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  • N&PD Moderators: Skorpio

getting neurotransmitters to cross the bbb

Elaborate.

What kind of neurotransmitters are you trying to induce?
 
Even if you could, this will still not work too well because pharmacology isn't a matter of "too much" or "too little" serotonin. It is much more complicated and in any case, too much of a given transmitter is just as bad as too little.
 
there'll be some mad way to do it for every inactive (in that sense) chemical with another inactive chemical.

remember watching on a ray mears prog once that his mate was testing mushrooms for some reason or another. prolly edibility. and he had some kind of mushroom, was fine, then went for a beer after work. started tripping out and stuff "everything went blue and i felt extremely light headed". passed out.
medics came and he was fine in the end.

but yea, all it took was a beer. like a couple of the chemicals shulgin found no?
can't remember which ones
 
^ Are you talking about the "tomso effect" thing?

Btw, I forgot to mention that MAOIs would be a horrible idea - they would cause whatever neurotransmitter you're taking orally to accumilate in your blood without crossing the BBB, causing all sorts of problems, especially with the circulatory system.

This is actually why levodopa should only be taken with carbidopa, otherwise a lot of it gets turned into Dopamine in the blood before reaching the brain, which in turn is converted into epinephrine, causing all sorts of disgusting peripheral effects.

(for the sake of clarity: carbidopa does not increase levodopa's BBB permiability, it just peripherally inhibits the enzyme that turns levodopa into dopamine, if I understand correctly)
 
Maybe it was a Coprine-containing mushroom such as an inky cap. These contain an "antabuse"-like drug as an active alkaloid and it obviously does not mix with EtOH.

monstanoodle said:
there'll be some mad way to do it for every inactive (in that sense) chemical with another inactive chemical.

remember watching on a ray mears prog once that his mate was testing mushrooms for some reason or another. prolly edibility. and he had some kind of mushroom, was fine, then went for a beer after work. started tripping out and stuff "everything went blue and i felt extremely light headed". passed out.
medics came and he was fine in the end.

but yea, all it took was a beer. like a couple of the chemicals shulgin found no?
can't remember which ones
Click to expand...
 
Jamshyd said:
^ Are you talking about the "tomso effect" thing?

Btw, I forgot to mention that MAOIs would be a horrible idea - they would cause whatever neurotransmitter you're taking orally to accumilate in your blood without crossing the BBB, causing all sorts of problems, especially with the circulatory system.

This is actually why levodopa should only be taken with carbidopa, otherwise a lot of it gets turned into Dopamine in the blood before reaching the brain, which in turn is converted into epinephrine, causing all sorts of disgusting peripheral effects.

(for the sake of clarity: carbidopa does not increase levodopa's BBB permiability, it just peripherally inhibits the enzyme that turns levodopa into dopamine, if I understand correctly)
Click to expand...

correct as it is a peripheral decarboxylase inhibitor (PDI) meaning it prevents the conversion of L-Dopa to Dopamine peripherally, but since Carbidopa and other PDIs can NOT cross the BBB they do NOT interfere with conversion of L-Dopa past the BBB where the conversion is desired
 
L-Dopa (the precursor to dopamine) is NOT a good thing to mess with. Its given to people with parkinson's disease to combat low levels of dopamine in their substantia nigra. It is possible if you start messing with it in an uncontrolled manner that you will develop schizophrenic like symptoms due to an overabudance of dopamine. Remember, more neurotransmitters does not necessarily equal pleasurable symptoms.
 
samadhi_smiles said:
L-Dopa (the precursor to dopamine) is NOT a good thing to mess with. Its given to people with parkinson's disease to combat low levels of dopamine in their substantia nigra. It is possible if you start messing with it in an uncontrolled manner that you will develop schizophrenic like symptoms due to an overabudance of dopamine. Remember, more neurotransmitters does not necessarily equal pleasurable symptoms.
Click to expand...

Are you aware if this has been used successfully as an experimental model?
 
samadhi_smiles said:
L-Dopa (the precursor to dopamine) is NOT a good thing to mess with. Its given to people with parkinson's disease to combat low levels of dopamine in their substantia nigra. It is possible if you start messing with it in an uncontrolled manner that you will develop schizophrenic like symptoms due to an overabudance of dopamine. Remember, more neurotransmitters does not necessarily equal pleasurable symptoms.
Click to expand...
Mucuna Pruriens seems like a great alternative, with neuroprotective properties



Neuroprotective effects of the antiparkinson drug Mucuna pruriens

Mucuna pruriens possesses significantly higher antiparkinson activity compared with levodopa in the 6-hydroxydopamine (6-OHDA) lesioned rat model of Parkinson's disease. The present study evaluated the neurorestorative effect of Mucuna pruriens cotyledon powder on the nigrostriatal tract of 6-OHDA lesioned rats. Mucuna pruriens cotyledon powder significantly increased the brain mitochondrial complex-I activity but did not affect the total monoamine oxidase activity (in vitro). Unlike synthetic levodopa treatment, Mucuna pruriens cotyledon powder treatment significantly restored the endogenous levodopa, dopamine, norepinephrine and serotonin content in the substantia nigra. Nicotine adenine dinucleotide (NADH) and coenzyme Q-10, that are shown to have a therapeutic benefit in Parkinson's disease, were present in the Mucuna pruriens cotyledon powder. Earlier studies showed that Mucuna pruriens treatment controls the symptoms of Parkinson's disease. This additional finding of a neurorestorative benefit by Mucuna pruriens cotyledon powder on the degenerating dopaminergic neurons in the substantia nigra may be due to increased complex-I activity and the presence of NADH and coenzyme Q-10. Copyright (c) 2004 John Wiley & Sons, Ltd.
 
^ Well, I don't know what part of repetative shaking, nausea, anxiety, high blood pressure, and delusions exactly constitutes as "nuroprotective"?

That was my experience with M. Pruriens, at least.

I know it contains Nicotine and buotenin besides l-dopa...
 
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