similar cns stimulation as (x)mg of Stim(B) (and give similar info. for pns stimulation)?

Hmm, maybe I should post this somewhere else...conduct a little poll-like study... hell Id do it myself if I had a reliable source of unadulterated (meth)amphetamine at this point in my life

I guess it couldnt hurt to leave this here for a day or two..as long as the mods are fine with it

Oh hey if a mod sees this and wants to close the thread or something Please dont delete my posts (at least not right away) cause since I havent studied this shit too much it takes me like a fucking half hour to write these posts, trying to figure out how to word them without sounding like a fucking retard, so Id wanna copy/paste at last some of the stuff I wrote

I wish, lawl

haha dont we all man

 

[negrogesic]

There are no true ratios of CNS/PNS activity. Even the most centrally acting stimulant (d-methamphetamine) has PNS effects......

 

[ebola?]

Can anyone here say that (x)mg of Stim(A) gave similar cns stimulation as (x)mg of Stim(B) (and give similar info. for pns stimulation)?

Oh, I see how this would be possible in principle. However, it wouldn't make sense to give a ratio of PNS to CNS activity within a given drug. They're just two qualitatively different domains. It would be like saying, when you take a given drug, the ratio of liver effects to kidney effects is x:y.

So we can get rough ideas of what is more selective for central activity, but nothing strictly quantitative.

Even the most centrally acting stimulant (d-methamphetamine)

It really hasn't been unseated by something more exotic, like desoxypipradrol?

ebola

 

[hamhurricane]

^^^
im pretty certain it has been surpassed dozens if not hundreds of times. amfonelic acid comes to mind, fencamfamine, most likely desoxypipradrol as well - but this returns one to the original question of can these ratios be measured (aside from subjective bioassays) the speed and ease with which it crosses the BBB is an import factor, as well as its affinity for receptor subtypes located predominantly in the PNS - im trying to remember but there was some tryptamine which was totally non-recreational but had a high affinity for intestinal 5HT receptors (it was relatively obscure not an RC like 5-MeO-aMT)

 

[Black]

the octanol/water coefficient is commonly used to measure lipophilicity of compounds and as the bbb is a 'lipid barrier' it is often proportional (more or less) to the amount that can get into the cns. very hydrophilic compounds cannot cross the bbb.

 

[seep]

the octanol/water coefficient is commonly used to measure lipophilicity of compounds and as the bbb is a 'lipid barrier' it is often proportional (more or less) to the amount that can get into the cns. very hydrophilic compounds cannot cross the bbb.

With exceptions. Like levodopa (LogP -0.23) crosses passively but dopamine (LogP 0.12) doesn't.

Glucose gets in there too, but it has ferrymen.

 

[Black]

sure, i just posted that to give the op a starting point for further research. with ephedrine -> amphetamine -> methamp is works that way.

 

[Lupus]

There's no way to measure this with ancedotes.

With traditional amphetamines after even a short time period of use its modulation of tyrosine hydroxylase could cause a permanent effect on perceptions of dopagenic stims. For positive or negative, we really dont know.

Dexedrine is my preferred stim because the quality of methamp and its legal status are far too much of a hurdle to make it worthwhile to do more than dabble with it. Besides, its just too much of a mental strain for me. (the ever looming threat of mania and psychosis)

 

[nods]

DESOXYN GRADUMETS SR15mg pre2000, smooth and lasted all day

 

[Thyme]

*snip* but this returns one to the original question of can these ratios be measured (aside from subjective bioassays) the speed and ease with which it crosses the BBB is an import factor, as well as its affinity for receptor subtypes located predominantly in the PNS - im trying to remember but there was some tryptamine which was totally non-recreational but had a high affinity for intestinal 5HT receptors (it was relatively obscure not an RC like 5-MeO-aMT)

Does anyone have knowledge of the receptor affinity and etc mentioned here? Have there been any studies done comparing stim(a) to stim(b) with regards to this? Is it cool to bump my old thread since the original inquiry is still relatively unsolved?

Thank you. I appreciate your time, mad scientists of ADD

 

[sekio]

Oh, I see how this would be possible in principle. However, it wouldn't make sense to give a ratio of PNS to CNS activity within a given drug. They're just two qualitatively different domains. It would be like saying, when you take a given drug, the ratio of liver effects to kidney effects is x:y.

Seeing as most stimulants act on transporters (DAT, SERT, NET) and not directly on receptors, there's no difference between "central" transporters and perhipheral ones as there sometimes is with e.g. dopamine or 5-ht receptors.

I think the best indicator of strong central stimulant effects is a high DA release/reuptake inh. capacity combined with some NE release/reuptake. "Pure" norepinephrine releasers are more often deconcestants or "perhipheral" stimulants (see: l-meth, pseudepehedrine). Stims that have affinity for direct adrenergic receptors are also considered to be "tweaky" and peripheral (see also: ephedrine & other beta-subst phens)

 

[ebola?]

Seeing as most stimulants act on transporters (DAT, SERT, NET) and not directly on receptors, there's no difference between "central" transporters and perhipheral ones as there sometimes is with e.g. dopamine or 5-ht receptors.

Mmmm...from the big and dandy thread, didn't it come out that the involvement of PKC differs between monoamine transporters in the gut versus the brain?

"Pure" norepinephrine releasers are more often deconcestants or "perhipheral" stimulants (see: l-meth, pseudepehedrine).

What about ethcathinone (which has a good ratio of PNS to CNS effects and negligible direct adrenergic agnoism but high selectivity for NE)?

ebola

 

[sekio]

Ethcathinone has cathinone as a 1' metabolite, which is a dopamine releaser, so it's not as "pure" a NE releaser as you'd think.

I haven't really been reading the B&Dbut to my knowledge any subtype differences in transporters is unlikely to be as wide as for direct receptors. I'm think ing of e.g. the 14 odd distinct types of serotonin receptors versus the 2 transporter protiens that carry it (SERT and VMAT). Don't think SERT/VMAT have multiple protiens.

 

[ebola?]

Ethcathinone has cathinone as a 1' metabolite, which is a dopamine releaser, so it's not as "pure" a NE releaser as you'd think.

Working by rough analogy, isn't the amount of methamphetamine catabolized to amphetamine around 7 percent of that ingested? The time-course and intensity of ethcathinone's effects suggest action as a prodrug for cathinone to play a relatively minor role in the drug's effects.

I'm think ing of e.g. the 14 odd distinct types of serotonin receptors versus the 2 transporter protiens that carry it (SERT and VMAT). Don't think SERT/VMAT have multiple protiens.

Very good point.

ebola

 

[Thyme]

Working by rough analogy, isn't the amount of methamphetamine catabolized to amphetamine around 7 percent of that ingested? *snip*

Etymologically, ethylamphetamine -> amphetamine sounds like it'd make a better roughish comparison imo
Though, is that percentage even known?

If not, this article
http://onlinelibrary.wiley.com/doi/10.1111/j.2042-7158.1969.tb08366.x/abstract
could possibly be used to calculate it, if someone knows how to convert urinary amphetamine levels into how much was in his system beforehand. Seems like it would be tricky though, based on what the very article addresses itself

I dunno. I cant even see past the abstract.