DOR1/bivalent DOR agonist speedballs anyone?

[Limpet_Chicken]

Alright...this is a bit...different, normally I'd put a question like this in OD.

However, this is of a sufficiently different kind of drug to be rather far out of the sphere of the usual experience range in OD. So, here it is going.

What is people's take here on the thought of a speedball, but rather than using a conventional DA/NA releaser, DARI or releaser-reuptake inhibitor, for the stimulant portion of a speedball, use of a delta opioid agonist? the one, or ligand I am as certain as I can be without setting up to perform a radioligand binding assay, that I have in mind is alpha-chloromorphide, which, since at the highest dose levels tried, although not at lower ones, there was mild clonus of the hands and feet, fingers. Nothing particularly threatening but I wouldn't push it higher than I did try, at a couple of hundred mg (tolerant to MOR agonists, not sure if that provides any crosstolerance with DOR ligands)

I am pretty confident that it is at least a DOR1 agonist, due to the clonus at high levels, but have no way of determining if it may be a DOR2 agonist also.
I'll test that out as soon as I can afford to, although I'm pretty snowed under at the moment. And have nothing to spare, money-wise, since I do have to eat something that isn't spent on the ol' skunk-works. Thankfully I don't tend to eat all that much anyway But this one has me curious, as it is SO like a psychostimulant, but coming from morphine, as a backbone and such a modest structural modification, I am pretty sure that it is an opioid of SOME variety. It does, after all relieve MOR agonist (morphine, oxy, dipropionyl or dibenzoylmorphine esters, opium, codeine, DHC. ) withdrawals

forgot to specify-the opiate(s) I had in mind are either dipropionylmorphine, desomorphine-D, or both.

 

[serotonin2A]

DOR activation can lead to convulsions but does not produce psychostimulant effects. Its possible you are detecting some type of off-target effect.

 

[Limpet_Chicken]

Seems rather strange given the pharmacology of DOR, in that they are highly expressed in the NAC, and activation results in DA release in striatum/NAC, and there are some other effects I'm still reading about on monoamine release, NMDA/possibly AMPAr modulation of DOR agonist ligands. Seemingly DOR agonists significantly increase DA efflux in response to DAT blockade or DA release, although not to DA agonists.

Haven't yet tried combining a serious dose of selective reuptake inhibitor vs selective releasers and D3, D1, D4 agonists with the alpha-chloromorphide. Surprising it isn't a more popular clandestine target, all things considered, because whilst it doesn't feel like a particularly strongly sedating type opioid, it nevertheless combines enough..err..well I'd say conventional opioid activity, I'm just not quite sure. Do delta (that is to say, selective DOR1 or DOR2 agonists, such as for instance some of the peptidic compounds typically used to label delta opioid receptors, or the likes of the SNC- and TAN- family nonpeptides produce a nod-like effect in human beings?)

Any idea what the off-target, if this proves not the case, effects might be?

I do take a DA agonist (pramipexole), but the book I'm currently reading specifies that DOR agonists do not complement DA agonists.
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