SSRI and Anti-Cholinergics

[apothecary]

Hmmm. Help my ignorance here guys

My understanding of anti cholinergics is that they block the flow of acetylcholine and thus fuck with the way serotonin/dopamine is distributed or somesuch.

I believe benztropine (synthetic tropine) is/was used to fight Parkinsonism.

So, if I were to partake of an SSRI, such as say, sceletium and then smoke some Datura flower, would this change the effect? I know from personal experience there is a definite difference in the combination compared to just the SSRI or just the Datura, but I'm curious from a brain chemistry perspective.

Would inhibiting serotonin reuptake for even a short while reduce the harmful effects of cholinoceptor antagonists such as scopolamine or atropine?

Also, random note of curiosity, is there such thing as a Dopamine Reuptake Inhibitor (selective or not)?

[Torsten]

Originally posted by apothecary:

Also, random note of curiosity, is there such thing as a Dopamine Reuptake Inhibitor (selective or not)?

Yes, SDRIs are used as antidepressants and for increasing libido. There are also selective norepinephrine reuptake inhibitors, although these are usually used in conjunction with SSRIs.

as for the first part of your post I am very curious, but have no idea.

[Salviador]

Acetylcholine antagonists are nicotine, datura, and most nerve gas/ fly spray. Acetylcholine has to do with our reflexes and central nervous system. Maybe thats why datura is less of a hallucinogen and more of a deliriant. Serotonin and dopamine involve most of our favourite substances

I think that the two are unrelated as far as any brain function can be unrelated to another. acetylcholine is a neurotransmitter just like serotonin and dopamine. Each has a relatively separate function. I havent any artiles to back this up tho

interesting point apo with benztropine, because SSRI's ie mdma also treat parkinsons, thus there could be some sort of link there.

My totally unsubstantiated guess would be that serotonin would be a good conductor for information sent to acetylcholine receptors to send to the muscles to tell them to tense up. Relating this to your question about the mixture of the two might mean trip that where you were more conscious of the delirium maybe?

Hypothetically if you were to partake, then i think it would fuck you up regardless

[Benzito]

Wellbutrin, or Zyban, is believed to be a Dopamine Re-uptake Inhibitor. I've got one spare tab, if you're interested Apo? I found it in the drawer, after I finished my course of Zyban. (Sorry, there aren't any more)

[apothecary]

Thanks Benz, but I'll be right!

I was kind of hoping a brain like Tryptameanie or tantra would have something to say on this one.

[oxydiser]

 

quote:

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My understanding of anti cholinergics is that they block the flow of acetylcholine and thus fuck with the way serotonin/dopamine is distributed or somesuch.

 

I believe benztropine (synthetic tropine) is/was used to fight Parkinsonism.

 

---

True, anticholinergics (atropine, scopolamine) block the action of acetylcholine on parasympathetic muscarinic receptors which account for all of the effects following administration, which some people may be familiar with - inhibition of secretions, modest increase in heart rate, dilated pupils, mild decrease in GI motility and of course the CNS excitation effects of restlessness, agitation and delerium. Anticholinergics also affect the extrapyramidal system, reducing the involuntary movement and rigidity of patients with Parkinson's.

Up until levodopa was discovered in the 1960s, the anticholinergics were the main form of treatment for Parkinson's. They are effective because acetylcholine receptors have an excitatory effect, which is opposite to that of dopamine, on the neurons involved in Parkinson's. Suppression of the excitatory effects (using anticholinergics) partly makes up for the lack of dopamine that is characteristic of Parkinson's.

As such, anticholinergics are used in Parkinson's as a physiological antagonists - the beneficial effects occur because anticholinergic are used to treat the symptoms rather than the underlying cause.

 

quote:

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So, if I were to partake of an SSRI, such as say, sceletium and then smoke some Datura flower, would this change the effect? I know from personal experience there is a definite difference in the combination compared to just the SSRI or just the Datura, but I'm curious from a brain chemistry perspective.

 

Would inhibiting serotonin reuptake for even a short while reduce the harmful effects of cholinoceptor antagonists such as scopolamine or atropine?

---

Vary interesting questions apoth, although I am no neuroscientist I am leaning strongly towards what Salviador has said and I would also suggest that the combination of an SSRI would not interact with anticholinergics with regard to brain chemistry. Care to elaborate more on the difference between sceletium, datura and sceletium+datura?

[apothecary]

I'd love to. In fact, a batch of some experimental material from a good friend (in the form of brug leaf and flower;)) has arrived to tide me over until my Datura recovers.

