Cocaine cocaine deliriant effects???

[cgdon]

can someone explain to me why cocaine gives me a nasty experiment? I feel as if I am under the influence of delirium.

I bought some cocaine and tested it with reagent test and then washed it twice with acetone. yes I lost a bit of weight.
the powder was odorless and beautifully white after washing. I placed a small line as a tester and felt some effect, but immediately followed by a nasty high that was very similar to delirium. I had fears about bad things and I saw flashes in the corner of my eye.
exactly as if I felt snakes in space.
this effect lasted 30-40 minutes and then disappeared.

reagent testing showed it was cocaine with an anesthetic such as lidocaine.

was this cocaine contaminated with bad procaine? was this cocaine contaminated with tropane akaloids?

I read that cocaine akaloids come from tropane akaloids such as deliriants?

 

[RJMac]

Sounds like intense anxiety.

 

[bigjackaal96]

Because very high D2 levels cause ACH levels to drop enough that you M1 antagonism & NE/NET hyperactivity. You literally had a mini DPH trip without the antihistamine effects. D2/DNRI Stimulants are Deliriants since I'm sure most of the even have direct M1 antagonism like Ritalin & It XR versions which in the 60s matched the 2nd most potent TCA. The only reason It not a issue Is because the Dopamine activity hides the body load from low ACH.

Anticholinergic's like Trihexyphenidyl & Scoplamine avoid the NE/NET hyperactivity because M1 antagonism Is also potent CNS depressent.

 

[4DQSAR]

Trihexyphenidyl & Scoplamine have much longer durations of action, do they not?

I've read lidocaine can produce psychosis and you did mention that your test revelaled lidocaine or similar.

None of us were there, don't know the source of the material or actually experienced the adverse effects so it's all guesswork.

I'm just thinking that if a test revealed an impurity, maybe look at what that impurity could do.

 

[bigjackaal96]

Trihexyphenidyl & Scoplamine have much longer durations of action, do they not?

I was comparing effects. M1 blocking Deliriants are ironiclly much safer because they aren't stressful on D2 receptors/neurons.

I literally got Deliriant effects from Alcohol where I went to bed without getting changed, I couldn't even walk the dog without It being a total blur. Atypical Deliriants are just as potent as DPH/Datura but they lack the dysphoric effects.

 

[4DQSAR]

Well atypical or idiopathic?

You may GUESS what underlying biochemistry is taking place, but you don't know.

I stuck to what was said, and even then only tacitly suggested a possible reason.

 

[someguyontheinternet]

Because very high D2 levels cause ACH levels to drop enough that you M1 antagonism & NE/NET hyperactivity. You literally had a mini DPH trip without the antihistamine effects. D2/DNRI Stimulants are Deliriants since I'm sure most of the even have direct M1 antagonism like Ritalin & It XR versions which in the 60s matched the 2nd most potent TCA. The only reason It not a issue Is because the Dopamine activity hides the body load from low ACH.

Anticholinergic's like Trihexyphenidyl & Scoplamine avoid the NE/NET hyperactivity because M1 antagonism Is also potent CNS depressent.

By what pathway does D2 activation cause a decrease in ACH and in which tissue or brain region does ACH decrease?

 

[someguyontheinternet]

D2 receptor antagonises ACH in the striatum which then leads to centrally low ACH. But what odd Is how the brain seems never display the typical traits of M1 antagonism when D2 is high.

What do you mean by the D2 receptor antagonizes ACH? You're talking about the inhibitory indirect BG circuit?

 

[someguyontheinternet]

It stops ACH form flowing in the area where Dopamine neurons live. It the same reason why Central Dopamine hyperactivity from NMDA hypoactivity in Autism/SZ. Causes very low CNS ACH mainly M1 receptors without any issues.

It more like competitive antagonism from D2. But D2 Is a far better exictory centre than ACH & NMDA will ever be. I view in psychosis 5HT2A mutates to respond to D1/D2 and AMPA hence why the effects are atypical.

Okay now I just think you're stringing words together without understanding what they mean. Do you have any citations at all that can back up your claims