So I can set out a few decent experiments and get back to you. My current experience is that the effect is much "nicer" that is to say lacking some of the raw psychological power I feel imbibed with sometimes with a much more cannabisy nice feeling replacing it.

If you have any good ideas for experimentation, post here and I'll give it a shot.

EDIT: Also , thanks for shedding light on the Parkinsons/benzitropine interaction, definitely fixed some misconceptions I had

[ 28. September 2005, 06:50: Message edited by: apothecary ]

[indigo264nm]

Just out of curiousity, what dosage levels are we talking about???

There is a very big difference in the subtle tropane alteration and the full blown delerium, so what range have you been dabbling with???

[hoodoo]

To notes:

First:

I have begun to try "Atrovent" (ipratropium bromide) is a synthetic atropine nasal inhaler used for allergies. ie. Might have nothing to do with what you are all talking about.

Secondly, here is interesting article which might help explain why some people more than others can have long term depression after taking ecstacy and also why some people do not respond to SSRIs yet otehrs do:

Depression, Genetics and the Drug Ecstasy

April - 2005

By Harold J. DeMonaco, M.S.

Massachusetts General Hospital

Ecstasy, a popular street drug used to create a sense of euphoria, has unexpectedly given scientists a better understanding of how much genetics can influence our reaction to medications.

Although news reports usually focus on the dangers of Ecstasy overdose, the amphetamine derivative is highly addictive and has other problems associated with long-term use, such as depression. Some studies report up to a 33% incidence of depression in long term users of Ecstasy. Although the way that the drug creates a euphoric feeling has been known for some time, we have not known why some users develop severe depression. Genetics may be the answer.

Ecstasy creates a euphoric sensation by changing the concentration of a chemical messenger in the brain called serotonin. Serotonin is an important brain chemical involved in the control of mood and emotion. Many antidepressant drugs, especially the SSRIs, or selective serotonin reuptake inhibitors (including Lexapro, Prozac, Zoloft and others), take advantage of serotonin's action in the brain to treat the disorder. They increase the amount of serotonin action in the brain by blocking the uptake and storage of serotonin back into brain cells. This is a slow, controlled process that keeps more serotonin molecules free to act on mood stimulation receptors.

Ecstasy not only blocks this uptake and storage, but it causes a massive release of serotonin that has built up inside storage sites. This massive release of serotonin is responsible for the short-lived, euphoric effects of the drug.

The serotonin storage system is different from person to person, in large part based upon the type of serotonin transporter genes that you inherited. Researchers have identified what they call a long and a short transporter gene. Because one transporter gene is inherited from each parent, you could have two long forms, two short forms or one of each, depending upon which ones ended up in the sperm and the egg that got you started.

To see how the different transporter genes correlate with depression in Ecstasy users, researchers recently studied the frequency of depression among 66 heavy users of Ecstasy, 30 users of marijuana and 28 people who did not use any drugs. The participants completed two standard questionnaires for diagnosing depression. Then, the researchers compared the depression test results with the patterns of serotonin transporter genes. Here’s what they found:

Heavy users of Ecstasy who had the two short transporter genes were more likely to have depression than those with either two long genes or one long and one short gene.

People who had two short versions of the transporter gene who do not use Ecstasy did not have any increased risk of depression.

Studies looking at people with depression who have less than optimal responses to SSRI drugs show a similar pattern. They are more likely to have inherited two short serotonin transporter genes rather than two longs or one of each.

Although genetic testing for the transporter genes is only a research tool at the moment, the U.S. Food and Drug Administration recently approved the first laboratory test kit (called Amplichip Cytochrome P450 Genotyping Test) that allows physicians to determine how well a person metabolizes certain drugs used for heart problems, cancer and depression. Although it is unlikely that we will ever see a test kit for Ecstasy, genetic testing to predict how effective a drug will be for a specific patient will be more common in the next few years.

.................................................. .......

Harold J. DeMonaco, M.S., is senior clinical associate in the Decision Support and Quality Management Unit at the Massachusetts General Hospital and is currently a Visiting Scholar at the MIT Sloan School of Management. He is author of over 20 publications in the pharmacy and medical literature and routinely reviews manuscript submissions for eight medical journals.

[blog]

Benzito:

Wellbutrin, or Zyban, is believed to be a Dopamine Re-uptake Inhibitor.

Yeah which is why schizophrenics are not prescribed zyban. Theory being they have too much dopamine or too many dopamine receptors. Though I don't think anyone really knows for sure.

Effexor is also a dopamine reuptake inhibitor at high dosages of 400-450mg per day

[ 29. September 2005, 04:54: Message edited by: blog ]